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hsv 1 infection  (ATCC)


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    ATCC hsv 1 infection
    Hsv 1 Infection, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    hsv 1 infection - by Bioz Stars, 2024-12
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    <t>HSV-1</t> infection of PDL cells. ( A ) Morphological changes in PDL cells 24 and 48 h post-infection (p.i.) with HSV-1 (MOI 100), showing ballooning and detachment of dead cells (10× magnification). ( B ) Visualization of HSV-1 infection in PDL cells by immunofluorescent staining (green) of immediate-early (ICP0) and early (ICP8) viral proteins (10× magnification). Cells were infected with HSV-1 (MOI 100), fixed at 1 h p.i. (ICP0) and 24 h p.i. (ICP8). Control: irrelevant mouse IgG1; nuclei stained with DAPI (blue). Panels ( A , B ) are representative of 6 independent infections. ( C ) RT-qPCR of PDL cells infected with HSV-1 at various MOIs (10 to 40,000), measuring immediate-early (ICP0, ICP4) and early (ICP8) transcripts at 1 and 6 h p.i. Bars show mean expression values; error bars indicate standard deviations (n = 3). Viral titer-dependent (MOI) response to HSV-1 infection in PDL cells was determined using repeated measures ANOVA. The statistical significance and P-values of the comparisons are presented in to avoid overcrowding the graph. ( D ) RT-qPCR of PDL fragments exposed to HSV-1 (4 × 10 7 TCID50/mL) for 4 h, showing Log 10 fold changes in ICP0, ICP4 and ICP8 transcripts from 3 donors (PDLs A, B and C). Baseline in ( C ) from mock-infected cells; in ( D ) from uninfected fragments of the same donors. Gene expression levels were calculated using the 2 −ΔΔCT method and normalized to GAPDH as a reference gene.
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    ATCC hsv 1 infection
    <t>HSV-1</t> infection of PDL cells. ( A ) Morphological changes in PDL cells 24 and 48 h post-infection (p.i.) with HSV-1 (MOI 100), showing ballooning and detachment of dead cells (10× magnification). ( B ) Visualization of HSV-1 infection in PDL cells by immunofluorescent staining (green) of immediate-early (ICP0) and early (ICP8) viral proteins (10× magnification). Cells were infected with HSV-1 (MOI 100), fixed at 1 h p.i. (ICP0) and 24 h p.i. (ICP8). Control: irrelevant mouse IgG1; nuclei stained with DAPI (blue). Panels ( A , B ) are representative of 6 independent infections. ( C ) RT-qPCR of PDL cells infected with HSV-1 at various MOIs (10 to 40,000), measuring immediate-early (ICP0, ICP4) and early (ICP8) transcripts at 1 and 6 h p.i. Bars show mean expression values; error bars indicate standard deviations (n = 3). Viral titer-dependent (MOI) response to HSV-1 infection in PDL cells was determined using repeated measures ANOVA. The statistical significance and P-values of the comparisons are presented in to avoid overcrowding the graph. ( D ) RT-qPCR of PDL fragments exposed to HSV-1 (4 × 10 7 TCID50/mL) for 4 h, showing Log 10 fold changes in ICP0, ICP4 and ICP8 transcripts from 3 donors (PDLs A, B and C). Baseline in ( C ) from mock-infected cells; in ( D ) from uninfected fragments of the same donors. Gene expression levels were calculated using the 2 −ΔΔCT method and normalized to GAPDH as a reference gene.
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    Thermo Fisher post hsv 1 infection
    <t>HSV-1</t> infection of PDL cells. ( A ) Morphological changes in PDL cells 24 and 48 h post-infection (p.i.) with HSV-1 (MOI 100), showing ballooning and detachment of dead cells (10× magnification). ( B ) Visualization of HSV-1 infection in PDL cells by immunofluorescent staining (green) of immediate-early (ICP0) and early (ICP8) viral proteins (10× magnification). Cells were infected with HSV-1 (MOI 100), fixed at 1 h p.i. (ICP0) and 24 h p.i. (ICP8). Control: irrelevant mouse IgG1; nuclei stained with DAPI (blue). Panels ( A , B ) are representative of 6 independent infections. ( C ) RT-qPCR of PDL cells infected with HSV-1 at various MOIs (10 to 40,000), measuring immediate-early (ICP0, ICP4) and early (ICP8) transcripts at 1 and 6 h p.i. Bars show mean expression values; error bars indicate standard deviations (n = 3). Viral titer-dependent (MOI) response to HSV-1 infection in PDL cells was determined using repeated measures ANOVA. The statistical significance and P-values of the comparisons are presented in to avoid overcrowding the graph. ( D ) RT-qPCR of PDL fragments exposed to HSV-1 (4 × 10 7 TCID50/mL) for 4 h, showing Log 10 fold changes in ICP0, ICP4 and ICP8 transcripts from 3 donors (PDLs A, B and C). Baseline in ( C ) from mock-infected cells; in ( D ) from uninfected fragments of the same donors. Gene expression levels were calculated using the 2 −ΔΔCT method and normalized to GAPDH as a reference gene.
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    Image Search Results


