quantitative synthetic human immunodeficiency virus 1 hiv 1 rna  (ATCC)


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    ATCC quantitative synthetic human immunodeficiency virus 1 hiv 1 rna
    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) <t>HIV-1</t> proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.
    Quantitative Synthetic Human Immunodeficiency Virus 1 Hiv 1 Rna, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/quantitative synthetic human immunodeficiency virus 1 hiv 1 rna/product/ATCC
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    quantitative synthetic human immunodeficiency virus 1 hiv 1 rna - by Bioz Stars, 2024-04
    94/100 stars

    Images

    1) Product Images from "Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy"

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    Journal: Cell Host & Microbe

    doi: 10.1016/j.chom.2022.12.002

    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) HIV-1 proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.
    Figure Legend Snippet: Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) HIV-1 proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.

    Techniques Used: Sequencing, Whisker Assay

    Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic trees for intact HIV-1 proviruses from long-term ART-treated individuals (LT01–LT08). Coordinates of chromosomal integration sites obtained by integration site loop amplification (ISLA) and corresponding gene name (if applicable) are indicated. Symbols indicate sequences generated by FLIP-seq, MIP-seq, PRIP-seq or from quantitative viral outgrowth assays (qVOAs). Proviruses integrated in highly repetitive satellite DNA could not always be definitively mapped to specific chromosomal locations; a detailed list of integration sites is shown in <xref ref-type=Table S1 . ∗ Sequences differ by 1 or 2 base pairs from adjacent clonal sequences. LADs, lamina-associated domains. (B) Proportions of intact proviruses with indicated integration site features in LT-ART individuals and comparison cohorts. (C) Chromosomal distance between integration sites of intact proviruses to most proximal host transcriptional start sites (TSSs), as determined by RNA-seq in CD4 T cells from reference datasets in total, effector-memory (EM), or central-memory (CM) primary CD4 T cells or from genome browser (GB). Box and Whisker plots show median, interquartile ranges and minimum/maximum. (D) Proportions of genome-intact proviral sequences in structural compartments/subcompartments A and B, as determined by Hi-C seq data. Integration sites not covered in the reference dataset were excluded. (B–D) Data from individuals with moderate ART treatment durations (m-ART) and from EC are shown for comparison. Clonal sequences are counted once. (B–D) p values were calculated by FDR-adjusted two-sided Kruskal-Wallis nonparametric tests or chi-square tests, adjusted for multiple comparison testing where applicable. n reflects the number of integration sites. " title="Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic trees for intact HIV-1 proviruses from long-term ART-treated individuals (LT01–LT08). Coordinates of chromosomal integration sites obtained by integration site loop amplification (ISLA) and corresponding gene name (if applicable) are indicated. Symbols indicate sequences generated by FLIP-seq, MIP-seq, PRIP-seq or from quantitative viral outgrowth assays (qVOAs). Proviruses integrated in highly repetitive satellite DNA could not always be definitively mapped to specific chromosomal locations; a detailed list of integration sites is shown in Table S1 . ∗ Sequences differ by 1 or 2 base pairs from adjacent clonal sequences. LADs, lamina-associated domains. (B) Proportions of intact proviruses with indicated integration site features in LT-ART individuals and comparison cohorts. (C) Chromosomal distance between integration sites of intact proviruses to most proximal host transcriptional start sites (TSSs), as determined by RNA-seq in CD4 T cells from reference datasets in total, effector-memory (EM), or central-memory (CM) primary CD4 T cells or from genome browser (GB). Box and Whisker plots show median, interquartile ranges and minimum/maximum. (D) Proportions of genome-intact proviral sequences in structural compartments/subcompartments A and B, as determined by Hi-C seq data. Integration sites not covered in the reference dataset were excluded. (B–D) Data from individuals with moderate ART treatment durations (m-ART) and from EC are shown for comparison. Clonal sequences are counted once. (B–D) p values were calculated by FDR-adjusted two-sided Kruskal-Wallis nonparametric tests or chi-square tests, adjusted for multiple comparison testing where applicable. n reflects the number of integration sites.

    Techniques Used: Amplification, Generated, RNA Sequencing Assay, Whisker Assay, Hi-C

    Transcriptional activity of single HIV-1 proviruses from study participant LT03 (A) Maximum-likelihood phylogenetic tree of individual proviruses isolated from LT03 using PRIP-seq. Chromosomal integration sites are indicated where available; genes harboring the integration site are shown where applicable. Color coding reflects the transcriptional activity of proviral species. (B) Genome browser snapshot indicating RNA-seq, Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and ChIP-seq reads surrounding the chromosomal integration site of the indicated proviral sequence from study participant LT03; RNA-seq and ATAC-seq reads are derived from reference data of HIV-1-infected ART-treated persons and were first described in Einkauf et al. ; ChIP-seq reads from the reference dataset of the ROADMAP consortium were used.
    Figure Legend Snippet: Transcriptional activity of single HIV-1 proviruses from study participant LT03 (A) Maximum-likelihood phylogenetic tree of individual proviruses isolated from LT03 using PRIP-seq. Chromosomal integration sites are indicated where available; genes harboring the integration site are shown where applicable. Color coding reflects the transcriptional activity of proviral species. (B) Genome browser snapshot indicating RNA-seq, Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and ChIP-seq reads surrounding the chromosomal integration site of the indicated proviral sequence from study participant LT03; RNA-seq and ATAC-seq reads are derived from reference data of HIV-1-infected ART-treated persons and were first described in Einkauf et al. ; ChIP-seq reads from the reference dataset of the ROADMAP consortium were used.

    Techniques Used: Activity Assay, Isolation, RNA Sequencing Assay, Sequencing, ChIP-sequencing, Derivative Assay, Infection

    Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots reflecting the chromosomal locations of defective proviruses at indicated time points in five study participants (LT01–LT04, LT08). Each symbol reflects one defective provirus. Clonal sequences, defined by integration sites and/or complete sequence identity, are highlighted. Color-coded arches around the plots indicate types of defects in HIV-1 genomes. (B) Proportions of intact and defective proviruses with indicated integration site features at time points T1–T3. (C) Chromosomal distance between integration sites of intact and defective proviruses to most proximal TSS, as determined by RNA-seq in CD4 T cells from reference datasets at indicated time points. Box and Whisker plots show median, interquartile ranges and minimum/maximum. (B and C) Data from defective proviruses after 20 years of suppressive antiretroviral therapy are cross-sectionally compared with corresponding data from intact proviruses. A complete list of defective proviruses and their corresponding chromosomal location is indicated in <xref ref-type=Table S1 . p values were calculated by a chi-square test in (B) and by an FDR-adjusted two-sided Kruskal-Wallis nonparametric test in (C), adjusted for multiple comparison testing where applicable. n reflects the number of integration sites. " title="Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots reflecting the chromosomal locations of defective proviruses at indicated time points in five study participants (LT01–LT04, LT08). Each symbol reflects one defective provirus. Clonal sequences, defined by integration sites and/or complete sequence identity, are highlighted. Color-coded arches around the plots indicate types of defects in HIV-1 genomes. (B) Proportions of intact and defective proviruses with indicated integration site features at time points T1–T3. (C) Chromosomal distance between integration sites of intact and defective proviruses to most proximal TSS, as determined by RNA-seq in CD4 T cells from reference datasets at indicated time points. Box and Whisker plots show median, interquartile ranges and minimum/maximum. (B and C) Data from defective proviruses after 20 years of suppressive antiretroviral therapy are cross-sectionally compared with corresponding data from intact proviruses. A complete list of defective proviruses and their corresponding chromosomal location is indicated in Table S1 . p values were calculated by a chi-square test in (B) and by an FDR-adjusted two-sided Kruskal-Wallis nonparametric test in (C), adjusted for multiple comparison testing where applicable. n reflects the number of integration sites.

    Techniques Used: Sequencing, RNA Sequencing Assay, Whisker Assay

    Longitudinal dynamics of intact proviruses in two individuals with post-treatment control (A) Longitudinal analysis of HIV-1 plasma viral load in study persons 04 and 30. PBMC sampling time points are indicated by arrows. Day 0 is the first day of treatment interruption. (B) CIRCOS plots indicating longitudinal evolution of intact proviruses and their corresponding chromosomal integration sites. Each symbol reflects one intact provirus. Clonal sequences, defined by identical integration sites and/or complete sequence identity, are highlighted. In study person 30, two clones were detected in repetitive genomic regions in immediate proximity to micro-satellite DNA; due to the repetitive nature of these regions, the exact chromosomal region could not be definitively identified. ∗ Intact proviral sequences analyzed without identification of integration sites that differ by 1 or 2 base pairs from adjacent clonal sequences and might be part of the respective clones. (C) CIRCOS plots indicating longitudinal evolution and chromosomal locations of defective HIV-1 proviruses in study persons 04 and 30. Color-coded arches around the plots indicate types of defects in HIV-1 genomes.
    Figure Legend Snippet: Longitudinal dynamics of intact proviruses in two individuals with post-treatment control (A) Longitudinal analysis of HIV-1 plasma viral load in study persons 04 and 30. PBMC sampling time points are indicated by arrows. Day 0 is the first day of treatment interruption. (B) CIRCOS plots indicating longitudinal evolution of intact proviruses and their corresponding chromosomal integration sites. Each symbol reflects one intact provirus. Clonal sequences, defined by identical integration sites and/or complete sequence identity, are highlighted. In study person 30, two clones were detected in repetitive genomic regions in immediate proximity to micro-satellite DNA; due to the repetitive nature of these regions, the exact chromosomal region could not be definitively identified. ∗ Intact proviral sequences analyzed without identification of integration sites that differ by 1 or 2 base pairs from adjacent clonal sequences and might be part of the respective clones. (C) CIRCOS plots indicating longitudinal evolution and chromosomal locations of defective HIV-1 proviruses in study persons 04 and 30. Color-coded arches around the plots indicate types of defects in HIV-1 genomes.

    Techniques Used: Sampling, Sequencing, Clone Assay

    Integration site profile of intact proviruses from study persons with virological rebound after ART interruption (A) Longitudinal analysis of HIV-1 plasma viral load in three study persons who developed rapid viral rebound following ART interruption. PBMC sampling time points are indicated by arrows. (B) Maximum likelihood phylogenetic tree for intact proviruses isolated from PBMC samples prior to ART interruption in three rebounders shown in (A). Chromosomal integration sites are indicated when available. (C) Proportions of intact and defective proviruses with indicated integration sites in PTC. Data from intact proviruses identified in rebounders are shown for comparison. Data from the time point immediately prior to treatment interruption are shown; clonal sequences are counted individually. Significance was calculated using a chi-square test, adjusted for multiple comparison testing. n reflects the number of integration sites.
    Figure Legend Snippet: Integration site profile of intact proviruses from study persons with virological rebound after ART interruption (A) Longitudinal analysis of HIV-1 plasma viral load in three study persons who developed rapid viral rebound following ART interruption. PBMC sampling time points are indicated by arrows. (B) Maximum likelihood phylogenetic tree for intact proviruses isolated from PBMC samples prior to ART interruption in three rebounders shown in (A). Chromosomal integration sites are indicated when available. (C) Proportions of intact and defective proviruses with indicated integration sites in PTC. Data from intact proviruses identified in rebounders are shown for comparison. Data from the time point immediately prior to treatment interruption are shown; clonal sequences are counted individually. Significance was calculated using a chi-square test, adjusted for multiple comparison testing. n reflects the number of integration sites.

    Techniques Used: Sampling, Isolation


    Figure Legend Snippet:

    Techniques Used: Western Blot, Recombinant, Activation Assay, Cell Isolation, Reporter Gene Assay, Isolation, Software, Sequencing, Digital PCR

    quantitative synthetic human immunodeficiency virus 1 hiv 1 rna  (ATCC)


    Bioz Verified Symbol ATCC is a verified supplier
    Bioz Manufacturer Symbol ATCC manufactures this product  
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  • 94

    Structured Review

    ATCC quantitative synthetic human immunodeficiency virus 1 hiv 1 rna
    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) <t>HIV-1</t> proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.
    Quantitative Synthetic Human Immunodeficiency Virus 1 Hiv 1 Rna, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/quantitative synthetic human immunodeficiency virus 1 hiv 1 rna/product/ATCC
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    quantitative synthetic human immunodeficiency virus 1 hiv 1 rna - by Bioz Stars, 2024-04
    94/100 stars

    Images

    1) Product Images from "Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy"

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    Journal: Cell Host & Microbe

    doi: 10.1016/j.chom.2022.12.002

    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) HIV-1 proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.
    Figure Legend Snippet: Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) HIV-1 proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.

