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    Structured Review

    Thermo Fisher hcv rna levels
    Charged-to-alanine mutations dispensable for Con1 <t>RNA</t> replication are not required for the production of infectious <t>HCV.</t> (A) Huh-7.5 cells were electroporated with 1 μg of full-length wild-type and mutant J6-JFH1 RNA, and at 24, 48, and 72 h posttransfection,
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    Images

    1) Product Images from "Charged Residues in Hepatitis C Virus NS4B Are Critical for Multiple NS4B Functions in RNA Replication ▿"

    Article Title: Charged Residues in Hepatitis C Virus NS4B Are Critical for Multiple NS4B Functions in RNA Replication ▿

    Journal: Journal of Virology

    doi: 10.1128/JVI.00858-11

    Charged-to-alanine mutations dispensable for Con1 RNA replication are not required for the production of infectious HCV. (A) Huh-7.5 cells were electroporated with 1 μg of full-length wild-type and mutant J6-JFH1 RNA, and at 24, 48, and 72 h posttransfection,
    Figure Legend Snippet: Charged-to-alanine mutations dispensable for Con1 RNA replication are not required for the production of infectious HCV. (A) Huh-7.5 cells were electroporated with 1 μg of full-length wild-type and mutant J6-JFH1 RNA, and at 24, 48, and 72 h posttransfection,

    Techniques Used: Mutagenesis

    Identification of charged amino acids in the N- and C-terminal domains of NS4B required for HCV RNA replication. (A) Amino acid sequence of the N- and C-terminal domains of Con1 NS4B. The numbers indicate the amino acid positions within the NS4B protein.
    Figure Legend Snippet: Identification of charged amino acids in the N- and C-terminal domains of NS4B required for HCV RNA replication. (A) Amino acid sequence of the N- and C-terminal domains of Con1 NS4B. The numbers indicate the amino acid positions within the NS4B protein.

    Techniques Used: Sequencing

    Second-site mutations at E15 and Q16 in NS4B suppress the replication defect of NS4B K20A. At 96 h posttransfection, NS5A protein expression was visualized by Western blotting, and HCV RNA in 1 μg of total cellular RNA was quantified by real-time
    Figure Legend Snippet: Second-site mutations at E15 and Q16 in NS4B suppress the replication defect of NS4B K20A. At 96 h posttransfection, NS5A protein expression was visualized by Western blotting, and HCV RNA in 1 μg of total cellular RNA was quantified by real-time

    Techniques Used: Expressing, Western Blot

    2) Product Images from "TM6SF2 Promotes Lipidation and Secretion of Hepatitis C Virus in Infected Hepatocytes"

    Article Title: TM6SF2 Promotes Lipidation and Secretion of Hepatitis C Virus in Infected Hepatocytes

    Journal: Gastroenterology

    doi: 10.1053/j.gastro.2018.08.027

    Overexpression of functional TM6SF2 increases the secretion of HCV RNA and infectious lipoviroparticles.
    Figure Legend Snippet: Overexpression of functional TM6SF2 increases the secretion of HCV RNA and infectious lipoviroparticles.

    Techniques Used: Over Expression, Functional Assay

    TM6SF2 knockdown blocks the secretion of HCV RNA and infectious particles.
    Figure Legend Snippet: TM6SF2 knockdown blocks the secretion of HCV RNA and infectious particles.

    Techniques Used:

    3) Product Images from "Lipoprotein Lipase Inhibits Hepatitis C Virus (HCV) Infection by Blocking Virus Cell Entry"

    Article Title: Lipoprotein Lipase Inhibits Hepatitis C Virus (HCV) Infection by Blocking Virus Cell Entry

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0026637

    The inhibitory effect of LPL on HCVcc infection is only partly related to its catalytic activity. (A) Huh7.5 cells were pre-incubated with 1 µg/ml LPL at 4°C in the presence or absence of 50 µg/ml THL before infection with JFH1. The infected cells were grown for 24 h and HCV RNA was then extracted and quantified by RT-qPCR. (B) THL does not influence HCV replication. Huh7.5 cells were pre-incubated with indicated concentrations of THL before cell infection with JFH-1, as for experiments with LPL. THL was maintained in the medium for 24 h post infection. HCV RNA was then extracted and quantified by RT-qPCR. Results are expressed as a percent of RNA as compared with control cells infected in the absence of LPL and THL.
    Figure Legend Snippet: The inhibitory effect of LPL on HCVcc infection is only partly related to its catalytic activity. (A) Huh7.5 cells were pre-incubated with 1 µg/ml LPL at 4°C in the presence or absence of 50 µg/ml THL before infection with JFH1. The infected cells were grown for 24 h and HCV RNA was then extracted and quantified by RT-qPCR. (B) THL does not influence HCV replication. Huh7.5 cells were pre-incubated with indicated concentrations of THL before cell infection with JFH-1, as for experiments with LPL. THL was maintained in the medium for 24 h post infection. HCV RNA was then extracted and quantified by RT-qPCR. Results are expressed as a percent of RNA as compared with control cells infected in the absence of LPL and THL.