    HSV-1 infection of PDL cells. ( A ) Morphological changes in PDL cells 24 and 48 h post-infection (p.i.) with HSV-1 (MOI 100), showing ballooning and detachment of dead cells (10× magnification). ( B ) Visualization of HSV-1 infection in PDL cells by immunofluorescent staining (green) of immediate-early (ICP0) and early (ICP8) viral proteins (10× magnification). Cells were infected with HSV-1 (MOI 100), fixed at 1 h p.i. (ICP0) and 24 h p.i. (ICP8). Control: irrelevant mouse IgG1; nuclei stained with DAPI (blue). Panels ( A , B ) are representative of 6 independent infections. ( C ) RT-qPCR of PDL cells infected with HSV-1 at various MOIs (10 to 40,000), measuring immediate-early (ICP0, ICP4) and early (ICP8) transcripts at 1 and 6 h p.i. Bars show mean expression values; error bars indicate standard deviations (n = 3). Viral titer-dependent (MOI) response to HSV-1 infection in PDL cells was determined using repeated measures ANOVA. The statistical significance and P-values of the comparisons are presented in to avoid overcrowding the graph. ( D ) RT-qPCR of PDL fragments exposed to HSV-1 (4 × 10 7 TCID50/mL) for 4 h, showing Log 10 fold changes in ICP0, ICP4 and ICP8 transcripts from 3 donors (PDLs A, B and C). Baseline in ( C ) from mock-infected cells; in ( D ) from uninfected fragments of the same donors. Gene expression levels were calculated using the 2 −ΔΔCT method and normalized to GAPDH as a reference gene.

    Journal: International Journal of Molecular Sciences

    Article Title: Herpes Simplex Virus Type 1 Infection of Human Periodontal Ligament

    doi: 10.3390/ijms25158466

    Figure Lengend Snippet: HSV-1 infection of PDL cells. ( A ) Morphological changes in PDL cells 24 and 48 h post-infection (p.i.) with HSV-1 (MOI 100), showing ballooning and detachment of dead cells (10× magnification). ( B ) Visualization of HSV-1 infection in PDL cells by immunofluorescent staining (green) of immediate-early (ICP0) and early (ICP8) viral proteins (10× magnification). Cells were infected with HSV-1 (MOI 100), fixed at 1 h p.i. (ICP0) and 24 h p.i. (ICP8). Control: irrelevant mouse IgG1; nuclei stained with DAPI (blue). Panels ( A , B ) are representative of 6 independent infections. ( C ) RT-qPCR of PDL cells infected with HSV-1 at various MOIs (10 to 40,000), measuring immediate-early (ICP0, ICP4) and early (ICP8) transcripts at 1 and 6 h p.i. Bars show mean expression values; error bars indicate standard deviations (n = 3). Viral titer-dependent (MOI) response to HSV-1 infection in PDL cells was determined using repeated measures ANOVA. The statistical significance and P-values of the comparisons are presented in to avoid overcrowding the graph. ( D ) RT-qPCR of PDL fragments exposed to HSV-1 (4 × 10 7 TCID50/mL) for 4 h, showing Log 10 fold changes in ICP0, ICP4 and ICP8 transcripts from 3 donors (PDLs A, B and C). Baseline in ( C ) from mock-infected cells; in ( D ) from uninfected fragments of the same donors. Gene expression levels were calculated using the 2 −ΔΔCT method and normalized to GAPDH as a reference gene.

    Article Snippet: HSV-1 infections were also performed in the presence of 1 and 10 µg/mL of peptidoglycan (PEG) from Micrococcus luteus (Sigma-Aldrich, St. Louis, MO, USA).

    Techniques: Infection, Staining, Control, Quantitative RT-PCR, Expressing

    Innate immune response in HSV-1-infected PDL exposed to bacterial peptidoglycan (PEG). ( A ) Expression of interferons (IFN-α, IFN-β, IFN-λ) and cytokines (IL1-β, TNF-α) in cultured PDL cells after 24 h of HSV-1 (MOI 100) exposure with or without PEG. Bars show Log 10 fold changes in gene expression. The synergy between PEG and HSV-1 was assessed by calculating the ratio (R, shown inside the bars) of the sum of Log 10 RQ values for the combined condition (HSV-1 + PEG) to the sum of individual conditions. R > 1 indicates synergy, R ≈ 1 additive effect, and R < 1 antagonism. ( B ) Expression of interferons (IFN-α, IFN-β, IFN-λ) in PDL fragments from 3 donors (PDLs A, B, C) after 4 h of HSV-1 (4 × 10 7 TCID50/mL) exposure. Bars represent fold changes in gene expression. ( A , B ) Gene expression was calculated using the 2 −ΔΔCT method, with GAPDH as the reference gene and mock condition as the reference sample.

    Journal: International Journal of Molecular Sciences

    Article Title: Herpes Simplex Virus Type 1 Infection of Human Periodontal Ligament

    doi: 10.3390/ijms25158466

    Figure Lengend Snippet: Innate immune response in HSV-1-infected PDL exposed to bacterial peptidoglycan (PEG). ( A ) Expression of interferons (IFN-α, IFN-β, IFN-λ) and cytokines (IL1-β, TNF-α) in cultured PDL cells after 24 h of HSV-1 (MOI 100) exposure with or without PEG. Bars show Log 10 fold changes in gene expression. The synergy between PEG and HSV-1 was assessed by calculating the ratio (R, shown inside the bars) of the sum of Log 10 RQ values for the combined condition (HSV-1 + PEG) to the sum of individual conditions. R > 1 indicates synergy, R ≈ 1 additive effect, and R < 1 antagonism. ( B ) Expression of interferons (IFN-α, IFN-β, IFN-λ) in PDL fragments from 3 donors (PDLs A, B, C) after 4 h of HSV-1 (4 × 10 7 TCID50/mL) exposure. Bars represent fold changes in gene expression. ( A , B ) Gene expression was calculated using the 2 −ΔΔCT method, with GAPDH as the reference gene and mock condition as the reference sample.

    Article Snippet: HSV-1 infections were also performed in the presence of 1 and 10 µg/mL of peptidoglycan (PEG) from Micrococcus luteus (Sigma-Aldrich, St. Louis, MO, USA).

    Techniques: Infection, Expressing, Cell Culture