    Techniques Used: Sequencing, Whisker Assay

    Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic trees for intact HIV-1 proviruses from long-term ART-treated individuals (LT01–LT08). Coordinates of chromosomal integration sites obtained by integration site loop amplification (ISLA) and corresponding gene name (if applicable) are indicated. Symbols indicate sequences generated by FLIP-seq, MIP-seq, PRIP-seq or from quantitative viral outgrowth assays (qVOAs). Proviruses integrated in highly repetitive satellite DNA could not always be definitively mapped to specific chromosomal locations; a detailed list of integration sites is shown in <xref ref-type=Table S1 . ∗ Sequences differ by 1 or 2 base pairs from adjacent clonal sequences. LADs, lamina-associated domains. (B) Proportions of intact proviruses with indicated integration site features in LT-ART individuals and comparison cohorts. (C) Chromosomal distance between integration sites of intact proviruses to most proximal host transcriptional start sites (TSSs), as determined by RNA-seq in CD4 T cells from reference datasets in total, effector-memory (EM), or central-memory (CM) primary CD4 T cells or from genome browser (GB). Box and Whisker plots show median, interquartile ranges and minimum/maximum. (D) Proportions of genome-intact proviral sequences in structural compartments/subcompartments A and B, as determined by Hi-C seq data. Integration sites not covered in the reference dataset were excluded. (B–D) Data from individuals with moderate ART treatment durations (m-ART) and from EC are shown for comparison. Clonal sequences are counted once. (B–D) p values were calculated by FDR-adjusted two-sided Kruskal-Wallis nonparametric tests or chi-square tests, adjusted for multiple comparison testing where applicable. n reflects the number of integration sites. " title="Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic trees for intact HIV-1 proviruses from long-term ART-treated individuals (LT01–LT08). Coordinates of chromosomal integration sites obtained by integration site loop amplification (ISLA) and corresponding gene name (if applicable) are indicated. Symbols indicate sequences generated by FLIP-seq, MIP-seq, PRIP-seq or from quantitative viral outgrowth assays (qVOAs). Proviruses integrated in highly repetitive satellite DNA could not always be definitively mapped to specific chromosomal locations; a detailed list of integration sites is shown in Table S1 . ∗ Sequences differ by 1 or 2 base pairs from adjacent clonal sequences. LADs, lamina-associated domains. (B) Proportions of intact proviruses with indicated integration site features in LT-ART individuals and comparison cohorts. (C) Chromosomal distance between integration sites of intact proviruses to most proximal host transcriptional start sites (TSSs), as determined by RNA-seq in CD4 T cells from reference datasets in total, effector-memory (EM), or central-memory (CM) primary CD4 T cells or from genome browser (GB). Box and Whisker plots show median, interquartile ranges and minimum/maximum. (D) Proportions of genome-intact proviral sequences in structural compartments/subcompartments A and B, as determined by Hi-C seq data. Integration sites not covered in the reference dataset were excluded. (B–D) Data from individuals with moderate ART treatment durations (m-ART) and from EC are shown for comparison. Clonal sequences are counted once. (B–D) p values were calculated by FDR-adjusted two-sided Kruskal-Wallis nonparametric tests or chi-square tests, adjusted for multiple comparison testing where applicable. n reflects the number of integration sites.

    Techniques Used: Amplification, Generated, RNA Sequencing Assay, Whisker Assay, Hi-C

    Transcriptional activity of single HIV-1 proviruses from study participant LT03 (A) Maximum-likelihood phylogenetic tree of individual proviruses isolated from LT03 using PRIP-seq. Chromosomal integration sites are indicated where available; genes harboring the integration site are shown where applicable. Color coding reflects the transcriptional activity of proviral species. (B) Genome browser snapshot indicating RNA-seq, Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and ChIP-seq reads surrounding the chromosomal integration site of the indicated proviral sequence from study participant LT03; RNA-seq and ATAC-seq reads are derived from reference data of HIV-1-infected ART-treated persons and were first described in Einkauf et al. ; ChIP-seq reads from the reference dataset of the ROADMAP consortium were used.
    Figure Legend Snippet: Transcriptional activity of single HIV-1 proviruses from study participant LT03 (A) Maximum-likelihood phylogenetic tree of individual proviruses isolated from LT03 using PRIP-seq. Chromosomal integration sites are indicated where available; genes harboring the integration site are shown where applicable. Color coding reflects the transcriptional activity of proviral species. (B) Genome browser snapshot indicating RNA-seq, Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and ChIP-seq reads surrounding the chromosomal integration site of the indicated proviral sequence from study participant LT03; RNA-seq and ATAC-seq reads are derived from reference data of HIV-1-infected ART-treated persons and were first described in Einkauf et al. ; ChIP-seq reads from the reference dataset of the ROADMAP consortium were used.

    Techniques Used: Activity Assay, Isolation, RNA Sequencing Assay, Sequencing, ChIP-sequencing, Derivative Assay, Infection

    Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots reflecting the chromosomal locations of defective proviruses at indicated time points in five study participants (LT01–LT04, LT08). Each symbol reflects one defective provirus. Clonal sequences, defined by integration sites and/or complete sequence identity, are highlighted. Color-coded arches around the plots indicate types of defects in HIV-1 genomes. (B) Proportions of intact and defective proviruses with indicated integration site features at time points T1–T3. (C) Chromosomal distance between integration sites of intact and defective proviruses to most proximal TSS, as determined by RNA-seq in CD4 T cells from reference datasets at indicated time points. Box and Whisker plots show median, interquartile ranges and minimum/maximum. (B and C) Data from defective proviruses after 20 years of suppressive antiretroviral therapy are cross-sectionally compared with corresponding data from intact proviruses. A complete list of defective proviruses and their corresponding chromosomal location is indicated in <xref ref-type=Table S1 . p values were calculated by a chi-square test in (B) and by an FDR-adjusted two-sided Kruskal-Wallis nonparametric test in (C), adjusted for multiple comparison testing where applicable. n reflects the number of integration sites. " title="Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots reflecting the chromosomal locations of defective proviruses at indicated time points in five study participants (LT01–LT04, LT08). Each symbol reflects one defective provirus. Clonal sequences, defined by integration sites and/or complete sequence identity, are highlighted. Color-coded arches around the plots indicate types of defects in HIV-1 genomes. (B) Proportions of intact and defective proviruses with indicated integration site features at time points T1–T3. (C) Chromosomal distance between integration sites of intact and defective proviruses to most proximal TSS, as determined by RNA-seq in CD4 T cells from reference datasets at indicated time points. Box and Whisker plots show median, interquartile ranges and minimum/maximum. (B and C) Data from defective proviruses after 20 years of suppressive antiretroviral therapy are cross-sectionally compared with corresponding data from intact proviruses. A complete list of defective proviruses and their corresponding chromosomal location is indicated in Table S1 . p values were calculated by a chi-square test in (B) and by an FDR-adjusted two-sided Kruskal-Wallis nonparametric test in (C), adjusted for multiple comparison testing where applicable. n reflects the number of integration sites.

    Techniques Used: Sequencing, RNA Sequencing Assay, Whisker Assay

    Longitudinal dynamics of intact proviruses in two individuals with post-treatment control (A) Longitudinal analysis of HIV-1 plasma viral load in study persons 04 and 30. PBMC sampling time points are indicated by arrows. Day 0 is the first day of treatment interruption. (B) CIRCOS plots indicating longitudinal evolution of intact proviruses and their corresponding chromosomal integration sites. Each symbol reflects one intact provirus. Clonal sequences, defined by identical integration sites and/or complete sequence identity, are highlighted. In study person 30, two clones were detected in repetitive genomic regions in immediate proximity to micro-satellite DNA; due to the repetitive nature of these regions, the exact chromosomal region could not be definitively identified. ∗ Intact proviral sequences analyzed without identification of integration sites that differ by 1 or 2 base pairs from adjacent clonal sequences and might be part of the respective clones. (C) CIRCOS plots indicating longitudinal evolution and chromosomal locations of defective HIV-1 proviruses in study persons 04 and 30. Color-coded arches around the plots indicate types of defects in HIV-1 genomes.
    Figure Legend Snippet: Longitudinal dynamics of intact proviruses in two individuals with post-treatment control (A) Longitudinal analysis of HIV-1 plasma viral load in study persons 04 and 30. PBMC sampling time points are indicated by arrows. Day 0 is the first day of treatment interruption. (B) CIRCOS plots indicating longitudinal evolution of intact proviruses and their corresponding chromosomal integration sites. Each symbol reflects one intact provirus. Clonal sequences, defined by identical integration sites and/or complete sequence identity, are highlighted. In study person 30, two clones were detected in repetitive genomic regions in immediate proximity to micro-satellite DNA; due to the repetitive nature of these regions, the exact chromosomal region could not be definitively identified. ∗ Intact proviral sequences analyzed without identification of integration sites that differ by 1 or 2 base pairs from adjacent clonal sequences and might be part of the respective clones. (C) CIRCOS plots indicating longitudinal evolution and chromosomal locations of defective HIV-1 proviruses in study persons 04 and 30. Color-coded arches around the plots indicate types of defects in HIV-1 genomes.

    Techniques Used: Sampling, Sequencing, Clone Assay

    Integration site profile of intact proviruses from study persons with virological rebound after ART interruption (A) Longitudinal analysis of HIV-1 plasma viral load in three study persons who developed rapid viral rebound following ART interruption. PBMC sampling time points are indicated by arrows. (B) Maximum likelihood phylogenetic tree for intact proviruses isolated from PBMC samples prior to ART interruption in three rebounders shown in (A). Chromosomal integration sites are indicated when available. (C) Proportions of intact and defective proviruses with indicated integration sites in PTC. Data from intact proviruses identified in rebounders are shown for comparison. Data from the time point immediately prior to treatment interruption are shown; clonal sequences are counted individually. Significance was calculated using a chi-square test, adjusted for multiple comparison testing. n reflects the number of integration sites.
    Figure Legend Snippet: Integration site profile of intact proviruses from study persons with virological rebound after ART interruption (A) Longitudinal analysis of HIV-1 plasma viral load in three study persons who developed rapid viral rebound following ART interruption. PBMC sampling time points are indicated by arrows. (B) Maximum likelihood phylogenetic tree for intact proviruses isolated from PBMC samples prior to ART interruption in three rebounders shown in (A). Chromosomal integration sites are indicated when available. (C) Proportions of intact and defective proviruses with indicated integration sites in PTC. Data from intact proviruses identified in rebounders are shown for comparison. Data from the time point immediately prior to treatment interruption are shown; clonal sequences are counted individually. Significance was calculated using a chi-square test, adjusted for multiple comparison testing. n reflects the number of integration sites.

    Techniques Used: Sampling, Isolation


    Figure Legend Snippet:

    Techniques Used: Western Blot, Recombinant, Activation Assay, Cell Isolation, Reporter Gene Assay, Isolation, Software, Sequencing, Digital PCR

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    ATCC quantitative synthetic human immunodeficiency virus 1 hiv 1 rna
    Simultaneous analysis of <t>HIV-1</t> DNA sequence, integration site, and transcriptional activity from individual infected cells (A) Schematic representation of the PRIP-seq assay design. (B) Proviral sequence classification in all analyzed HIV-1-infected cells and in long LTR RNA-expressing HIV-1-infected cells (PSC, premature stop codon). (C) Proportions of proviruses in genic versus nongenic positions, introns/exons/promoters (genic sites only), same or opposite orientation to host genes (genic sites only), and repetitive genomic elements. (D) Proportion of HIV-1 long LTR RNA-expressing proviruses among analyzed proviruses, stratified according to proviral sequence intactness/defects. Data are shown separately for all proviruses, all proviruses collected during aviremic time points, and for a subset of proviruses with experimentally confirmed intact core promoter regions. (E) Circos plots reflecting the chromosomal locations of transcriptionally active (RNA+) and silent (RNA−) proviruses in genic versus nongenic DNA. (F) Proportion of transcriptionally active proviruses among proviruses integrated in either genic, nongenic, or nongenic satellite DNA regions. (G) Contribution of proviruses in nongenic or nongenic satellite DNA to the total number of transcriptionally active (RNA+) or silent proviruses (RNA−) with detectable chromosomal IS. (E–G) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+.” ( ∗∗∗ p < 0.001, Fisher’s exact tests were used for all comparisons. Error bars represent standard errors of proportions ).
    Quantitative Synthetic Human Immunodeficiency Virus 1 Hiv 1 Rna, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses"

    Article Title: Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses

    Journal: Cell

    doi: 10.1016/j.cell.2021.12.011

    Simultaneous analysis of HIV-1 DNA sequence, integration site, and transcriptional activity from individual infected cells (A) Schematic representation of the PRIP-seq assay design. (B) Proviral sequence classification in all analyzed HIV-1-infected cells and in long LTR RNA-expressing HIV-1-infected cells (PSC, premature stop codon). (C) Proportions of proviruses in genic versus nongenic positions, introns/exons/promoters (genic sites only), same or opposite orientation to host genes (genic sites only), and repetitive genomic elements. (D) Proportion of HIV-1 long LTR RNA-expressing proviruses among analyzed proviruses, stratified according to proviral sequence intactness/defects. Data are shown separately for all proviruses, all proviruses collected during aviremic time points, and for a subset of proviruses with experimentally confirmed intact core promoter regions. (E) Circos plots reflecting the chromosomal locations of transcriptionally active (RNA+) and silent (RNA−) proviruses in genic versus nongenic DNA. (F) Proportion of transcriptionally active proviruses among proviruses integrated in either genic, nongenic, or nongenic satellite DNA regions. (G) Contribution of proviruses in nongenic or nongenic satellite DNA to the total number of transcriptionally active (RNA+) or silent proviruses (RNA−) with detectable chromosomal IS. (E–G) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+.” ( ∗∗∗ p < 0.001, Fisher’s exact tests were used for all comparisons. Error bars represent standard errors of proportions ).
    Figure Legend Snippet: Simultaneous analysis of HIV-1 DNA sequence, integration site, and transcriptional activity from individual infected cells (A) Schematic representation of the PRIP-seq assay design. (B) Proviral sequence classification in all analyzed HIV-1-infected cells and in long LTR RNA-expressing HIV-1-infected cells (PSC, premature stop codon). (C) Proportions of proviruses in genic versus nongenic positions, introns/exons/promoters (genic sites only), same or opposite orientation to host genes (genic sites only), and repetitive genomic elements. (D) Proportion of HIV-1 long LTR RNA-expressing proviruses among analyzed proviruses, stratified according to proviral sequence intactness/defects. Data are shown separately for all proviruses, all proviruses collected during aviremic time points, and for a subset of proviruses with experimentally confirmed intact core promoter regions. (E) Circos plots reflecting the chromosomal locations of transcriptionally active (RNA+) and silent (RNA−) proviruses in genic versus nongenic DNA. (F) Proportion of transcriptionally active proviruses among proviruses integrated in either genic, nongenic, or nongenic satellite DNA regions. (G) Contribution of proviruses in nongenic or nongenic satellite DNA to the total number of transcriptionally active (RNA+) or silent proviruses (RNA−) with detectable chromosomal IS. (E–G) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+.” ( ∗∗∗ p < 0.001, Fisher’s exact tests were used for all comparisons. Error bars represent standard errors of proportions ).