    Techniques Used: Infection, Activity Assay, Incubation, Quantitative RT-PCR

    LPL inhibits cell infection by the JFH-1 and J6/JFH-1 strains produced in vitro and in vivo in a chimeric uPA-SCID mouse model. The HCVcc strains JFH-1 (A) and J6/JFH-1 (B) were produced in the Huh7.5 hepatoma cell line. Cells were incubated with (or without) LPL for 30 min at 4°C and then with virus preparations for 2 h at 37°C to allow infection. RNA was extracted from cells 24 h post infection and HCV RNA was quantified by RT-qPCR. The data obtained were normalized with respect to levels of GADPH. The mJFH-1 (A) and mJ6/JFH-1 (B) correspond to HCVcc strains produced in chimeric uPA-SCID mice into which we transplanted human hepatocytes. Serum samples collected from infected mice were pooled and their capacity to infect Huh7.5 cells was assessed in the presence and absence of LPL, as outlined above. Cells infected in the absence (black bar) and in the presence of LPL (gray bar). The data are expressed as the amount of HCV RNA detected in cells infected in the presence of LPL as compared with the amount of HCV RNA in cells infected in the absence of LPL, expressed as a percentage.
    Figure Legend Snippet: LPL inhibits cell infection by the JFH-1 and J6/JFH-1 strains produced in vitro and in vivo in a chimeric uPA-SCID mouse model. The HCVcc strains JFH-1 (A) and J6/JFH-1 (B) were produced in the Huh7.5 hepatoma cell line. Cells were incubated with (or without) LPL for 30 min at 4°C and then with virus preparations for 2 h at 37°C to allow infection. RNA was extracted from cells 24 h post infection and HCV RNA was quantified by RT-qPCR. The data obtained were normalized with respect to levels of GADPH. The mJFH-1 (A) and mJ6/JFH-1 (B) correspond to HCVcc strains produced in chimeric uPA-SCID mice into which we transplanted human hepatocytes. Serum samples collected from infected mice were pooled and their capacity to infect Huh7.5 cells was assessed in the presence and absence of LPL, as outlined above. Cells infected in the absence (black bar) and in the presence of LPL (gray bar). The data are expressed as the amount of HCV RNA detected in cells infected in the presence of LPL as compared with the amount of HCV RNA in cells infected in the absence of LPL, expressed as a percentage.

    Techniques Used: Infection, Produced, In Vitro, In Vivo, Incubation, Quantitative RT-PCR, Mouse Assay

    LPL affects HCV attachment and early stages of the virus cell cycle. (A) Effect of LPL on virus attachment to Huh7.5 cells. Huh7.5 cells were pre-incubated with various concentrations of LPL (1–9 µg/ml) for 30 min at 4°C. An aliquot of cell culture supernatant containing JFH-1 was incubated with LPL-pretreated Huh7.5 cells for 30 min at 4°C. The cells were washed and the RNA associated with them was extracted. HCV RNA was quantified by RT-qPCR. (B) Effect of LPL on early steps of HCV infection. JFH-1 was first adsorbed onto Huh7.5 cells by incubation for 45 min at 4°C. Cells were washed with cold medium to remove any unbound virus. Complete medium, warmed to 37°C, was then added and incubated with the cells at 37°C. LPL was added to a concentration of 1 µg/ml at various time points (0, 5, 10, 15 or 20 min) after the transfer of cells to 37°C, with or without the addition of 50 µg/ml THL to block its enzymatic activity. Cells were grown for 24 h. RNA was then extracted and HCV RNA was quantified by RT-qPCR. Results are expressed as a percent of RNA as compared with control cells infected in the absence of LPL.
    Figure Legend Snippet: LPL affects HCV attachment and early stages of the virus cell cycle. (A) Effect of LPL on virus attachment to Huh7.5 cells. Huh7.5 cells were pre-incubated with various concentrations of LPL (1–9 µg/ml) for 30 min at 4°C. An aliquot of cell culture supernatant containing JFH-1 was incubated with LPL-pretreated Huh7.5 cells for 30 min at 4°C. The cells were washed and the RNA associated with them was extracted. HCV RNA was quantified by RT-qPCR. (B) Effect of LPL on early steps of HCV infection. JFH-1 was first adsorbed onto Huh7.5 cells by incubation for 45 min at 4°C. Cells were washed with cold medium to remove any unbound virus. Complete medium, warmed to 37°C, was then added and incubated with the cells at 37°C. LPL was added to a concentration of 1 µg/ml at various time points (0, 5, 10, 15 or 20 min) after the transfer of cells to 37°C, with or without the addition of 50 µg/ml THL to block its enzymatic activity. Cells were grown for 24 h. RNA was then extracted and HCV RNA was quantified by RT-qPCR. Results are expressed as a percent of RNA as compared with control cells infected in the absence of LPL.

    Techniques Used: Incubation, Cell Culture, Quantitative RT-PCR, Infection, Concentration Assay, Blocking Assay, Activity Assay

    Cell infection with low- and high-density virus populations from iodixanol gradients in the presence or absence of LPL. The pooled peak fractions of the low- and high-density virus populations obtained after centrifugation through iodixanol gradients of JFH1 grown in cell culture (A) and serum samples from the m-JFH1 chimeric mouse model (B) (both gradients are shown in Figure 2 ) were used to infect cells in the presence or absence of 1 µg/ml LPL, as described in the Materials and Methods section. Cells were grown for 48 h at 37°C and HCV RNA was extracted and quantified by RT-qPCR. The results were normalized with respect to the cellular gene GAPDH, with the GAPDH Control Kit. The data are expressed as the amount of HCV RNA detected in cells infected with the pooled fractions from the two major virus populations in the presence of LPL as compared with the amount of HCV RNA in cells infected with the same fractions in the absence of LPL, expressed as a percentage.
    Figure Legend Snippet: Cell infection with low- and high-density virus populations from iodixanol gradients in the presence or absence of LPL. The pooled peak fractions of the low- and high-density virus populations obtained after centrifugation through iodixanol gradients of JFH1 grown in cell culture (A) and serum samples from the m-JFH1 chimeric mouse model (B) (both gradients are shown in Figure 2 ) were used to infect cells in the presence or absence of 1 µg/ml LPL, as described in the Materials and Methods section. Cells were grown for 48 h at 37°C and HCV RNA was extracted and quantified by RT-qPCR. The results were normalized with respect to the cellular gene GAPDH, with the GAPDH Control Kit. The data are expressed as the amount of HCV RNA detected in cells infected with the pooled fractions from the two major virus populations in the presence of LPL as compared with the amount of HCV RNA in cells infected with the same fractions in the absence of LPL, expressed as a percentage.