    Techniques Used: Sequencing, Activity Assay, Infection, Expressing

    Technical evaluation of PRIP-seq assay, related to <xref ref-type=Figure 1 (A and B) Schematic representation of the experimental workflow for isolation, reverse transcription, and amplification of HIV-1 RNA/cDNA (A) and of the primer/probe binding sites for ddPCR-based detection of indicated HIV-1 cDNA products (B). (C and D) Known HIV-1 RNA copy numbers were serially diluted in 96-well plates and added to cell lysates of 10,000 PBMC from an HIV-1-uninfected person; afterward, a standard PRIP-seq assay was performed. (C) Proportion of wells with detectable HIV-1 cDNA at the indicated number of input HIV-1 RNA copies. (D) Correlation between input HIV-1 RNA copy numbers and numbers of postamplification HIV-1 cDNA copies detectable by the PRIP-seq assay; Spearman correlation coefficient is shown. (E) Evaluation of possible HIV-1 cDNA contamination by genomic HIV-1 DNA. PRIP-seq was applied to 48 wells, each containing 12,000 PBMC/well from an HIV-infected participant; 40 separate control wells were subjected to the same protocol, except for exclusion of reverse transcriptase from the workflow. Graph demonstrates number of wells with detectable HIV-1 cDNA in samples and controls. (F) Gene expression intensity (determined by RNA-seq) of all human protein-coding genes compared with host genes harboring proviral IS recovered by PRIP-seq in all study subjects. (∗∗∗∗ p < 0.0001, Mann-Whitney U test). (G) Circos plot indicating positioning of long LTR RNA-expressing proviruses (RNA+) and transcriptionally silent (RNA-) proviruses relative to genome-wide assessments of indicated transcriptional (RNA-seq), epigenetic (ATAC-seq and ChIP-seq) and three-dimensional chromatin contact (Hi-C) features. Data from all analyzed proviruses for which IS were available are shown. " title="... workflow for isolation, reverse transcription, and amplification of HIV-1 RNA/cDNA (A) and of the primer/probe binding sites ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Technical evaluation of PRIP-seq assay, related to Figure 1 (A and B) Schematic representation of the experimental workflow for isolation, reverse transcription, and amplification of HIV-1 RNA/cDNA (A) and of the primer/probe binding sites for ddPCR-based detection of indicated HIV-1 cDNA products (B). (C and D) Known HIV-1 RNA copy numbers were serially diluted in 96-well plates and added to cell lysates of 10,000 PBMC from an HIV-1-uninfected person; afterward, a standard PRIP-seq assay was performed. (C) Proportion of wells with detectable HIV-1 cDNA at the indicated number of input HIV-1 RNA copies. (D) Correlation between input HIV-1 RNA copy numbers and numbers of postamplification HIV-1 cDNA copies detectable by the PRIP-seq assay; Spearman correlation coefficient is shown. (E) Evaluation of possible HIV-1 cDNA contamination by genomic HIV-1 DNA. PRIP-seq was applied to 48 wells, each containing 12,000 PBMC/well from an HIV-infected participant; 40 separate control wells were subjected to the same protocol, except for exclusion of reverse transcriptase from the workflow. Graph demonstrates number of wells with detectable HIV-1 cDNA in samples and controls. (F) Gene expression intensity (determined by RNA-seq) of all human protein-coding genes compared with host genes harboring proviral IS recovered by PRIP-seq in all study subjects. (∗∗∗∗ p < 0.0001, Mann-Whitney U test). (G) Circos plot indicating positioning of long LTR RNA-expressing proviruses (RNA+) and transcriptionally silent (RNA-) proviruses relative to genome-wide assessments of indicated transcriptional (RNA-seq), epigenetic (ATAC-seq and ChIP-seq) and three-dimensional chromatin contact (Hi-C) features. Data from all analyzed proviruses for which IS were available are shown.

    Techniques Used: Isolation, Amplification, Binding Assay, Infection, Expressing, RNA Sequencing Assay, MANN-WHITNEY, Genome Wide, ChIP-sequencing, Hi-C

    Clinical characteristics of study participants, related to <xref ref-type=Figure 1 (A) Diagrams reflecting CD4 + T cell counts and HIV-1 plasma viral loads of the six study participants (P1–P6). Sampling time points are indicated by red arrows. ART exposure time is indicated by yellow shading. Horizontal dotted lines indicate limits of detection for viral load assays; empty squares indicate participant viral loads at/below the associated limit of detection. (B) Table summarizing number of cells, wells and plates analyzed by PRIP-seq for each participant at indicated PBMC sampling time points. " title="... Diagrams reflecting CD4 + T cell counts and HIV-1 plasma viral loads of the six study participants ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Clinical characteristics of study participants, related to Figure 1 (A) Diagrams reflecting CD4 + T cell counts and HIV-1 plasma viral loads of the six study participants (P1–P6). Sampling time points are indicated by red arrows. ART exposure time is indicated by yellow shading. Horizontal dotted lines indicate limits of detection for viral load assays; empty squares indicate participant viral loads at/below the associated limit of detection. (B) Table summarizing number of cells, wells and plates analyzed by PRIP-seq for each participant at indicated PBMC sampling time points.

    Techniques Used: Sampling

    Chromatin features of HIV-1 proviruses integrated in non-genic DNA, related to and (A–D) Sum of local RNA-seq reads (A), ChIP-seq reads corresponding to activating (B), inhibitory (C) histone modifications, and ATAC-seq reads (D) within 5 kb upstream or downstream of proviral IS in genic versus nongenic locations. (E and F) Chromosomal distances of proviruses in genic versus nongenic positions to frequently interacting regions (FIREs) (E) and to topologically associated domains (TADs) (F), determined at 10 kb binning resolution of Hi-C data. (G and H) Numbers of intrachromosomal (G) and interchromosomal (H) contact regions, determined by FiTHiC2-seq ( <xref ref-type=Kaul et al., 2020 ) (p < 0.05, binning resolution of 20 kb), for proviruses in genic versus nongenic locations. Pie charts reflect proportions of proviruses with no detectable intra- or interchromosomal contacts. (A–H) Clones of proviruses are counted as single datapoints; IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded because of the reduced ability to map next-generation sequencing reads onto repetitive genomic DNA regions. (E and F) Proviral sequences without FIRE annotation by FIREcaller ( Crowley et al., 2021 ) or without TAD annotation by Homer (version 4.10.3) were excluded from the respective analyses. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; Mann-Whitney U tests or Fisher’s exact tests were used for all comparisons). " title="Chromatin features of HIV-1 proviruses integrated in non-genic DNA, related to and ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Chromatin features of HIV-1 proviruses integrated in non-genic DNA, related to and (A–D) Sum of local RNA-seq reads (A), ChIP-seq reads corresponding to activating (B), inhibitory (C) histone modifications, and ATAC-seq reads (D) within 5 kb upstream or downstream of proviral IS in genic versus nongenic locations. (E and F) Chromosomal distances of proviruses in genic versus nongenic positions to frequently interacting regions (FIREs) (E) and to topologically associated domains (TADs) (F), determined at 10 kb binning resolution of Hi-C data. (G and H) Numbers of intrachromosomal (G) and interchromosomal (H) contact regions, determined by FiTHiC2-seq ( Kaul et al., 2020 ) (p < 0.05, binning resolution of 20 kb), for proviruses in genic versus nongenic locations. Pie charts reflect proportions of proviruses with no detectable intra- or interchromosomal contacts. (A–H) Clones of proviruses are counted as single datapoints; IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded because of the reduced ability to map next-generation sequencing reads onto repetitive genomic DNA regions. (E and F) Proviral sequences without FIRE annotation by FIREcaller ( Crowley et al., 2021 ) or without TAD annotation by Homer (version 4.10.3) were excluded from the respective analyses. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; Mann-Whitney U tests or Fisher’s exact tests were used for all comparisons).

    Techniques Used: RNA Sequencing Assay, ChIP-sequencing, Hi-C, Clone Assay, Next-Generation Sequencing, MANN-WHITNEY

    Epigenetic features in linear and three-dimensional contact regions of transcriptionally active proviruses (A) Genome browser snapshot of RNA-seq, ATAC-seq, and ChIP-seq reads in proximity of the indicated representative proviral integration site. (B and C) Dot plots showing ChIP-seq reads corresponding to activating histone features (H3K4me1, H3K4me3, and H3K27ac) (B) and ATAC-seq reads (C) in linear proximity (±5 kb) of RNA-positive or -negative proviruses. (D) Proportion of proviruses with 100% methylated cytosine residues within 2,500 bp upstream of the proviral 5′-LTR HIV-1 promoter. Proviruses with 0 CpGs in this region were excluded. (E) Genome browser snapshot and circos plot highlighting intra- and interchromosomal contact regions of the representative provirus indicated in (A). (F–I) Number of total (intra- and interchromosomal) contacts (F), chromosomal distances to FIREs (G), activating histone-specific ChIP-seq reads in 3D contact regions (H), and ATAC-seq reads in 3D contact regions (I) among HIV-1 RNA-positive or -negative proviruses. In (G), proviral sequences without FIRE annotation by FIREcaller ( <xref ref-type=Crowley et al., 2021 ) were excluded from the analysis. (J) Sum of ATAC-seq reads in linear (±5 kb) and all 3D contact regions. (K) Sum of activating histone-specific (upper panel) and H3K4me1 (lower panel) ChIP-seq reads in linear (±5 kb) and interchromosomal 3D contact regions. (L) Transcriptional activity of proviruses stratified according to multiple integration site features. Proviruses were categorized based on the number of features within the upper 50 th percentile for (B, C, and F) and within the lower 50 th percentile for (D and G), relative to the indicated data distributions. (M) Receiver operating characteristic (ROC) curve for a logistic regression model trained to predict proviral transcriptional activity as evaluated on a holdout testing dataset. (N) Dot plot displaying model-predicted confidence scores of HIV-1 RNA expression in RNA-positive or -negative proviruses in the test dataset. (O) Coefficients of each feature in the logistic regression model after training. Positive coefficients are associated with proviral transcriptional activity and negative coefficients are associated with proviral transcriptional silence. (B–D and F–O) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+”; clonal proviral sequences are counted once and shown as RNA+ when at least one member of a clonal cluster had detectable HIV-1 long LTR RNA; IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. (F–K) Hi-C data at binning resolution of 10 kb are shown. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, Mann-Whitney U tests or Fisher’s exact tests were used for all comparisons. Error bars in bar diagrams D, F, and L represent SEM or SEP). " title="... within 2,500 bp upstream of the proviral 5′-LTR HIV-1 promoter. Proviruses with 0 CpGs in this region ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Epigenetic features in linear and three-dimensional contact regions of transcriptionally active proviruses (A) Genome browser snapshot of RNA-seq, ATAC-seq, and ChIP-seq reads in proximity of the indicated representative proviral integration site. (B and C) Dot plots showing ChIP-seq reads corresponding to activating histone features (H3K4me1, H3K4me3, and H3K27ac) (B) and ATAC-seq reads (C) in linear proximity (±5 kb) of RNA-positive or -negative proviruses. (D) Proportion of proviruses with 100% methylated cytosine residues within 2,500 bp upstream of the proviral 5′-LTR HIV-1 promoter. Proviruses with 0 CpGs in this region were excluded. (E) Genome browser snapshot and circos plot highlighting intra- and interchromosomal contact regions of the representative provirus indicated in (A). (F–I) Number of total (intra- and interchromosomal) contacts (F), chromosomal distances to FIREs (G), activating histone-specific ChIP-seq reads in 3D contact regions (H), and ATAC-seq reads in 3D contact regions (I) among HIV-1 RNA-positive or -negative proviruses. In (G), proviral sequences without FIRE annotation by FIREcaller ( Crowley et al., 2021 ) were excluded from the analysis. (J) Sum of ATAC-seq reads in linear (±5 kb) and all 3D contact regions. (K) Sum of activating histone-specific (upper panel) and H3K4me1 (lower panel) ChIP-seq reads in linear (±5 kb) and interchromosomal 3D contact regions. (L) Transcriptional activity of proviruses stratified according to multiple integration site features. Proviruses were categorized based on the number of features within the upper 50 th percentile for (B, C, and F) and within the lower 50 th percentile for (D and G), relative to the indicated data distributions. (M) Receiver operating characteristic (ROC) curve for a logistic regression model trained to predict proviral transcriptional activity as evaluated on a holdout testing dataset. (N) Dot plot displaying model-predicted confidence scores of HIV-1 RNA expression in RNA-positive or -negative proviruses in the test dataset. (O) Coefficients of each feature in the logistic regression model after training. Positive coefficients are associated with proviral transcriptional activity and negative coefficients are associated with proviral transcriptional silence. (B–D and F–O) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+”; clonal proviral sequences are counted once and shown as RNA+ when at least one member of a clonal cluster had detectable HIV-1 long LTR RNA; IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. (F–K) Hi-C data at binning resolution of 10 kb are shown. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, Mann-Whitney U tests or Fisher’s exact tests were used for all comparisons. Error bars in bar diagrams D, F, and L represent SEM or SEP).