    Techniques Used: Infection, Centrifugation, Cell Culture, Quantitative RT-PCR

    Iodixanol gradient analysis of the JFH-1 and J6/JFH-1 strains produced in vitro and in vivo . The supernatants from infected Huh7.5 cells producing JFH-1 (JFH-1, shown in A and B) and J6/JFH-1 (shown in E) were subjected to isopycnic centrifugation through iodixanol gradients, as described in Materials and Methods . Pooled serum samples from the chimeric uPA-SCID mice were also subjected to centrifugation on the same type of gradient. Representative profiles are shown in C and D for mice inoculated with JFH-1 (mJFH-1) and in F for mice inoculated with J6/JFH-1 (mJ6/JFH-1). HCV core antigen in gradient fractions was quantified by ELISA, HCV RNA was quantified by RT-qPCR, and ApoB and cholesterol were determined by ELISA. Infectivity for fractionated J6/JFH-1 (representative for both strains) grown in Huh7.5 cells is shown in E and that for the corresponding mouse serum (mJ6/JFH-1) is shown in F. The fractions (25 µl) were used to infect Huh7.5 cells. Cells were incubated for 48 h at 37°C; total RNA was then extracted and HCV-RNA levels were quantified by RT-qPCR. The results were normalized, taking into account the initial HCV-RNA content in each sample analyzed, as determined by RT-qPCR, and are expressed as a ratio of these two values.
    Figure Legend Snippet: Iodixanol gradient analysis of the JFH-1 and J6/JFH-1 strains produced in vitro and in vivo . The supernatants from infected Huh7.5 cells producing JFH-1 (JFH-1, shown in A and B) and J6/JFH-1 (shown in E) were subjected to isopycnic centrifugation through iodixanol gradients, as described in Materials and Methods . Pooled serum samples from the chimeric uPA-SCID mice were also subjected to centrifugation on the same type of gradient. Representative profiles are shown in C and D for mice inoculated with JFH-1 (mJFH-1) and in F for mice inoculated with J6/JFH-1 (mJ6/JFH-1). HCV core antigen in gradient fractions was quantified by ELISA, HCV RNA was quantified by RT-qPCR, and ApoB and cholesterol were determined by ELISA. Infectivity for fractionated J6/JFH-1 (representative for both strains) grown in Huh7.5 cells is shown in E and that for the corresponding mouse serum (mJ6/JFH-1) is shown in F. The fractions (25 µl) were used to infect Huh7.5 cells. Cells were incubated for 48 h at 37°C; total RNA was then extracted and HCV-RNA levels were quantified by RT-qPCR. The results were normalized, taking into account the initial HCV-RNA content in each sample analyzed, as determined by RT-qPCR, and are expressed as a ratio of these two values.

    Techniques Used: Produced, In Vitro, In Vivo, Infection, Centrifugation, Mouse Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Incubation

    4) Product Images from "In Vitro Characterization of GSK2485852, a Novel Hepatitis C Virus Polymerase Inhibitor"

    Article Title: In Vitro Characterization of GSK2485852, a Novel Hepatitis C Virus Polymerase Inhibitor

    Journal: Antimicrobial Agents and Chemotherapy

    doi: 10.1128/AAC.00874-13

    HCV RNA reduction assay. Genotype 1a (A) or 1b (B) replicon cells were treated with compounds and reductions in replicon RNA determined as described in Materials and Methods. ●, DMSO control; ■, 3× EC 90 GSK5852; □, 10×
    Figure Legend Snippet: HCV RNA reduction assay. Genotype 1a (A) or 1b (B) replicon cells were treated with compounds and reductions in replicon RNA determined as described in Materials and Methods. ●, DMSO control; ■, 3× EC 90 GSK5852; □, 10×

    Techniques Used:

    5) Product Images from "Targeting Innate Immunity for Antiviral Therapy through Small Molecule Agonists of the RLR Pathway"

    Article Title: Targeting Innate Immunity for Antiviral Therapy through Small Molecule Agonists of the RLR Pathway

    Journal: Journal of Virology

    doi: 10.1128/JVI.02202-15

    KIN1400 inhibits HCV (JFH-1) infection. (A) Huh7 cells were pretreated with 0.5% DMSO, 20 μM KIN1000 or KIN1400, or 100 IU/ml IFN-β for 24 h before they were infected with HCV (MOI, 1). The HCV RNA levels in the cell culture supernatant
    Figure Legend Snippet: KIN1400 inhibits HCV (JFH-1) infection. (A) Huh7 cells were pretreated with 0.5% DMSO, 20 μM KIN1000 or KIN1400, or 100 IU/ml IFN-β for 24 h before they were infected with HCV (MOI, 1). The HCV RNA levels in the cell culture supernatant

    Techniques Used: Infection, Cell Culture

    6) Product Images from "Neutralizing antibody response during acute and chronic hepatitis C virus infection"

    Article Title: Neutralizing antibody response during acute and chronic hepatitis C virus infection

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.0403519101

    The nAb response in experimentally infected chimpanzees. Sequential plasma samples from six chronically H77-virus-infected chimpanzees were monitored for viral RNA levels, nAb for pseudotype virus bearing autologous H77 gp (HIV-HCV H77), and anti-E1E2 and anti-HVR reactivity. All plasma samples were tested at a dilution of 1/100. Data are shown as percentage neutralization. The anti-E1E2 and anti-HVR Ab data are represented as a P/N ratio, calculated by dividing the OD value of the test sera by that obtained with a preimmune serum. P/N values > 2 were considered positive. All assays were performed in quadruplicate, and the data are representative of two independent experiments.
    Figure Legend Snippet: The nAb response in experimentally infected chimpanzees. Sequential plasma samples from six chronically H77-virus-infected chimpanzees were monitored for viral RNA levels, nAb for pseudotype virus bearing autologous H77 gp (HIV-HCV H77), and anti-E1E2 and anti-HVR reactivity. All plasma samples were tested at a dilution of 1/100. Data are shown as percentage neutralization. The anti-E1E2 and anti-HVR Ab data are represented as a P/N ratio, calculated by dividing the OD value of the test sera by that obtained with a preimmune serum. P/N values > 2 were considered positive. All assays were performed in quadruplicate, and the data are representative of two independent experiments.