    Techniques Used: RNA Sequencing Assay, ChIP-sequencing, Methylation, Activity Assay, RNA Expression, Expressing, Hi-C, MANN-WHITNEY

    Additional distinguishing features of transcriptionally active HIV-1 proviruses, related to <xref ref-type=Figure 2 (A and B) Chromosomal distance between transcriptionally active (RNA+) and transcriptionally silent (RNA-) proviruses and the most proximal host transcriptional start site (TSS) in same (A) or opposite (B) orientation. (C and D) H3K4me1- (C) and H3K27me3-specific (D) ChIP-seq reads in linear proximity (±5 kb) to proviral IS. (E and F) Average numbers of intrachromosomal (E) and interchromosomal (F) proviral chromatin contacts; error bars indicate standard error of the mean. (G and H) RNA-seq reads (G) and H3K4me1-specific ChIP-seq reads (H) in all proviral 3D contact regions. (I) Sum of H3K4me3- (upper panel) and H3K27ac-specific (lower panel) ChIP-seq reads in linear proximity and interchromosomal proviral contact regions. (E–I) 3D contacts were determined by Hi-C at 10 kb binning resolution. (J) Network reflecting chromosomal interactions (p < 0.05, 20 kb binning resolution) between IS of transcriptionally active (red) and silent (blue) proviruses from all six study subjects. Circles suggest transcriptional interactomes between HIV-1 RNA+ proviruses. (A–J) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+”; clonal sequences were counted once and were counted as RNA+ when at least one member of a clonal cluster had detectable expression of HIV-1 long LTR RNA. IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. ( ∗ p < 0.05, ∗∗ p < 0.01, Mann-Whitney U tests or Fisher’s exact tests were used for all comparisons). " title="Additional distinguishing features of transcriptionally active HIV-1 proviruses, related to Figure 2 (A ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Additional distinguishing features of transcriptionally active HIV-1 proviruses, related to Figure 2 (A and B) Chromosomal distance between transcriptionally active (RNA+) and transcriptionally silent (RNA-) proviruses and the most proximal host transcriptional start site (TSS) in same (A) or opposite (B) orientation. (C and D) H3K4me1- (C) and H3K27me3-specific (D) ChIP-seq reads in linear proximity (±5 kb) to proviral IS. (E and F) Average numbers of intrachromosomal (E) and interchromosomal (F) proviral chromatin contacts; error bars indicate standard error of the mean. (G and H) RNA-seq reads (G) and H3K4me1-specific ChIP-seq reads (H) in all proviral 3D contact regions. (I) Sum of H3K4me3- (upper panel) and H3K27ac-specific (lower panel) ChIP-seq reads in linear proximity and interchromosomal proviral contact regions. (E–I) 3D contacts were determined by Hi-C at 10 kb binning resolution. (J) Network reflecting chromosomal interactions (p < 0.05, 20 kb binning resolution) between IS of transcriptionally active (red) and silent (blue) proviruses from all six study subjects. Circles suggest transcriptional interactomes between HIV-1 RNA+ proviruses. (A–J) HIV-1 long LTR RNA-expressing proviruses were considered “RNA+”; clonal sequences were counted once and were counted as RNA+ when at least one member of a clonal cluster had detectable expression of HIV-1 long LTR RNA. IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. ( ∗ p < 0.05, ∗∗ p < 0.01, Mann-Whitney U tests or Fisher’s exact tests were used for all comparisons).

    Techniques Used: ChIP-sequencing, RNA Sequencing Assay, Hi-C, Expressing, MANN-WHITNEY

    Longitudinal changes in frequency of transcriptionally active and silent proviruses, related to <xref ref-type=Figure 3 (A–C, E–G, and I–K) Proportions and frequencies of proviruses expressing any HIV-1 RNA, high-level (>10,000 postamplification copies) HIV-1 RNA or elongated HIV-1 RNA (containing pol, nef, spliced tat-rev, or poly-A sequences) at indicated time points in participants 1–3 (P1–P3). Data for all proviruses (A, E, and I), proviruses integrated in genic locations (B, F, and J), and proviruses in nongenic locations (C, G, and K) are shown; (B, C, F, G, J, and K) only include proviruses for which IS are available. (D, H, and L) Frequencies of long LTR RNA-positive or -negative intact or defective proviruses at indicated time points in P1–P3. L.O.D., limit of detection. (M–O) Proportion of long LTR RNA-expressing HIV-1 proviruses in study participants 1–4. Data for all proviruses (M), proviruses in genic locations (N), and proviruses in nongenic locations (O) are shown. Horizontal dashes indicate available time points from each participant. (P and Q) Among proviruses detected once and positioned in either same (P) or opposite (Q) orientation to the nearest host TSS, proportion of proviruses expressing HIV-1 long LTR RNA; longitudinal data are pooled from study subjects 1–3 at indicated time points. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, Fisher’s exact tests were used for all comparisons. Error bars in bar diagrams represent SEP). " title="... I–K) Proportions and frequencies of proviruses expressing any HIV-1 RNA, high-level (>10,000 postamplification copies) HIV-1 RNA or ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Longitudinal changes in frequency of transcriptionally active and silent proviruses, related to Figure 3 (A–C, E–G, and I–K) Proportions and frequencies of proviruses expressing any HIV-1 RNA, high-level (>10,000 postamplification copies) HIV-1 RNA or elongated HIV-1 RNA (containing pol, nef, spliced tat-rev, or poly-A sequences) at indicated time points in participants 1–3 (P1–P3). Data for all proviruses (A, E, and I), proviruses integrated in genic locations (B, F, and J), and proviruses in nongenic locations (C, G, and K) are shown; (B, C, F, G, J, and K) only include proviruses for which IS are available. (D, H, and L) Frequencies of long LTR RNA-positive or -negative intact or defective proviruses at indicated time points in P1–P3. L.O.D., limit of detection. (M–O) Proportion of long LTR RNA-expressing HIV-1 proviruses in study participants 1–4. Data for all proviruses (M), proviruses in genic locations (N), and proviruses in nongenic locations (O) are shown. Horizontal dashes indicate available time points from each participant. (P and Q) Among proviruses detected once and positioned in either same (P) or opposite (Q) orientation to the nearest host TSS, proportion of proviruses expressing HIV-1 long LTR RNA; longitudinal data are pooled from study subjects 1–3 at indicated time points. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, Fisher’s exact tests were used for all comparisons. Error bars in bar diagrams represent SEP).

    Techniques Used: Expressing

    Longitudinal evolution of HIV-1 proviruses (A–C) Relative proportions of proviruses expressing any HIV-1 RNA or high-level (>10,000 postamplification copies) HIV-1 RNA at indicated time points for participants 1–3 (P1–P3). Data for all proviruses (A), proviruses integrated in genic locations (B), and proviruses in nongenic locations (C) are shown; (B) and (C) only include proviruses for which IS are available. (D) Proportion of proviruses integrated in nongenic and nongenic, satellite DNA in a combined longitudinal analysis of participants 1–3. (E) Relative contribution of RNA-positive or -negative proviruses in genic versus nongenic chromosomal locations to the total number of proviruses with known IS in P1–P3. (F and G) Proportions of intact (F) and defective (G) proviruses that were transcriptionally active in P1–P3 at indicated longitudinal time points. (H) Contribution of indicated proviruses to the total number of proviruses in participants 1–3. (A–G) Horizontal dashes indicate available time points from each participant; HIV-1 long LTR RNA-expressing proviruses were considered “RNA+.” (I–K and N–P) Frequencies and proportions of proviruses expressing any HIV-1 RNA, high-level (>10,000 postamplification copies) HIV-1 RNA, elongated HIV-1 RNA (containing pol, nef, spliced tat-rev, or poly-A sequences), or no HIV-1 RNA in study participants 5 (P5, I–K) and 6 (P6, N–P). Data for all proviruses (I and N), for proviruses with IS detected once (J and O), and for proviruses with IS detected more than once (K and P) are shown. (J, K, O, and P) Only include proviruses for which IS are available. (L and Q) Contribution of proviruses with IS detected once or multiple times to the total number of proviruses with known IS in participants 5 (L) and 6 (Q). In (M/R), proviruses are additionally stratified by HIV-1 RNA expression status. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, Mann-Whitney U tests, Fisher’s exact tests, or G tests were used for all comparisons. Error bars in bar diagrams represent SEP).
    Figure Legend Snippet: Longitudinal evolution of HIV-1 proviruses (A–C) Relative proportions of proviruses expressing any HIV-1 RNA or high-level (>10,000 postamplification copies) HIV-1 RNA at indicated time points for participants 1–3 (P1–P3). Data for all proviruses (A), proviruses integrated in genic locations (B), and proviruses in nongenic locations (C) are shown; (B) and (C) only include proviruses for which IS are available. (D) Proportion of proviruses integrated in nongenic and nongenic, satellite DNA in a combined longitudinal analysis of participants 1–3. (E) Relative contribution of RNA-positive or -negative proviruses in genic versus nongenic chromosomal locations to the total number of proviruses with known IS in P1–P3. (F and G) Proportions of intact (F) and defective (G) proviruses that were transcriptionally active in P1–P3 at indicated longitudinal time points. (H) Contribution of indicated proviruses to the total number of proviruses in participants 1–3. (A–G) Horizontal dashes indicate available time points from each participant; HIV-1 long LTR RNA-expressing proviruses were considered “RNA+.” (I–K and N–P) Frequencies and proportions of proviruses expressing any HIV-1 RNA, high-level (>10,000 postamplification copies) HIV-1 RNA, elongated HIV-1 RNA (containing pol, nef, spliced tat-rev, or poly-A sequences), or no HIV-1 RNA in study participants 5 (P5, I–K) and 6 (P6, N–P). Data for all proviruses (I and N), for proviruses with IS detected once (J and O), and for proviruses with IS detected more than once (K and P) are shown. (J, K, O, and P) Only include proviruses for which IS are available. (L and Q) Contribution of proviruses with IS detected once or multiple times to the total number of proviruses with known IS in participants 5 (L) and 6 (Q). In (M/R), proviruses are additionally stratified by HIV-1 RNA expression status. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, Mann-Whitney U tests, Fisher’s exact tests, or G tests were used for all comparisons. Error bars in bar diagrams represent SEP).

    Techniques Used: Expressing, RNA Expression, MANN-WHITNEY

    Transcriptional behavior of clonal HIV-1 proviruses Phylogenetic trees of clonal HIV-1 proviruses from the six study participants. Each symbol reflects one single provirus. Proviral sequence calls and host genes harboring IS are indicated. Clones that are transcriptionally silent across all members are boxed. PSC, premature stop codon; large del, large deletion; hypermut, hypermutation.
    Figure Legend Snippet: Transcriptional behavior of clonal HIV-1 proviruses Phylogenetic trees of clonal HIV-1 proviruses from the six study participants. Each symbol reflects one single provirus. Proviral sequence calls and host genes harboring IS are indicated. Clones that are transcriptionally silent across all members are boxed. PSC, premature stop codon; large del, large deletion; hypermut, hypermutation.

    Techniques Used: Sequencing, Clone Assay

    Epigenetic features of transcriptionally active clonal HIV-1 proviruses (A and B) Genome browser snapshots reflecting the local chromatin environment surrounding the proviral IS of selected transcriptionally active clonal proviruses from study persons 5 (A) and 6 (B). (C–E) ATAC-seq (C), H3K4me1-specific ChIP-seq (D), and all activating (H3K4me1, H3K4me3, and H3K27ac) ChIP-seq (E) reads surrounding (±5 kb) the proviral IS of clonal proviruses and of proviruses detected once (here termed “nonclonal”). (F–H) Sum of ATAC-seq (F), RNA-seq (G), and all activating ChIP-seq (H) reads in linear proximity and 3D interchromosomal contact regions of clonal proviruses and proviruses detected once (“nonclonal”) using Hi-C data at 10 kb binning resolution. (C–H) HIV-1 Long LTR RNA-expressing proviruses were considered “RNA+”; HIV-1 Long-LTR RNA-negative proviruses are considered Amemiya et al., 2019 ) were excluded. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, Mann-Whitney U tests were used for all comparisons). " title="Epigenetic features of transcriptionally active clonal HIV-1 proviruses (A and B) Genome browser snapshots reflecting ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Epigenetic features of transcriptionally active clonal HIV-1 proviruses (A and B) Genome browser snapshots reflecting the local chromatin environment surrounding the proviral IS of selected transcriptionally active clonal proviruses from study persons 5 (A) and 6 (B). (C–E) ATAC-seq (C), H3K4me1-specific ChIP-seq (D), and all activating (H3K4me1, H3K4me3, and H3K27ac) ChIP-seq (E) reads surrounding (±5 kb) the proviral IS of clonal proviruses and of proviruses detected once (here termed “nonclonal”). (F–H) Sum of ATAC-seq (F), RNA-seq (G), and all activating ChIP-seq (H) reads in linear proximity and 3D interchromosomal contact regions of clonal proviruses and proviruses detected once (“nonclonal”) using Hi-C data at 10 kb binning resolution. (C–H) HIV-1 Long LTR RNA-expressing proviruses were considered “RNA+”; HIV-1 Long-LTR RNA-negative proviruses are considered "RNA-". Clonal sequences were counted only once; clones were counted as transcriptionally active when at least one member of a clonal cluster had detectable expression of HIV-1 long LTR RNA. IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, Mann-Whitney U tests were used for all comparisons).

    Techniques Used: ChIP-sequencing, RNA Sequencing Assay, Hi-C, Expressing, Clone Assay, MANN-WHITNEY

    Longitudinal evolution of proviral integration site features (A and B) Proportion of methylated CpG (mCpG) residues within 2,500 bp upstream of the HIV-1 5′-LTR promoter for IS. Proportions of IS with 100% upstream CpG methylation and the average ratio of methylated CpGs to total CpGs are also indicated. Proviruses with 0 CpGs within 2,500 bp upstream of the integration site were excluded. (C) Median distance between proviral IS and the most proximal host transcriptional start site (TSS) with indicated orientation to the proviral sequence. (D) Median RNA-seq-derived gene expression intensity at nearest host TSS with indicated directional orientation to proviral sequence. (E–G) Among proviruses in the same directional orientation as the nearest host TSS, plots indicate the longitudinal evolution of ATAC-seq reads (E) and H3K4me3-specific (F) and all activating (H3K4me1, H3K4me3, and H3K27ac) ChIP-seq reads (G) surrounding (±10 kb) proviral IS. (H–J) Among proviruses in opposite orientation to the nearest host TSS, plots indicate the longitudinal evolution of ATAC-seq reads (H), H3K4me1-specific (I), and all activating (H3K4me1, H3K4me3, and H3K27ac) ChIP-seq reads (J) surrounding (±10 kb) proviral IS. (E–J) Kendall’s rank correlation coefficients (τ) and corresponding p values are indicated in the upper right of each plot. (A–J) Longitudinal data from all proviruses in genic regions from study subjects 1, 2, and 5 are included; IS located in chromosomal regions in the ENCODE blacklist ( <xref ref-type=Amemiya et al., 2019 ) were excluded; clonal IS are counted only once and assigned to the time point contributing the majority of clonal members or to the earliest time point in the case of a tie. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, Mann-Whitney U tests, Fisher’s exact tests, or G tests were used for all comparisons). " title="... (mCpG) residues within 2,500 bp upstream of the HIV-1 5′-LTR promoter for IS. Proportions of IS with ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Longitudinal evolution of proviral integration site features (A and B) Proportion of methylated CpG (mCpG) residues within 2,500 bp upstream of the HIV-1 5′-LTR promoter for IS. Proportions of IS with 100% upstream CpG methylation and the average ratio of methylated CpGs to total CpGs are also indicated. Proviruses with 0 CpGs within 2,500 bp upstream of the integration site were excluded. (C) Median distance between proviral IS and the most proximal host transcriptional start site (TSS) with indicated orientation to the proviral sequence. (D) Median RNA-seq-derived gene expression intensity at nearest host TSS with indicated directional orientation to proviral sequence. (E–G) Among proviruses in the same directional orientation as the nearest host TSS, plots indicate the longitudinal evolution of ATAC-seq reads (E) and H3K4me3-specific (F) and all activating (H3K4me1, H3K4me3, and H3K27ac) ChIP-seq reads (G) surrounding (±10 kb) proviral IS. (H–J) Among proviruses in opposite orientation to the nearest host TSS, plots indicate the longitudinal evolution of ATAC-seq reads (H), H3K4me1-specific (I), and all activating (H3K4me1, H3K4me3, and H3K27ac) ChIP-seq reads (J) surrounding (±10 kb) proviral IS. (E–J) Kendall’s rank correlation coefficients (τ) and corresponding p values are indicated in the upper right of each plot. (A–J) Longitudinal data from all proviruses in genic regions from study subjects 1, 2, and 5 are included; IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded; clonal IS are counted only once and assigned to the time point contributing the majority of clonal members or to the earliest time point in the case of a tie. ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, Mann-Whitney U tests, Fisher’s exact tests, or G tests were used for all comparisons).

    Techniques Used: Methylation, CpG Methylation Assay, Sequencing, RNA Sequencing Assay, Derivative Assay, Expressing, ChIP-sequencing, MANN-WHITNEY

    Transcriptional activity of individual proviruses after in vitro stimulation (A) Proportion of proviruses producing any HIV-1 RNA or elongated HIV-1 RNA after 12 h of stimulation with PMA/ionomycin or control media. (B and C) Per-cell levels of HIV-1 long LTR (B) and elongated (C) transcripts from single HIV-1-infected cells after 12 h of stimulation with PMA/ionomycin or control media. Only proviruses with detectable HIV-1 RNA are included. (D) Chromosomal distance between proviral IS and nearest ChIP-seq peaks corresponding to repressive histone marks (H3K27me3 and H3K9me3) among viral RNA-positive or -negative proviruses stimulated with PMA/ionomycin. IS are annotated with ChIP-seq data from the ROADMAP project (resting primary CD4 + T cells, <xref ref-type=Kundaje et al., 2015 ) or from ENCODE (activated primary CD4 + T cells ). IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. (E) Phylogenetic tree of clonal proviral species that were detected in stimulated and nonstimulated experimental conditions. (F) Per-cell levels of total HIV-1 transcripts detected in clonal HIV-1-infected cells analyzed in the presence or absence of stimulation with PMA/ionomycin. ( ∗ p < 0.05, ∗∗∗ p < 0.001, Mann-Whitney U tests were used for all comparisons. Error bars represent SEP). " title="... vitro stimulation (A) Proportion of proviruses producing any HIV-1 RNA or elongated HIV-1 RNA after 12 h ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Transcriptional activity of individual proviruses after in vitro stimulation (A) Proportion of proviruses producing any HIV-1 RNA or elongated HIV-1 RNA after 12 h of stimulation with PMA/ionomycin or control media. (B and C) Per-cell levels of HIV-1 long LTR (B) and elongated (C) transcripts from single HIV-1-infected cells after 12 h of stimulation with PMA/ionomycin or control media. Only proviruses with detectable HIV-1 RNA are included. (D) Chromosomal distance between proviral IS and nearest ChIP-seq peaks corresponding to repressive histone marks (H3K27me3 and H3K9me3) among viral RNA-positive or -negative proviruses stimulated with PMA/ionomycin. IS are annotated with ChIP-seq data from the ROADMAP project (resting primary CD4 + T cells, Kundaje et al., 2015 ) or from ENCODE (activated primary CD4 + T cells ). IS located in chromosomal regions in the ENCODE blacklist ( Amemiya et al., 2019 ) were excluded. (E) Phylogenetic tree of clonal proviral species that were detected in stimulated and nonstimulated experimental conditions. (F) Per-cell levels of total HIV-1 transcripts detected in clonal HIV-1-infected cells analyzed in the presence or absence of stimulation with PMA/ionomycin. ( ∗ p < 0.05, ∗∗∗ p < 0.001, Mann-Whitney U tests were used for all comparisons. Error bars represent SEP).

    Techniques Used: Activity Assay, In Vitro, Infection, ChIP-sequencing, MANN-WHITNEY


    Figure Legend Snippet:

    Techniques Used: Recombinant, Activation Assay, Cell Isolation, Isolation, Software, Sequencing, Digital PCR

    rna standard  (ATCC)


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    ATCC rna standard

    Rna Standard, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rna standard/product/ATCC
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    rna standard - by Bioz Stars, 2024-04
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    1) Product Images from "Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses"

    Article Title: Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses

    Journal: Cell

    doi: 10.1016/j.cell.2021.12.011


    Figure Legend Snippet:

    Techniques Used: Recombinant, Activation Assay, Cell Isolation, Isolation, Software, Sequencing, Digital PCR

    hiv 1 standard  (ATCC)


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    ATCC hiv 1 standard
    CODEHOP-mediated PCR amplification of the pol gene from different <t>HIV-1</t> CRFs. (A) Nested RT-PCR amplification of protease and reverse transcriptase genes. Lane 1, CRF35_AD; lane 2, CRF07_BC; lane 3, CRF08_BC; lane 4, CRF63_02A; lane 5, CRF67_01B; lane 6, CRF16_A2D; lane 7, CRF10_CD; lane 8, CRF02_AG; lane 9, CRF50_A1D; lane 10, CRF43_02G; lane 11, negative control; lane 12, high-DNA mass ladder. (B) Seminested RT-PCR amplification of integrase gene. Lane 1, low-DNA mass ladder, lane 2, CRF35_AD; lane 3, CRF07_BC; lane 4, CRF08_BC; lane 5, CRF63_02A; lane 6, CRF67_01B; lane 7, CRF16_A2D; lane 8, CRF10_CD; lane 9, CRF02_AG; lane 10, CRF50_A1D; lane 11, CRF43_02G; lane 12, CRF32_06A1; lane 13, CRF25_cpx.
    Hiv 1 Standard, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "CODEHOP-Mediated PCR Improves HIV-1 Genotyping and Detection of Variants by MinION Sequencing"

    Article Title: CODEHOP-Mediated PCR Improves HIV-1 Genotyping and Detection of Variants by MinION Sequencing

    Journal: Microbiology Spectrum

    doi: 10.1128/Spectrum.01432-21

    CODEHOP-mediated PCR amplification of the pol gene from different HIV-1 CRFs. (A) Nested RT-PCR amplification of protease and reverse transcriptase genes. Lane 1, CRF35_AD; lane 2, CRF07_BC; lane 3, CRF08_BC; lane 4, CRF63_02A; lane 5, CRF67_01B; lane 6, CRF16_A2D; lane 7, CRF10_CD; lane 8, CRF02_AG; lane 9, CRF50_A1D; lane 10, CRF43_02G; lane 11, negative control; lane 12, high-DNA mass ladder. (B) Seminested RT-PCR amplification of integrase gene. Lane 1, low-DNA mass ladder, lane 2, CRF35_AD; lane 3, CRF07_BC; lane 4, CRF08_BC; lane 5, CRF63_02A; lane 6, CRF67_01B; lane 7, CRF16_A2D; lane 8, CRF10_CD; lane 9, CRF02_AG; lane 10, CRF50_A1D; lane 11, CRF43_02G; lane 12, CRF32_06A1; lane 13, CRF25_cpx.
    Figure Legend Snippet: CODEHOP-mediated PCR amplification of the pol gene from different HIV-1 CRFs. (A) Nested RT-PCR amplification of protease and reverse transcriptase genes. Lane 1, CRF35_AD; lane 2, CRF07_BC; lane 3, CRF08_BC; lane 4, CRF63_02A; lane 5, CRF67_01B; lane 6, CRF16_A2D; lane 7, CRF10_CD; lane 8, CRF02_AG; lane 9, CRF50_A1D; lane 10, CRF43_02G; lane 11, negative control; lane 12, high-DNA mass ladder. (B) Seminested RT-PCR amplification of integrase gene. Lane 1, low-DNA mass ladder, lane 2, CRF35_AD; lane 3, CRF07_BC; lane 4, CRF08_BC; lane 5, CRF63_02A; lane 6, CRF67_01B; lane 7, CRF16_A2D; lane 8, CRF10_CD; lane 9, CRF02_AG; lane 10, CRF50_A1D; lane 11, CRF43_02G; lane 12, CRF32_06A1; lane 13, CRF25_cpx.