    Techniques Used: Infection, Neutralization

    7) Product Images from "Single Particle Imaging of Polarized Hepatoma Organoids upon Hepatitis C Virus Infection Reveals an Ordered and Sequential Entry Process"

    Article Title: Single Particle Imaging of Polarized Hepatoma Organoids upon Hepatitis C Virus Infection Reveals an Ordered and Sequential Entry Process

    Journal: Cell host & microbe

    doi: 10.1016/j.chom.2018.02.005

    Activated EGFR Is Associated with DID-HCV at the Tight Junction prior to Internalization (A–E) Huh-7.5 organoids were infected with DiD-HCV for 1 hr at 4C, shifted to 37°C for the indicated times, fixed, and probed for either total EGFR or phosphoEGFR 1045. (A, B, and D) Arrows indicate area enlarged in insets; dashed arrows indicate DiD colocalization while solid arrows denote DiD-HCV particles lacking colocalization. (A) DiD-HCV colocalization over a time course of infection. (B) DiD-HCV colocalization with phospho-EGFR at 120 min post shift. Lower inset is merged and enlarged in upper inset. (D) DiD-HCV colocalization at 0 min post shift, analyzed for localization of DiD-HCV particles. (C and E) Quantification of (A) and (C), respectively. (F) Huh-7.5 organoids were serum starved, infected with concentrated HCV for 1 hr at 4C, shifted to 37°C, processed with Matrigel cell recovery solution, and lysed at the indicated times. Lysate samples were immunoblotted for the specified proteins. (G) Wild-type, shEGFR, and shEGFR cells expressing wild-type or mutant EGFR were seeded into 6-well plates, lysed, and analyzed via immunoblot with indicated antibodies. (H) Wild-type, shEGFR, or complemented cells were seeded onto 96-well plates, infected with HCV for 48 hr, and then analyzed for relative HCV RNA levels. n = total DiD signal, mean ± SD. *p
    Figure Legend Snippet: Activated EGFR Is Associated with DID-HCV at the Tight Junction prior to Internalization (A–E) Huh-7.5 organoids were infected with DiD-HCV for 1 hr at 4C, shifted to 37°C for the indicated times, fixed, and probed for either total EGFR or phosphoEGFR 1045. (A, B, and D) Arrows indicate area enlarged in insets; dashed arrows indicate DiD colocalization while solid arrows denote DiD-HCV particles lacking colocalization. (A) DiD-HCV colocalization over a time course of infection. (B) DiD-HCV colocalization with phospho-EGFR at 120 min post shift. Lower inset is merged and enlarged in upper inset. (D) DiD-HCV colocalization at 0 min post shift, analyzed for localization of DiD-HCV particles. (C and E) Quantification of (A) and (C), respectively. (F) Huh-7.5 organoids were serum starved, infected with concentrated HCV for 1 hr at 4C, shifted to 37°C, processed with Matrigel cell recovery solution, and lysed at the indicated times. Lysate samples were immunoblotted for the specified proteins. (G) Wild-type, shEGFR, and shEGFR cells expressing wild-type or mutant EGFR were seeded into 6-well plates, lysed, and analyzed via immunoblot with indicated antibodies. (H) Wild-type, shEGFR, or complemented cells were seeded onto 96-well plates, infected with HCV for 48 hr, and then analyzed for relative HCV RNA levels. n = total DiD signal, mean ± SD. *p

    Techniques Used: Infection, Expressing, Mutagenesis

    8) Product Images from "Liver-targeted cyclosporine A-encapsulated poly (lactic-co-glycolic) acid nanoparticles inhibit hepatitis C virus replication"

    Article Title: Liver-targeted cyclosporine A-encapsulated poly (lactic-co-glycolic) acid nanoparticles inhibit hepatitis C virus replication

    Journal: International Journal of Nanomedicine

    doi: 10.2147/IJN.S74723

    Effect of targeted CsA encapsulated poly (lactic-co-glycolic) acid nanoparticles in an HCV mouse model. Notes: ( A ) HCV RNA levels. ( B ) NS5A protein levels. ( C ) Confocal microscopy analysis of Huh7 cells containing the HCV-Con1b replicon for human hepatocytes (green) and HCV NS5A (red), in the liver tissue of an HCV mouse model (n=3) after continuous treatment with CsA or CsANP-LTP at 48-hour intervals for 21 days. Sustained antiviral effects of free CsA, CsANP, or CsANP-LTP after treatment withdrawal on ( D ) HCV RNA levels and ( E ) NS5A protein levels. For withdrawal experiments (n=3), injections were given on days 1, 3, and 5 and HCV RNA and NS5A protein levels were assessed after day 21. In both experiments, HCV RNA levels were normalized by human GAPDH levels, and the data are presented as the average ± SD from three mice. * P
    Figure Legend Snippet: Effect of targeted CsA encapsulated poly (lactic-co-glycolic) acid nanoparticles in an HCV mouse model. Notes: ( A ) HCV RNA levels. ( B ) NS5A protein levels. ( C ) Confocal microscopy analysis of Huh7 cells containing the HCV-Con1b replicon for human hepatocytes (green) and HCV NS5A (red), in the liver tissue of an HCV mouse model (n=3) after continuous treatment with CsA or CsANP-LTP at 48-hour intervals for 21 days. Sustained antiviral effects of free CsA, CsANP, or CsANP-LTP after treatment withdrawal on ( D ) HCV RNA levels and ( E ) NS5A protein levels. For withdrawal experiments (n=3), injections were given on days 1, 3, and 5 and HCV RNA and NS5A protein levels were assessed after day 21. In both experiments, HCV RNA levels were normalized by human GAPDH levels, and the data are presented as the average ± SD from three mice. * P

    Techniques Used: Confocal Microscopy, Mouse Assay

    9) Product Images from "Spatiotemporal Analysis of Hepatitis C Virus Infection"

    Article Title: Spatiotemporal Analysis of Hepatitis C Virus Infection

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1004758

    Strand specific HCV RNA detection in fixed cells. A . Huh-7.5 cells were electroporated with the indicated HCV RNA constructs and cells were fixed and processed for RNA detection at 6 and 96 hours post-electroporation. Scale bar is 5 μm. B . Quantification of images in panel A. Error bars represent standard deviation from 25 different images. ND = not detected. ** p = 0.0008.
    Figure Legend Snippet: Strand specific HCV RNA detection in fixed cells. A . Huh-7.5 cells were electroporated with the indicated HCV RNA constructs and cells were fixed and processed for RNA detection at 6 and 96 hours post-electroporation. Scale bar is 5 μm. B . Quantification of images in panel A. Error bars represent standard deviation from 25 different images. ND = not detected. ** p = 0.0008.

    Techniques Used: RNA Detection, Construct, Electroporation, Standard Deviation

    Colocalization of (−) and (+) HCV RNA strands. A . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post infection cells were fixed and processed for strand specific RNA detection. Scale bar is 5 μm. Solid arrows point to (+) strand RNA colocalizing with (−) strand RNA. B . Quantitation of % colocalization in (A).
    Figure Legend Snippet: Colocalization of (−) and (+) HCV RNA strands. A . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post infection cells were fixed and processed for strand specific RNA detection. Scale bar is 5 μm. Solid arrows point to (+) strand RNA colocalizing with (−) strand RNA. B . Quantitation of % colocalization in (A).

    Techniques Used: Infection, RNA Detection, Quantitation Assay

    Kinetic analysis of genomic RNA fate. A . Huh-7.5 cells were infected with HCV at MOI = 1.5. RNA was collected at the indicated time points post-infection and quantified with real-time RT-PCR. Error bar, standard deviation. B . Intra- and extra-cellular viral supernatants from infections in panel A were collected at the indicated time points and titered by limiting dilution assay. Shown are the averages of two sets of titer data. Error bar, standard deviation. C . Total (+) puncta or D . Percent of (+) strand puncta colocalizing with translation (puromycylated ribosomes), replication (NS5A + NS3), assembly (core) and virion (E2) markers over the indicated time course (Figs. 3 – 6 ) were plotted using the smooth graph function in Microsoft Excel. E . Percent of (−) strand puncta colocalizing with active replication compartments (NS5A), active replication ((+) strands) and active replication (NS3) over the indicated time course plotted using the smooth graph function in Microsoft Excel.
    Figure Legend Snippet: Kinetic analysis of genomic RNA fate. A . Huh-7.5 cells were infected with HCV at MOI = 1.5. RNA was collected at the indicated time points post-infection and quantified with real-time RT-PCR. Error bar, standard deviation. B . Intra- and extra-cellular viral supernatants from infections in panel A were collected at the indicated time points and titered by limiting dilution assay. Shown are the averages of two sets of titer data. Error bar, standard deviation. C . Total (+) puncta or D . Percent of (+) strand puncta colocalizing with translation (puromycylated ribosomes), replication (NS5A + NS3), assembly (core) and virion (E2) markers over the indicated time course (Figs. 3 – 6 ) were plotted using the smooth graph function in Microsoft Excel. E . Percent of (−) strand puncta colocalizing with active replication compartments (NS5A), active replication ((+) strands) and active replication (NS3) over the indicated time course plotted using the smooth graph function in Microsoft Excel.

    Techniques Used: Infection, Quantitative RT-PCR, Standard Deviation, Limiting Dilution Assay

    Kinetics of HCV RNA accumulation during infection. A . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post-infection cells were fixed and processed for strand specific RNA detection. Scale bar is 5 μm. B . Individual (+) and (−) strand puncta for each time point were quantified and graphed using Prism software.
    Figure Legend Snippet: Kinetics of HCV RNA accumulation during infection. A . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post-infection cells were fixed and processed for strand specific RNA detection. Scale bar is 5 μm. B . Individual (+) and (−) strand puncta for each time point were quantified and graphed using Prism software.

    Techniques Used: Infection, RNA Detection, Software

    Colocalization of (+) and (−) strand HCV RNAs with NS5A and NS3. Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post-infection the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for A . NS5A or C . NS3. For 6 and 12 hpi samples, antibody signal was amplified using the tyramide signal amplification kit (TSA) as described in the materials and methods section. Scale bar is 5 μm. B . Quantitation of (A) D . Quantitation of (C). Each error bar indicates standard deviation from 25 different images. Scale bar is 5 μm. Insets represent 10 times magnification of the merged image. Solid arrows point to (+) strand RNA colocalizing with NS5A and NS3; arrowheads point to (−) strand RNA colocalizing with NS5A and NS3.
    Figure Legend Snippet: Colocalization of (+) and (−) strand HCV RNAs with NS5A and NS3. Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post-infection the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for A . NS5A or C . NS3. For 6 and 12 hpi samples, antibody signal was amplified using the tyramide signal amplification kit (TSA) as described in the materials and methods section. Scale bar is 5 μm. B . Quantitation of (A) D . Quantitation of (C). Each error bar indicates standard deviation from 25 different images. Scale bar is 5 μm. Insets represent 10 times magnification of the merged image. Solid arrows point to (+) strand RNA colocalizing with NS5A and NS3; arrowheads point to (−) strand RNA colocalizing with NS5A and NS3.