    Techniques Used: Amplification, Reverse Transcription Polymerase Chain Reaction, Negative Control

    synthetic hiv 1 rna standard  (ATCC)


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    ATCC synthetic hiv 1 rna standard
    Schematic presentation of <t>HIV-1</t> detection using the cellphone system. The developed system integrates cellphone-based optical sensing, loop-mediated isothermal amplification and micromotor motion (CALM). a A loop-mediated isothermal amplification (LAMP) reaction is performed to amplify the nucleic acid of HIV-1 and large-size looped amplicons. b The formed amplicons are mixed with DNA-modified micromotors that are specifically designed using 6-μm polystyrene (PS) beads covered with a hybrid surface layer of platinum (Pt) and gold (Au) nanoparticles to power the catalytic motion of motors in the presence of hydrogen peroxide. c The capture of LAMP amplicons on the surface of motors results in the formation of motile assemblies with a catalytic head of motors and large tail of DNA. d The motion of these assemblies can be detected and measured using a cellphone system on-chip for qualitative HIV-1 detection
    Synthetic Hiv 1 Rna Standard, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/synthetic hiv 1 rna standard/product/ATCC
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    1) Product Images from "DNA engineered micromotors powered by metal nanoparticles for motion based cellphone diagnostics"

    Article Title: DNA engineered micromotors powered by metal nanoparticles for motion based cellphone diagnostics

    Journal: Nature Communications

    doi: 10.1038/s41467-018-06727-8

    Schematic presentation of HIV-1 detection using the cellphone system. The developed system integrates cellphone-based optical sensing, loop-mediated isothermal amplification and micromotor motion (CALM). a A loop-mediated isothermal amplification (LAMP) reaction is performed to amplify the nucleic acid of HIV-1 and large-size looped amplicons. b The formed amplicons are mixed with DNA-modified micromotors that are specifically designed using 6-μm polystyrene (PS) beads covered with a hybrid surface layer of platinum (Pt) and gold (Au) nanoparticles to power the catalytic motion of motors in the presence of hydrogen peroxide. c The capture of LAMP amplicons on the surface of motors results in the formation of motile assemblies with a catalytic head of motors and large tail of DNA. d The motion of these assemblies can be detected and measured using a cellphone system on-chip for qualitative HIV-1 detection
    Figure Legend Snippet: Schematic presentation of HIV-1 detection using the cellphone system. The developed system integrates cellphone-based optical sensing, loop-mediated isothermal amplification and micromotor motion (CALM). a A loop-mediated isothermal amplification (LAMP) reaction is performed to amplify the nucleic acid of HIV-1 and large-size looped amplicons. b The formed amplicons are mixed with DNA-modified micromotors that are specifically designed using 6-μm polystyrene (PS) beads covered with a hybrid surface layer of platinum (Pt) and gold (Au) nanoparticles to power the catalytic motion of motors in the presence of hydrogen peroxide. c The capture of LAMP amplicons on the surface of motors results in the formation of motile assemblies with a catalytic head of motors and large tail of DNA. d The motion of these assemblies can be detected and measured using a cellphone system on-chip for qualitative HIV-1 detection

    Techniques Used: Amplification, Modification

    Validation of the CALM system using HIV-1 LAMP amplicon. Detection sensitivity: a agarose gel electrophoresis image of serially diluted HIV-1 RNA samples (0 copies/μl–10 5 copies/μl). Lane M: 1-kb DNA ladder marker; Lane NC: negative control (without target RNA template); b average velocity of motors ( n = 30) with (in red box) and without (in blue box) HIV-1 LAMP amplicons generated from HIV-1 RNA concentration of 10 4 copies/μl. The digital images show motion trajectories of motors in the presence and absence of LAMP amplicons tested in 5% H 2 O 2 (scale bar = 100 μm); c average velocity of motors in the presence of 0% (no LAMP, control) to 100% dilutions of HIV-1 LAMP amplification products (10 4 copies/μl) prepared in LAMP reaction buffer. Detection specificity: d agarose gel electrophoresis image of HIV-1 and human papillomavirus 16 (HPV-16) and different non-targeted viruses, including hepatitis C virus (HCV), hepatitis B virus (HBV), and herpes simplex virus type-1 (HSV-1); Lane M: 1-kb DNA ladder marker; Lane 1: HSV-1; Lane2: HBV; Lane 3: HCV; Lane 4: HIV-1; Lane 5: HPV-16; e average velocity of motors ( n = 30) in the presence of the amplification products of the target and non-target viruses; f representative digital images show the motion trajectories of motors in the presence of LAMP amplification products generated with the target and non-target viruses (scale bar = 100 μm). The concentration of the nucleic acid of all of the tested viruses was adjusted to 10 4 copies/μl before LAMP amplification. The results are expressed as the average values of three independent experiments. Error bars represent standard deviations. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the corresponding group with the target HIV-1, calculated using unpaired t test
    Figure Legend Snippet: Validation of the CALM system using HIV-1 LAMP amplicon. Detection sensitivity: a agarose gel electrophoresis image of serially diluted HIV-1 RNA samples (0 copies/μl–10 5 copies/μl). Lane M: 1-kb DNA ladder marker; Lane NC: negative control (without target RNA template); b average velocity of motors ( n = 30) with (in red box) and without (in blue box) HIV-1 LAMP amplicons generated from HIV-1 RNA concentration of 10 4 copies/μl. The digital images show motion trajectories of motors in the presence and absence of LAMP amplicons tested in 5% H 2 O 2 (scale bar = 100 μm); c average velocity of motors in the presence of 0% (no LAMP, control) to 100% dilutions of HIV-1 LAMP amplification products (10 4 copies/μl) prepared in LAMP reaction buffer. Detection specificity: d agarose gel electrophoresis image of HIV-1 and human papillomavirus 16 (HPV-16) and different non-targeted viruses, including hepatitis C virus (HCV), hepatitis B virus (HBV), and herpes simplex virus type-1 (HSV-1); Lane M: 1-kb DNA ladder marker; Lane 1: HSV-1; Lane2: HBV; Lane 3: HCV; Lane 4: HIV-1; Lane 5: HPV-16; e average velocity of motors ( n = 30) in the presence of the amplification products of the target and non-target viruses; f representative digital images show the motion trajectories of motors in the presence of LAMP amplification products generated with the target and non-target viruses (scale bar = 100 μm). The concentration of the nucleic acid of all of the tested viruses was adjusted to 10 4 copies/μl before LAMP amplification. The results are expressed as the average values of three independent experiments. Error bars represent standard deviations. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the corresponding group with the target HIV-1, calculated using unpaired t test

    Techniques Used: Amplification, Agarose Gel Electrophoresis, Marker, Negative Control, Generated, Concentration Assay

    HIV-1 detection using the CALM system. Synthetic HIV-1 RNA standard detection: a bar graph shows the average velocity of motors recorded by the CALM system for phosphate-buffered saline (1× PBS, pH 7.4) samples ( n = 45) spiked with different HIV-1 RNA concentrations. Vertical black dotted line indicates the average velocity at the threshold concentration of 1000 virus particles/ml; b representative digital images show the motion trajectories of motors in the absence of HIV-1 RNA (control) or the presence of HIV-1 RNA at concentrations above and below the threshold of 1000 copies/ml (scale bar = 100 μm). HIV-1 particles detection: c heatmap of the average motor velocity measured by the CALM system for different virus concentrations spiked in 1× PBS ( n = 35) and serum ( n = 20). The average velocity of HIV-1 positive samples (≥1000 virus particles/ml) is ≤0.704 ± 0.08 µm/s (yellow in color) and the average velocity of HIV-1 negative samples (<1000 virus particles/ml) is >0.704 ± 0.08 µm/s (red in color); d receiver-operating characteristics (ROC) curve analysis of 1× PBS ( n = 35) and serum ( n = 20) samples spiked with different HIV-1 concentrations showing the assay detection sensitivity (sens) and specificity (spec) compared to real-time polymerase chain reaction (RT-PCR). The threshold value for virus concentration applied here was 1000 particles/ml. Samples with virus concentrations above and below 1000 particles/ml were classified as positive and negative, respectively; e vertical scatterplot analysis of virus spiked samples ( n = 54). The threshold value for average motor velocity applied here was 0.704 µm/s that corresponds to 1000 particles/ml. Samples with velocities above and below 0.704 µm/s were classified as 1 (positive) and 0 (negative), respectively; f representative digital images show the motion trajectories of motors in the absence of HIV-1 particle (control) and the presence of HIV-1 at concentrations above and below 1000 virus particles/ml (scale bar = 100 μm). The results are expressed as the average values of three independent experiments and error bars represent standard deviations
    Figure Legend Snippet: HIV-1 detection using the CALM system. Synthetic HIV-1 RNA standard detection: a bar graph shows the average velocity of motors recorded by the CALM system for phosphate-buffered saline (1× PBS, pH 7.4) samples ( n = 45) spiked with different HIV-1 RNA concentrations. Vertical black dotted line indicates the average velocity at the threshold concentration of 1000 virus particles/ml; b representative digital images show the motion trajectories of motors in the absence of HIV-1 RNA (control) or the presence of HIV-1 RNA at concentrations above and below the threshold of 1000 copies/ml (scale bar = 100 μm). HIV-1 particles detection: c heatmap of the average motor velocity measured by the CALM system for different virus concentrations spiked in 1× PBS ( n = 35) and serum ( n = 20). The average velocity of HIV-1 positive samples (≥1000 virus particles/ml) is ≤0.704 ± 0.08 µm/s (yellow in color) and the average velocity of HIV-1 negative samples (<1000 virus particles/ml) is >0.704 ± 0.08 µm/s (red in color); d receiver-operating characteristics (ROC) curve analysis of 1× PBS ( n = 35) and serum ( n = 20) samples spiked with different HIV-1 concentrations showing the assay detection sensitivity (sens) and specificity (spec) compared to real-time polymerase chain reaction (RT-PCR). The threshold value for virus concentration applied here was 1000 particles/ml. Samples with virus concentrations above and below 1000 particles/ml were classified as positive and negative, respectively; e vertical scatterplot analysis of virus spiked samples ( n = 54). The threshold value for average motor velocity applied here was 0.704 µm/s that corresponds to 1000 particles/ml. Samples with velocities above and below 0.704 µm/s were classified as 1 (positive) and 0 (negative), respectively; f representative digital images show the motion trajectories of motors in the absence of HIV-1 particle (control) and the presence of HIV-1 at concentrations above and below 1000 virus particles/ml (scale bar = 100 μm). The results are expressed as the average values of three independent experiments and error bars represent standard deviations

    Techniques Used: Concentration Assay, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

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  • 94
    ATCC quantitative synthetic human immunodeficiency virus 1 hiv 1 rna
    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) <t>HIV-1</t> proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.
    Quantitative Synthetic Human Immunodeficiency Virus 1 Hiv 1 Rna, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    quantitative synthetic human immunodeficiency virus 1 hiv 1 rna - by Bioz Stars, 2024-04
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    94
    ATCC synthetic hiv 1 rna
    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) <t>HIV-1</t> proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.
    Synthetic Hiv 1 Rna, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    ATCC rna standard

    Rna Standard, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rna standard/product/ATCC
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    rna standard - by Bioz Stars, 2024-04
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    94
    ATCC hiv 1 standard
    CODEHOP-mediated PCR amplification of the pol gene from different <t>HIV-1</t> CRFs. (A) Nested RT-PCR amplification of protease and reverse transcriptase genes. Lane 1, CRF35_AD; lane 2, CRF07_BC; lane 3, CRF08_BC; lane 4, CRF63_02A; lane 5, CRF67_01B; lane 6, CRF16_A2D; lane 7, CRF10_CD; lane 8, CRF02_AG; lane 9, CRF50_A1D; lane 10, CRF43_02G; lane 11, negative control; lane 12, high-DNA mass ladder. (B) Seminested RT-PCR amplification of integrase gene. Lane 1, low-DNA mass ladder, lane 2, CRF35_AD; lane 3, CRF07_BC; lane 4, CRF08_BC; lane 5, CRF63_02A; lane 6, CRF67_01B; lane 7, CRF16_A2D; lane 8, CRF10_CD; lane 9, CRF02_AG; lane 10, CRF50_A1D; lane 11, CRF43_02G; lane 12, CRF32_06A1; lane 13, CRF25_cpx.
    Hiv 1 Standard, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    ATCC synthetic hiv 1 rna standard
    Schematic presentation of <t>HIV-1</t> detection using the cellphone system. The developed system integrates cellphone-based optical sensing, loop-mediated isothermal amplification and micromotor motion (CALM). a A loop-mediated isothermal amplification (LAMP) reaction is performed to amplify the nucleic acid of HIV-1 and large-size looped amplicons. b The formed amplicons are mixed with DNA-modified micromotors that are specifically designed using 6-μm polystyrene (PS) beads covered with a hybrid surface layer of platinum (Pt) and gold (Au) nanoparticles to power the catalytic motion of motors in the presence of hydrogen peroxide. c The capture of LAMP amplicons on the surface of motors results in the formation of motile assemblies with a catalytic head of motors and large tail of DNA. d The motion of these assemblies can be detected and measured using a cellphone system on-chip for qualitative HIV-1 detection
    Synthetic Hiv 1 Rna Standard, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) HIV-1 proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet: Proviral reservoir profile in long-term ART-treated individuals (A and B) Frequency of total (A) and intact (B) HIV-1 proviruses in long-term ART-treated individuals (LT-ART), in people living with HIV (PLHIV) undergoing moderate durations of treatment (median of 9 years) (m-ART), and in elite controllers (ECs). Open circles indicate data at the limit of detection. (C) Proportion of intact proviruses within total HIV-1 proviruses in indicated study cohorts. (D) Proportion of proviruses with genome-intact or defective sequences in indicated study cohorts. (E) Average genetic distance between intact proviruses from indicated study cohorts, determined by pairwise comparisons between all intact proviruses from a given study participant. (F) Pie charts reflecting proportions of intact proviruses detected once (non-clonal) or multiple times (clonal) in the three indicated study cohorts. (G) Proportions of clonally expanded intact HIV-1 proviruses within the total pool of intact HIV-1-proviruses from each study participant. (H) (Left panel) Proportion of wild-type clade B CTL epitopes restricted by autologous HLA class I alleles within intact proviruses from indicated study cohorts. Each symbol represents one intact proviral sequence; all intact clade B sequences were included. (Right panel) Numbers of base pair variations significantly associated with autologous HLA class I alleles, determined as described by Carlson et al., within intact HIV-1 proviruses from indicated study participants. Each symbol reflects one intact provirus. Clonal sequences were counted once. Box and Whisker plots demonstrate median, interquartile ranges, and minimum/maximum. (A–H) FDR-adjusted two-sided Kruskal-Wallis nonparametric test or FDR-adjusted Fisher’s exact test were used, as appropriate. (A–C, E, and G) Horizontal bars indicate the median and n represents the number of study subjects. (D, F, and H) n reflects the number of viral sequences.

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Sequencing, Whisker Assay

    Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic trees for intact HIV-1 proviruses from long-term ART-treated individuals (LT01–LT08). Coordinates of chromosomal integration sites obtained by integration site loop amplification (ISLA) and corresponding gene name (if applicable) are indicated. Symbols indicate sequences generated by FLIP-seq, MIP-seq, PRIP-seq or from quantitative viral outgrowth assays (qVOAs). Proviruses integrated in highly repetitive satellite DNA could not always be definitively mapped to specific chromosomal locations; a detailed list of integration sites is shown in <xref ref-type=Table S1 . ∗ Sequences differ by 1 or 2 base pairs from adjacent clonal sequences. LADs, lamina-associated domains. (B) Proportions of intact proviruses with indicated integration site features in LT-ART individuals and comparison cohorts. (C) Chromosomal distance between integration sites of intact proviruses to most proximal host transcriptional start sites (TSSs), as determined by RNA-seq in CD4 T cells from reference datasets in total, effector-memory (EM), or central-memory (CM) primary CD4 T cells or from genome browser (GB). Box and Whisker plots show median, interquartile ranges and minimum/maximum. (D) Proportions of genome-intact proviral sequences in structural compartments/subcompartments A and B, as determined by Hi-C seq data. Integration sites not covered in the reference dataset were excluded. (B–D) Data from individuals with moderate ART treatment durations (m-ART) and from EC are shown for comparison. Clonal sequences are counted once. (B–D) p values were calculated by FDR-adjusted two-sided Kruskal-Wallis nonparametric tests or chi-square tests, adjusted for multiple comparison testing where applicable. n reflects the number of integration sites. " width="100%" height="100%">

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet: Chromosomal positioning of intact HIV-1 proviruses in long-term ART-treated individuals (A) Maximum-likelihood phylogenetic trees for intact HIV-1 proviruses from long-term ART-treated individuals (LT01–LT08). Coordinates of chromosomal integration sites obtained by integration site loop amplification (ISLA) and corresponding gene name (if applicable) are indicated. Symbols indicate sequences generated by FLIP-seq, MIP-seq, PRIP-seq or from quantitative viral outgrowth assays (qVOAs). Proviruses integrated in highly repetitive satellite DNA could not always be definitively mapped to specific chromosomal locations; a detailed list of integration sites is shown in Table S1 . ∗ Sequences differ by 1 or 2 base pairs from adjacent clonal sequences. LADs, lamina-associated domains. (B) Proportions of intact proviruses with indicated integration site features in LT-ART individuals and comparison cohorts. (C) Chromosomal distance between integration sites of intact proviruses to most proximal host transcriptional start sites (TSSs), as determined by RNA-seq in CD4 T cells from reference datasets in total, effector-memory (EM), or central-memory (CM) primary CD4 T cells or from genome browser (GB). Box and Whisker plots show median, interquartile ranges and minimum/maximum. (D) Proportions of genome-intact proviral sequences in structural compartments/subcompartments A and B, as determined by Hi-C seq data. Integration sites not covered in the reference dataset were excluded. (B–D) Data from individuals with moderate ART treatment durations (m-ART) and from EC are shown for comparison. Clonal sequences are counted once. (B–D) p values were calculated by FDR-adjusted two-sided Kruskal-Wallis nonparametric tests or chi-square tests, adjusted for multiple comparison testing where applicable. n reflects the number of integration sites.

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Amplification, Generated, RNA Sequencing Assay, Whisker Assay, Hi-C

    Transcriptional activity of single HIV-1 proviruses from study participant LT03 (A) Maximum-likelihood phylogenetic tree of individual proviruses isolated from LT03 using PRIP-seq. Chromosomal integration sites are indicated where available; genes harboring the integration site are shown where applicable. Color coding reflects the transcriptional activity of proviral species. (B) Genome browser snapshot indicating RNA-seq, Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and ChIP-seq reads surrounding the chromosomal integration site of the indicated proviral sequence from study participant LT03; RNA-seq and ATAC-seq reads are derived from reference data of HIV-1-infected ART-treated persons and were first described in Einkauf et al. ; ChIP-seq reads from the reference dataset of the ROADMAP consortium were used.

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet: Transcriptional activity of single HIV-1 proviruses from study participant LT03 (A) Maximum-likelihood phylogenetic tree of individual proviruses isolated from LT03 using PRIP-seq. Chromosomal integration sites are indicated where available; genes harboring the integration site are shown where applicable. Color coding reflects the transcriptional activity of proviral species. (B) Genome browser snapshot indicating RNA-seq, Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and ChIP-seq reads surrounding the chromosomal integration site of the indicated proviral sequence from study participant LT03; RNA-seq and ATAC-seq reads are derived from reference data of HIV-1-infected ART-treated persons and were first described in Einkauf et al. ; ChIP-seq reads from the reference dataset of the ROADMAP consortium were used.

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Activity Assay, Isolation, RNA Sequencing Assay, Sequencing, ChIP-sequencing, Derivative Assay, Infection

    Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots reflecting the chromosomal locations of defective proviruses at indicated time points in five study participants (LT01–LT04, LT08). Each symbol reflects one defective provirus. Clonal sequences, defined by integration sites and/or complete sequence identity, are highlighted. Color-coded arches around the plots indicate types of defects in HIV-1 genomes. (B) Proportions of intact and defective proviruses with indicated integration site features at time points T1–T3. (C) Chromosomal distance between integration sites of intact and defective proviruses to most proximal TSS, as determined by RNA-seq in CD4 T cells from reference datasets at indicated time points. Box and Whisker plots show median, interquartile ranges and minimum/maximum. (B and C) Data from defective proviruses after 20 years of suppressive antiretroviral therapy are cross-sectionally compared with corresponding data from intact proviruses. A complete list of defective proviruses and their corresponding chromosomal location is indicated in <xref ref-type=Table S1 . p values were calculated by a chi-square test in (B) and by an FDR-adjusted two-sided Kruskal-Wallis nonparametric test in (C), adjusted for multiple comparison testing where applicable. n reflects the number of integration sites. " width="100%" height="100%">

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet: Proviral landscape of defective HIV-1 proviruses in long-term ART-treated individuals (A) CIRCOS plots reflecting the chromosomal locations of defective proviruses at indicated time points in five study participants (LT01–LT04, LT08). Each symbol reflects one defective provirus. Clonal sequences, defined by integration sites and/or complete sequence identity, are highlighted. Color-coded arches around the plots indicate types of defects in HIV-1 genomes. (B) Proportions of intact and defective proviruses with indicated integration site features at time points T1–T3. (C) Chromosomal distance between integration sites of intact and defective proviruses to most proximal TSS, as determined by RNA-seq in CD4 T cells from reference datasets at indicated time points. Box and Whisker plots show median, interquartile ranges and minimum/maximum. (B and C) Data from defective proviruses after 20 years of suppressive antiretroviral therapy are cross-sectionally compared with corresponding data from intact proviruses. A complete list of defective proviruses and their corresponding chromosomal location is indicated in Table S1 . p values were calculated by a chi-square test in (B) and by an FDR-adjusted two-sided Kruskal-Wallis nonparametric test in (C), adjusted for multiple comparison testing where applicable. n reflects the number of integration sites.

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Sequencing, RNA Sequencing Assay, Whisker Assay

    Longitudinal dynamics of intact proviruses in two individuals with post-treatment control (A) Longitudinal analysis of HIV-1 plasma viral load in study persons 04 and 30. PBMC sampling time points are indicated by arrows. Day 0 is the first day of treatment interruption. (B) CIRCOS plots indicating longitudinal evolution of intact proviruses and their corresponding chromosomal integration sites. Each symbol reflects one intact provirus. Clonal sequences, defined by identical integration sites and/or complete sequence identity, are highlighted. In study person 30, two clones were detected in repetitive genomic regions in immediate proximity to micro-satellite DNA; due to the repetitive nature of these regions, the exact chromosomal region could not be definitively identified. ∗ Intact proviral sequences analyzed without identification of integration sites that differ by 1 or 2 base pairs from adjacent clonal sequences and might be part of the respective clones. (C) CIRCOS plots indicating longitudinal evolution and chromosomal locations of defective HIV-1 proviruses in study persons 04 and 30. Color-coded arches around the plots indicate types of defects in HIV-1 genomes.

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet: Longitudinal dynamics of intact proviruses in two individuals with post-treatment control (A) Longitudinal analysis of HIV-1 plasma viral load in study persons 04 and 30. PBMC sampling time points are indicated by arrows. Day 0 is the first day of treatment interruption. (B) CIRCOS plots indicating longitudinal evolution of intact proviruses and their corresponding chromosomal integration sites. Each symbol reflects one intact provirus. Clonal sequences, defined by identical integration sites and/or complete sequence identity, are highlighted. In study person 30, two clones were detected in repetitive genomic regions in immediate proximity to micro-satellite DNA; due to the repetitive nature of these regions, the exact chromosomal region could not be definitively identified. ∗ Intact proviral sequences analyzed without identification of integration sites that differ by 1 or 2 base pairs from adjacent clonal sequences and might be part of the respective clones. (C) CIRCOS plots indicating longitudinal evolution and chromosomal locations of defective HIV-1 proviruses in study persons 04 and 30. Color-coded arches around the plots indicate types of defects in HIV-1 genomes.

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Sampling, Sequencing, Clone Assay

    Integration site profile of intact proviruses from study persons with virological rebound after ART interruption (A) Longitudinal analysis of HIV-1 plasma viral load in three study persons who developed rapid viral rebound following ART interruption. PBMC sampling time points are indicated by arrows. (B) Maximum likelihood phylogenetic tree for intact proviruses isolated from PBMC samples prior to ART interruption in three rebounders shown in (A). Chromosomal integration sites are indicated when available. (C) Proportions of intact and defective proviruses with indicated integration sites in PTC. Data from intact proviruses identified in rebounders are shown for comparison. Data from the time point immediately prior to treatment interruption are shown; clonal sequences are counted individually. Significance was calculated using a chi-square test, adjusted for multiple comparison testing. n reflects the number of integration sites.

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet: Integration site profile of intact proviruses from study persons with virological rebound after ART interruption (A) Longitudinal analysis of HIV-1 plasma viral load in three study persons who developed rapid viral rebound following ART interruption. PBMC sampling time points are indicated by arrows. (B) Maximum likelihood phylogenetic tree for intact proviruses isolated from PBMC samples prior to ART interruption in three rebounders shown in (A). Chromosomal integration sites are indicated when available. (C) Proportions of intact and defective proviruses with indicated integration sites in PTC. Data from intact proviruses identified in rebounders are shown for comparison. Data from the time point immediately prior to treatment interruption are shown; clonal sequences are counted individually. Significance was calculated using a chi-square test, adjusted for multiple comparison testing. n reflects the number of integration sites.

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Sampling, Isolation

    Journal: Cell Host & Microbe

    Article Title: Progressive transformation of the HIV-1 reservoir cell profile over two decades of antiviral therapy

    doi: 10.1016/j.chom.2022.12.002

    Figure Lengend Snippet:

    Article Snippet: Quantitative Synthetic Human immunodeficiency virus 1 (HIV-1) RNA , ATCC , Cat#VR-3245S.

    Techniques: Western Blot, Recombinant, Activation Assay, Cell Isolation, Reporter Gene Assay, Isolation, Software, Sequencing, Digital PCR

    Journal: Cell

    Article Title: Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses

    doi: 10.1016/j.cell.2021.12.011

    Figure Lengend Snippet:

    Article Snippet: In selected cases, these experiments were performed using an RNA standard (ATCC, VR-3245SD) with known viral copy numbers spiked into a background population of 10,000 cells from an HIV-1-negative person for technical validation of the assay workflow.