    Techniques Used: Infection, RNA Detection, Immunofluorescence, Staining, Amplification, Quantitation Assay, Standard Deviation

    Colocalization of (+) and (−) strand HCV RNAs with active translating ribosomes. A . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at 48 hours post-infection cells were left untreated or pre-treated with anisomycin (Ani) (competitive inhibitor of puromycin; 9.4 uM) followed by puromycin (Puro) labeling and digitonin extraction before fixation. Cells were processed for immunofluorescence using the anti-puromycin PMY-2A4 monoclonal antibody. Scale bar is 5 μm. B . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post-infection the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for puromycylated ribosomes. Scale bar is 5 μm. Insets represent 10 times magnification of the merged image. Solid arrows point to (+) strand RNA colocalizing with ribosomes; arrowheads point to (−) strand RNA colocalizing with ribosomes. C . Quantitation of % colocalization in (B). Each error bar indicates standard deviation from 25 different images. D . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at 6 hpi the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for calnexin.
    Figure Legend Snippet: Colocalization of (+) and (−) strand HCV RNAs with active translating ribosomes. A . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at 48 hours post-infection cells were left untreated or pre-treated with anisomycin (Ani) (competitive inhibitor of puromycin; 9.4 uM) followed by puromycin (Puro) labeling and digitonin extraction before fixation. Cells were processed for immunofluorescence using the anti-puromycin PMY-2A4 monoclonal antibody. Scale bar is 5 μm. B . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at the indicated times post-infection the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for puromycylated ribosomes. Scale bar is 5 μm. Insets represent 10 times magnification of the merged image. Solid arrows point to (+) strand RNA colocalizing with ribosomes; arrowheads point to (−) strand RNA colocalizing with ribosomes. C . Quantitation of % colocalization in (B). Each error bar indicates standard deviation from 25 different images. D . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at 6 hpi the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for calnexin.

    Techniques Used: Infection, Labeling, Immunofluorescence, RNA Detection, Staining, Quantitation Assay, Standard Deviation

    Colocalization of (+) and (−) strand HCV RNAs with core protein and virion E2. A . Huh-7.5 cells were infected with HCV at MOI = 1.5, fixed at the indicated times post-infection and processed for strand specific RNA detection followed by immunofluorescence staining for core. Scale bar is 5 um. Solid arrows indicate (+) strand (red) colocalization; arrowheads indicate (−) strand (magenta) colocalization with core (green). Insets represent 10 times magnification of the merged image. The asterisk indicates juxtaposition of (−) strand with core. B . Quantification of images in panel A. C . A merged image of core colocalization with (+) and (−) HCV RNAs at 48 hpi is shown together with an ImageJ color intensity plot for the white line drawn in the merged image. D, E . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at 48 and 72 hpi the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for E2 protein using CBH-5 antibody and quantified. Insets represent 10 times magnification of the merged image.
    Figure Legend Snippet: Colocalization of (+) and (−) strand HCV RNAs with core protein and virion E2. A . Huh-7.5 cells were infected with HCV at MOI = 1.5, fixed at the indicated times post-infection and processed for strand specific RNA detection followed by immunofluorescence staining for core. Scale bar is 5 um. Solid arrows indicate (+) strand (red) colocalization; arrowheads indicate (−) strand (magenta) colocalization with core (green). Insets represent 10 times magnification of the merged image. The asterisk indicates juxtaposition of (−) strand with core. B . Quantification of images in panel A. C . A merged image of core colocalization with (+) and (−) HCV RNAs at 48 hpi is shown together with an ImageJ color intensity plot for the white line drawn in the merged image. D, E . Huh-7.5 cells were infected with HCV at MOI = 1.5 and at 48 and 72 hpi the cells were fixed and processed for strand specific RNA detection followed by immunofluorescence staining for E2 protein using CBH-5 antibody and quantified. Insets represent 10 times magnification of the merged image.

    Techniques Used: Infection, RNA Detection, Immunofluorescence, Staining

    10) Product Images from "Identification of AP80978, a Novel Small-Molecule Inhibitor of Hepatitis C Virus Replication That Targets NS4B"

    Article Title: Identification of AP80978, a Novel Small-Molecule Inhibitor of Hepatitis C Virus Replication That Targets NS4B

    Journal: Antimicrobial Agents and Chemotherapy

    doi: 10.1128/AAC.00113-14

    Clearance of HCV RNA from replicon cells by treatment with AP80978. (A) Schematic of the genotype 1b replicon [Con1/SG-Neo(I)hRluc2aUb] used in the replicon clearance assay. (B) Replicon cells were untreated or treated with AP80978 (15 μM or 3.75 μM) or control compounds (2.5 μM cyclosporine [CsA] and 7.5 μM VX950) in the absence of G418 selection for four passages. Cells were then cultured in selection media in the absence of compound to determine when replicon is present and to allow “rebound.” HCV RNA levels from each treatment and time point were quantified and are expressed as log 10 change compared with HCV RNA levels in untreated samples at day 0, with all values normalized relative to GAPDH RNA. No rebound was observed in replicon cells that had been cultured in the presence of CsA, VX950, or AP80978 during the clearance phase of the assay. Values are means ± standard deviations (error bars) from three replicates.
    Figure Legend Snippet: Clearance of HCV RNA from replicon cells by treatment with AP80978. (A) Schematic of the genotype 1b replicon [Con1/SG-Neo(I)hRluc2aUb] used in the replicon clearance assay. (B) Replicon cells were untreated or treated with AP80978 (15 μM or 3.75 μM) or control compounds (2.5 μM cyclosporine [CsA] and 7.5 μM VX950) in the absence of G418 selection for four passages. Cells were then cultured in selection media in the absence of compound to determine when replicon is present and to allow “rebound.” HCV RNA levels from each treatment and time point were quantified and are expressed as log 10 change compared with HCV RNA levels in untreated samples at day 0, with all values normalized relative to GAPDH RNA. No rebound was observed in replicon cells that had been cultured in the presence of CsA, VX950, or AP80978 during the clearance phase of the assay. Values are means ± standard deviations (error bars) from three replicates.

    Techniques Used: Selection, Cell Culture

    11) Product Images from "TM6SF2 Promotes Lipidation and Secretion of Hepatitis C Virus in Infected Hepatocytes"

    Article Title: TM6SF2 Promotes Lipidation and Secretion of Hepatitis C Virus in Infected Hepatocytes

    Journal: Gastroenterology

    doi: 10.1053/j.gastro.2018.08.027

    Overexpression of functional TM6SF2 increases the secretion of HCV RNA and infectious lipoviroparticles.
    Figure Legend Snippet: Overexpression of functional TM6SF2 increases the secretion of HCV RNA and infectious lipoviroparticles.

    Techniques Used: Over Expression, Functional Assay

    TM6SF2 knockdown blocks the secretion of HCV RNA and infectious particles.
    Figure Legend Snippet: TM6SF2 knockdown blocks the secretion of HCV RNA and infectious particles.

    Techniques Used:

    12) Product Images from "Identification of AP80978, a Novel Small-Molecule Inhibitor of Hepatitis C Virus Replication That Targets NS4B"

    Article Title: Identification of AP80978, a Novel Small-Molecule Inhibitor of Hepatitis C Virus Replication That Targets NS4B

    Journal: Antimicrobial Agents and Chemotherapy

    doi: 10.1128/AAC.00113-14

    Clearance of HCV RNA from replicon cells by treatment with AP80978. (A) Schematic of the genotype 1b replicon [Con1/SG-Neo(I)hRluc2aUb] used in the replicon clearance assay. (B) Replicon cells were untreated or treated with AP80978 (15 μM or 3.75 μM) or control compounds (2.5 μM cyclosporine [CsA] and 7.5 μM VX950) in the absence of G418 selection for four passages. Cells were then cultured in selection media in the absence of compound to determine when replicon is present and to allow “rebound.” HCV RNA levels from each treatment and time point were quantified and are expressed as log 10 change compared with HCV RNA levels in untreated samples at day 0, with all values normalized relative to GAPDH RNA. No rebound was observed in replicon cells that had been cultured in the presence of CsA, VX950, or AP80978 during the clearance phase of the assay. Values are means ± standard deviations (error bars) from three replicates.
    Figure Legend Snippet: Clearance of HCV RNA from replicon cells by treatment with AP80978. (A) Schematic of the genotype 1b replicon [Con1/SG-Neo(I)hRluc2aUb] used in the replicon clearance assay. (B) Replicon cells were untreated or treated with AP80978 (15 μM or 3.75 μM) or control compounds (2.5 μM cyclosporine [CsA] and 7.5 μM VX950) in the absence of G418 selection for four passages. Cells were then cultured in selection media in the absence of compound to determine when replicon is present and to allow “rebound.” HCV RNA levels from each treatment and time point were quantified and are expressed as log 10 change compared with HCV RNA levels in untreated samples at day 0, with all values normalized relative to GAPDH RNA. No rebound was observed in replicon cells that had been cultured in the presence of CsA, VX950, or AP80978 during the clearance phase of the assay. Values are means ± standard deviations (error bars) from three replicates.

    Techniques Used: Selection, Cell Culture

    13) Product Images from "Inhibition of RNA binding to hepatitis C virus RNA-dependent RNA polymerase: a new mechanism for antiviral intervention"

    Article Title: Inhibition of RNA binding to hepatitis C virus RNA-dependent RNA polymerase: a new mechanism for antiviral intervention

    Journal: Nucleic Acids Research

    doi: 10.1093/nar/gku632

    (A) RNA binding assay with increasing concentrations of HCV-NS5BΔ21 incubated 30 min with 1 μg of RNA, then loaded onto a non-denaturing agarose gel. (B) RNA binding assay with 500 ng/ml of HCV-NS5BΔ21 incubated 30 min with 1 μg of RNA in the presence of increasing concentrations of quercetagetin, then loaded onto a non-denaturing agarose gel. The control contained no HCV-NS5BΔ21. (C) Dose-dependent inhibition of RNA binding to HCV-RdRp by quercetagetin in a quantitative HCV-NS5BΔ21-RNA ELISA assay.
    Figure Legend Snippet: (A) RNA binding assay with increasing concentrations of HCV-NS5BΔ21 incubated 30 min with 1 μg of RNA, then loaded onto a non-denaturing agarose gel. (B) RNA binding assay with 500 ng/ml of HCV-NS5BΔ21 incubated 30 min with 1 μg of RNA in the presence of increasing concentrations of quercetagetin, then loaded onto a non-denaturing agarose gel. The control contained no HCV-NS5BΔ21. (C) Dose-dependent inhibition of RNA binding to HCV-RdRp by quercetagetin in a quantitative HCV-NS5BΔ21-RNA ELISA assay.

    Techniques Used: RNA Binding Assay, Incubation, Agarose Gel Electrophoresis, Inhibition, Enzyme-linked Immunosorbent Assay

    Superimposition of the HCV-NS5BΔ21-quercetagetin complex with the HCV-NS5BΔ21-RNA complex (PDB code 4E7A) in ribbon representation (palm in red and orange, thumb in green and pale green, fingers in blue and marine). Quercetagetin and RNA are in stick representation (yellow and pink, respectively). (A) Superimposition of the global structures. (B) Zoom on the quercetagetin binding domain.
    Figure Legend Snippet: Superimposition of the HCV-NS5BΔ21-quercetagetin complex with the HCV-NS5BΔ21-RNA complex (PDB code 4E7A) in ribbon representation (palm in red and orange, thumb in green and pale green, fingers in blue and marine). Quercetagetin and RNA are in stick representation (yellow and pink, respectively). (A) Superimposition of the global structures. (B) Zoom on the quercetagetin binding domain.

    Techniques Used: Binding Assay

    Related Articles

    Polymerase Chain Reaction:

    Article Title: Automated Extraction of Viral-Pathogen RNA and DNA for High-Throughput Quantitative Real-Time PCR
    Article Snippet: .. In the first part of the study, the linearity and accuracy of the in-house real-time HCV and HBV PCR with the automated sample preparation protocol was determined with dilutions of commercially available HCV and HBV controls (NAP-HCV007 and NAP-HBV006; Acrometrix) and the samples of the HCV and HBV 2004 QCMD proficiency program panels. .. In the second part, the intrarun and interrun variations for the HCV and HBV assays with automated sample preparation were determined using three different dilutions of a positive sample for both assays.

    Sample Prep:

    Article Title: Automated Extraction of Viral-Pathogen RNA and DNA for High-Throughput Quantitative Real-Time PCR
    Article Snippet: .. In the first part of the study, the linearity and accuracy of the in-house real-time HCV and HBV PCR with the automated sample preparation protocol was determined with dilutions of commercially available HCV and HBV controls (NAP-HCV007 and NAP-HBV006; Acrometrix) and the samples of the HCV and HBV 2004 QCMD proficiency program panels. .. In the second part, the intrarun and interrun variations for the HCV and HBV assays with automated sample preparation were determined using three different dilutions of a positive sample for both assays.

    Purification:

    Article Title: Multiplexed quantification of nucleic acids with large dynamic range using multivolume digital RT-PCR on a rotational SlipChip tested with HIV and Hepatitis C viral load
    Article Snippet: .. HIV viral RNA was purified from an archived sample of plasma containing HIV (viral RNA estimated to be ∼1.5×106 molecules/mL) from a deidentified patient sample, and HCV control viral RNA was purified from a commercial sample containing control HCV virus (25 million IU/ml, OptiQuant-S HCV Quantification Panel, Acrometrix) using the iPrep purification instrument (see Experimental Section in ). .. As the final elution volume of purified nucleic acid is generally smaller than the starting volume of plasma, there is a concentrating effect on viral RNA after sample purification.

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    Thermo Fisher gapdh sirna
    Concentration optimisation using <t>GAPDH</t> <t>siRNA.</t> All values were expressed as relative expression value (REV) with mean ± SD, n = 9
    Gapdh Sirna, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher rs6051702
    The Linkage Disequilibrium Analysis Plot of rs1127354, rs7270101 and <t>rs6051702</t> A, D’; B, r 2 .
    Rs6051702, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Concentration optimisation using GAPDH siRNA. All values were expressed as relative expression value (REV) with mean ± SD, n = 9

    Journal: Open Access Macedonian Journal of Medical Sciences

    Article Title: Silencing HCV Replication in Its Reservoir

    doi: 10.3889/oamjms.2018.372

    Figure Lengend Snippet: Concentration optimisation using GAPDH siRNA. All values were expressed as relative expression value (REV) with mean ± SD, n = 9

    Article Snippet: Infected PBMCs that were untreated and transfected non-targeting (scrambled) siRNA (siNTC) served as negative controls while PBMCs that were untreated and transfected with GAPDH siRNA served as positive controls, and illustrate viral RNA levels and protein expression for both transfected and control PBMCs, as quantitated by qPCR at 72 h after transfection. siRNA was significantly able to suppress HCV replication at 100 nM compared with untreated PBMCs (P < 0.01).

    Techniques: Concentration Assay, Expressing

    Concentration optimisation using GAPDH siRNA. All values were expressed as relative expression value (REV) with mean ± SD, n = 9

    Journal: Open Access Macedonian Journal of Medical Sciences

    Article Title: Silencing HCV Replication in Its Reservoir

    doi: 10.3889/oamjms.2018.372

    Figure Lengend Snippet: Concentration optimisation using GAPDH siRNA. All values were expressed as relative expression value (REV) with mean ± SD, n = 9

    Article Snippet: Also, there are no significant inhibition levels- for HCV in cells transfected with either the NTC siRNA nor those with GAPDH siRNA- was detected.

    Techniques: Concentration Assay, Expressing

    The Linkage Disequilibrium Analysis Plot of rs1127354, rs7270101 and rs6051702 A, D’; B, r 2 .

    Journal: Hepatitis Monthly

    Article Title: The ITPA and C20orf194 Polymorphisms and Hematological Changes During Treatment With Pegylated-Interferon Plus Ribavirin in Patients With Chronic Hepatitis C

    doi: 10.5812/hepatmon.35278

    Figure Lengend Snippet: The Linkage Disequilibrium Analysis Plot of rs1127354, rs7270101 and rs6051702 A, D’; B, r 2 .

    Article Snippet: Evaluation of Factors Affecting Hemoglobin-Decline at Week 4 of Treatment With Pegylated-Interferon Plus Ribavirin In univariate analysis, no association was found between the age, sex, BMI, ALT, AST, HCV RNA level, rs7270101, rs6051702 and RBV dose with Hb-decline at week 4 of the treatment (P > 0.05) ( ).

    Techniques:

    The Effect of rs1127354, rs7270101 and rs6051702 SNPs on the Change of Hematological Components at Week 4 of Treatment With Pegylated-Interferon Plus Ribavirin A – C, rs1127354, rs7270101 and rs6051702 (respectively) and Hb-decline at week 4 of the treatment; D –F, rs1127354, rs7270101 and rs6051702 (respectively) and Plt-decline at week 4 of the treatment; G – I, rs1127354, rs7270101 and rs6051702 (respectively) and WBC-decline at week 4 of the treatment, The lines and bars are representative of mean and standard deviation. P values were obtained by t-test.

    Journal: Hepatitis Monthly

    Article Title: The ITPA and C20orf194 Polymorphisms and Hematological Changes During Treatment With Pegylated-Interferon Plus Ribavirin in Patients With Chronic Hepatitis C

    doi: 10.5812/hepatmon.35278

    Figure Lengend Snippet: The Effect of rs1127354, rs7270101 and rs6051702 SNPs on the Change of Hematological Components at Week 4 of Treatment With Pegylated-Interferon Plus Ribavirin A – C, rs1127354, rs7270101 and rs6051702 (respectively) and Hb-decline at week 4 of the treatment; D –F, rs1127354, rs7270101 and rs6051702 (respectively) and Plt-decline at week 4 of the treatment; G – I, rs1127354, rs7270101 and rs6051702 (respectively) and WBC-decline at week 4 of the treatment, The lines and bars are representative of mean and standard deviation. P values were obtained by t-test.

    Article Snippet: Evaluation of Factors Affecting Hemoglobin-Decline at Week 4 of Treatment With Pegylated-Interferon Plus Ribavirin In univariate analysis, no association was found between the age, sex, BMI, ALT, AST, HCV RNA level, rs7270101, rs6051702 and RBV dose with Hb-decline at week 4 of the treatment (P > 0.05) ( ).

    Techniques: Standard Deviation