    Techniques: Recombinant, Activation Assay, Cell Isolation, Isolation, Software, Sequencing, Digital PCR

    CODEHOP-mediated PCR amplification of the pol gene from different HIV-1 CRFs. (A) Nested RT-PCR amplification of protease and reverse transcriptase genes. Lane 1, CRF35_AD; lane 2, CRF07_BC; lane 3, CRF08_BC; lane 4, CRF63_02A; lane 5, CRF67_01B; lane 6, CRF16_A2D; lane 7, CRF10_CD; lane 8, CRF02_AG; lane 9, CRF50_A1D; lane 10, CRF43_02G; lane 11, negative control; lane 12, high-DNA mass ladder. (B) Seminested RT-PCR amplification of integrase gene. Lane 1, low-DNA mass ladder, lane 2, CRF35_AD; lane 3, CRF07_BC; lane 4, CRF08_BC; lane 5, CRF63_02A; lane 6, CRF67_01B; lane 7, CRF16_A2D; lane 8, CRF10_CD; lane 9, CRF02_AG; lane 10, CRF50_A1D; lane 11, CRF43_02G; lane 12, CRF32_06A1; lane 13, CRF25_cpx.

    Journal: Microbiology Spectrum

    Article Title: CODEHOP-Mediated PCR Improves HIV-1 Genotyping and Detection of Variants by MinION Sequencing

    doi: 10.1128/Spectrum.01432-21

    Figure Lengend Snippet: CODEHOP-mediated PCR amplification of the pol gene from different HIV-1 CRFs. (A) Nested RT-PCR amplification of protease and reverse transcriptase genes. Lane 1, CRF35_AD; lane 2, CRF07_BC; lane 3, CRF08_BC; lane 4, CRF63_02A; lane 5, CRF67_01B; lane 6, CRF16_A2D; lane 7, CRF10_CD; lane 8, CRF02_AG; lane 9, CRF50_A1D; lane 10, CRF43_02G; lane 11, negative control; lane 12, high-DNA mass ladder. (B) Seminested RT-PCR amplification of integrase gene. Lane 1, low-DNA mass ladder, lane 2, CRF35_AD; lane 3, CRF07_BC; lane 4, CRF08_BC; lane 5, CRF63_02A; lane 6, CRF67_01B; lane 7, CRF16_A2D; lane 8, CRF10_CD; lane 9, CRF02_AG; lane 10, CRF50_A1D; lane 11, CRF43_02G; lane 12, CRF32_06A1; lane 13, CRF25_cpx.

    Article Snippet: The analytical sensitivity of the assay, also known as the limit of detection (LOD), was determined by probit regression analysis using 12 replicates of each dilution of the HIV-1 standard (ATCC VR-3245SD; ATCC, Manassas, VA, USA).

    Techniques: Amplification, Reverse Transcription Polymerase Chain Reaction, Negative Control

    Schematic presentation of HIV-1 detection using the cellphone system. The developed system integrates cellphone-based optical sensing, loop-mediated isothermal amplification and micromotor motion (CALM). a A loop-mediated isothermal amplification (LAMP) reaction is performed to amplify the nucleic acid of HIV-1 and large-size looped amplicons. b The formed amplicons are mixed with DNA-modified micromotors that are specifically designed using 6-μm polystyrene (PS) beads covered with a hybrid surface layer of platinum (Pt) and gold (Au) nanoparticles to power the catalytic motion of motors in the presence of hydrogen peroxide. c The capture of LAMP amplicons on the surface of motors results in the formation of motile assemblies with a catalytic head of motors and large tail of DNA. d The motion of these assemblies can be detected and measured using a cellphone system on-chip for qualitative HIV-1 detection

    Journal: Nature Communications

    Article Title: DNA engineered micromotors powered by metal nanoparticles for motion based cellphone diagnostics

    doi: 10.1038/s41467-018-06727-8

    Figure Lengend Snippet: Schematic presentation of HIV-1 detection using the cellphone system. The developed system integrates cellphone-based optical sensing, loop-mediated isothermal amplification and micromotor motion (CALM). a A loop-mediated isothermal amplification (LAMP) reaction is performed to amplify the nucleic acid of HIV-1 and large-size looped amplicons. b The formed amplicons are mixed with DNA-modified micromotors that are specifically designed using 6-μm polystyrene (PS) beads covered with a hybrid surface layer of platinum (Pt) and gold (Au) nanoparticles to power the catalytic motion of motors in the presence of hydrogen peroxide. c The capture of LAMP amplicons on the surface of motors results in the formation of motile assemblies with a catalytic head of motors and large tail of DNA. d The motion of these assemblies can be detected and measured using a cellphone system on-chip for qualitative HIV-1 detection

    Article Snippet: The cellphone system was calibrated with PBS samples spiked with synthetic HIV-1 RNA standard (0–1 × 10 7 copies/ml) purchased from ATCC (VR-3245SD) and then compared to the standard RT-PCR using 1× PBS (pH 7.4) and serum samples spiked with HIV-1 particles at concentrations between 0 and 1.5 × 10 4 virus particles/ml.

    Techniques: Amplification, Modification

    Validation of the CALM system using HIV-1 LAMP amplicon. Detection sensitivity: a agarose gel electrophoresis image of serially diluted HIV-1 RNA samples (0 copies/μl–10 5 copies/μl). Lane M: 1-kb DNA ladder marker; Lane NC: negative control (without target RNA template); b average velocity of motors ( n = 30) with (in red box) and without (in blue box) HIV-1 LAMP amplicons generated from HIV-1 RNA concentration of 10 4 copies/μl. The digital images show motion trajectories of motors in the presence and absence of LAMP amplicons tested in 5% H 2 O 2 (scale bar = 100 μm); c average velocity of motors in the presence of 0% (no LAMP, control) to 100% dilutions of HIV-1 LAMP amplification products (10 4 copies/μl) prepared in LAMP reaction buffer. Detection specificity: d agarose gel electrophoresis image of HIV-1 and human papillomavirus 16 (HPV-16) and different non-targeted viruses, including hepatitis C virus (HCV), hepatitis B virus (HBV), and herpes simplex virus type-1 (HSV-1); Lane M: 1-kb DNA ladder marker; Lane 1: HSV-1; Lane2: HBV; Lane 3: HCV; Lane 4: HIV-1; Lane 5: HPV-16; e average velocity of motors ( n = 30) in the presence of the amplification products of the target and non-target viruses; f representative digital images show the motion trajectories of motors in the presence of LAMP amplification products generated with the target and non-target viruses (scale bar = 100 μm). The concentration of the nucleic acid of all of the tested viruses was adjusted to 10 4 copies/μl before LAMP amplification. The results are expressed as the average values of three independent experiments. Error bars represent standard deviations. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the corresponding group with the target HIV-1, calculated using unpaired t test

    Journal: Nature Communications

    Article Title: DNA engineered micromotors powered by metal nanoparticles for motion based cellphone diagnostics

    doi: 10.1038/s41467-018-06727-8

    Figure Lengend Snippet: Validation of the CALM system using HIV-1 LAMP amplicon. Detection sensitivity: a agarose gel electrophoresis image of serially diluted HIV-1 RNA samples (0 copies/μl–10 5 copies/μl). Lane M: 1-kb DNA ladder marker; Lane NC: negative control (without target RNA template); b average velocity of motors ( n = 30) with (in red box) and without (in blue box) HIV-1 LAMP amplicons generated from HIV-1 RNA concentration of 10 4 copies/μl. The digital images show motion trajectories of motors in the presence and absence of LAMP amplicons tested in 5% H 2 O 2 (scale bar = 100 μm); c average velocity of motors in the presence of 0% (no LAMP, control) to 100% dilutions of HIV-1 LAMP amplification products (10 4 copies/μl) prepared in LAMP reaction buffer. Detection specificity: d agarose gel electrophoresis image of HIV-1 and human papillomavirus 16 (HPV-16) and different non-targeted viruses, including hepatitis C virus (HCV), hepatitis B virus (HBV), and herpes simplex virus type-1 (HSV-1); Lane M: 1-kb DNA ladder marker; Lane 1: HSV-1; Lane2: HBV; Lane 3: HCV; Lane 4: HIV-1; Lane 5: HPV-16; e average velocity of motors ( n = 30) in the presence of the amplification products of the target and non-target viruses; f representative digital images show the motion trajectories of motors in the presence of LAMP amplification products generated with the target and non-target viruses (scale bar = 100 μm). The concentration of the nucleic acid of all of the tested viruses was adjusted to 10 4 copies/μl before LAMP amplification. The results are expressed as the average values of three independent experiments. Error bars represent standard deviations. ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the corresponding group with the target HIV-1, calculated using unpaired t test

    Article Snippet: The cellphone system was calibrated with PBS samples spiked with synthetic HIV-1 RNA standard (0–1 × 10 7 copies/ml) purchased from ATCC (VR-3245SD) and then compared to the standard RT-PCR using 1× PBS (pH 7.4) and serum samples spiked with HIV-1 particles at concentrations between 0 and 1.5 × 10 4 virus particles/ml.

    Techniques: Amplification, Agarose Gel Electrophoresis, Marker, Negative Control, Generated, Concentration Assay

    HIV-1 detection using the CALM system. Synthetic HIV-1 RNA standard detection: a bar graph shows the average velocity of motors recorded by the CALM system for phosphate-buffered saline (1× PBS, pH 7.4) samples ( n = 45) spiked with different HIV-1 RNA concentrations. Vertical black dotted line indicates the average velocity at the threshold concentration of 1000 virus particles/ml; b representative digital images show the motion trajectories of motors in the absence of HIV-1 RNA (control) or the presence of HIV-1 RNA at concentrations above and below the threshold of 1000 copies/ml (scale bar = 100 μm). HIV-1 particles detection: c heatmap of the average motor velocity measured by the CALM system for different virus concentrations spiked in 1× PBS ( n = 35) and serum ( n = 20). The average velocity of HIV-1 positive samples (≥1000 virus particles/ml) is ≤0.704 ± 0.08 µm/s (yellow in color) and the average velocity of HIV-1 negative samples (<1000 virus particles/ml) is >0.704 ± 0.08 µm/s (red in color); d receiver-operating characteristics (ROC) curve analysis of 1× PBS ( n = 35) and serum ( n = 20) samples spiked with different HIV-1 concentrations showing the assay detection sensitivity (sens) and specificity (spec) compared to real-time polymerase chain reaction (RT-PCR). The threshold value for virus concentration applied here was 1000 particles/ml. Samples with virus concentrations above and below 1000 particles/ml were classified as positive and negative, respectively; e vertical scatterplot analysis of virus spiked samples ( n = 54). The threshold value for average motor velocity applied here was 0.704 µm/s that corresponds to 1000 particles/ml. Samples with velocities above and below 0.704 µm/s were classified as 1 (positive) and 0 (negative), respectively; f representative digital images show the motion trajectories of motors in the absence of HIV-1 particle (control) and the presence of HIV-1 at concentrations above and below 1000 virus particles/ml (scale bar = 100 μm). The results are expressed as the average values of three independent experiments and error bars represent standard deviations

    Journal: Nature Communications

    Article Title: DNA engineered micromotors powered by metal nanoparticles for motion based cellphone diagnostics

    doi: 10.1038/s41467-018-06727-8

    Figure Lengend Snippet: HIV-1 detection using the CALM system. Synthetic HIV-1 RNA standard detection: a bar graph shows the average velocity of motors recorded by the CALM system for phosphate-buffered saline (1× PBS, pH 7.4) samples ( n = 45) spiked with different HIV-1 RNA concentrations. Vertical black dotted line indicates the average velocity at the threshold concentration of 1000 virus particles/ml; b representative digital images show the motion trajectories of motors in the absence of HIV-1 RNA (control) or the presence of HIV-1 RNA at concentrations above and below the threshold of 1000 copies/ml (scale bar = 100 μm). HIV-1 particles detection: c heatmap of the average motor velocity measured by the CALM system for different virus concentrations spiked in 1× PBS ( n = 35) and serum ( n = 20). The average velocity of HIV-1 positive samples (≥1000 virus particles/ml) is ≤0.704 ± 0.08 µm/s (yellow in color) and the average velocity of HIV-1 negative samples (<1000 virus particles/ml) is >0.704 ± 0.08 µm/s (red in color); d receiver-operating characteristics (ROC) curve analysis of 1× PBS ( n = 35) and serum ( n = 20) samples spiked with different HIV-1 concentrations showing the assay detection sensitivity (sens) and specificity (spec) compared to real-time polymerase chain reaction (RT-PCR). The threshold value for virus concentration applied here was 1000 particles/ml. Samples with virus concentrations above and below 1000 particles/ml were classified as positive and negative, respectively; e vertical scatterplot analysis of virus spiked samples ( n = 54). The threshold value for average motor velocity applied here was 0.704 µm/s that corresponds to 1000 particles/ml. Samples with velocities above and below 0.704 µm/s were classified as 1 (positive) and 0 (negative), respectively; f representative digital images show the motion trajectories of motors in the absence of HIV-1 particle (control) and the presence of HIV-1 at concentrations above and below 1000 virus particles/ml (scale bar = 100 μm). The results are expressed as the average values of three independent experiments and error bars represent standard deviations

    Article Snippet: The cellphone system was calibrated with PBS samples spiked with synthetic HIV-1 RNA standard (0–1 × 10 7 copies/ml) purchased from ATCC (VR-3245SD) and then compared to the standard RT-PCR using 1× PBS (pH 7.4) and serum samples spiked with HIV-1 particles at concentrations between 0 and 1.5 × 10 4 virus particles/ml.

    Techniques: Concentration Assay, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction