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    Santa Cruz Biotechnology hsv 1 infection
    A (upper panel). Polarized tonsil epithelial cells were treated with active or inactive recombinant HIV tat and gp120 in combination for 5 days, and TER was then measured. A (lower panel). The same cells were used to evaluate paracellular permeability after 5 days of treatment, as determined by leakage of IgG (Fab’) 2 from the apical chamber to the basolateral chamber. OD, optical density. B. The same cells were immunostained for ZO-1 (green). Cell nuclei are stained in blue. C. <t>HSV-1</t> at an MOI of 10 PFU per cell was added to the upper chamber of polarized cells, and culture medium was collected from the basolateral chamber after 1, 2, or 4 h. HSV-1 paracellular spread was confirmed by detection of ICP4 protein in Vero cells (green) 4 h after infection. Cell nuclei were stained with propidium iodide (red). Yellow indicates colocalization of ICP4 with the nuclear marker. D. HSV-1 paracellular spread was quantified by counting of HSV-1-infected Vero cells in 10 random microscopic fields and determining the percentage of cells positive for ICP4. A, D: Error bars indicate SEM (n = 3).
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    A (upper panel). Polarized tonsil epithelial cells were treated with active or inactive recombinant HIV tat and gp120 in combination for 5 days, and TER was then measured. A (lower panel). The same cells were used to evaluate paracellular permeability after 5 days of treatment, as determined by leakage of IgG (Fab’) 2 from the apical chamber to the basolateral chamber. OD, optical density. B. The same cells were immunostained for ZO-1 (green). Cell nuclei are stained in blue. C. HSV-1 at an MOI of 10 PFU per cell was added to the upper chamber of polarized cells, and culture medium was collected from the basolateral chamber after 1, 2, or 4 h. HSV-1 paracellular spread was confirmed by detection of ICP4 protein in Vero cells (green) 4 h after infection. Cell nuclei were stained with propidium iodide (red). Yellow indicates colocalization of ICP4 with the nuclear marker. D. HSV-1 paracellular spread was quantified by counting of HSV-1-infected Vero cells in 10 random microscopic fields and determining the percentage of cells positive for ICP4. A, D: Error bars indicate SEM (n = 3).

    Journal: PLoS ONE

    Article Title: HIV-Associated Disruption of Tight and Adherens Junctions of Oral Epithelial Cells Facilitates HSV-1 Infection and Spread

    doi: 10.1371/journal.pone.0088803

    Figure Lengend Snippet: A (upper panel). Polarized tonsil epithelial cells were treated with active or inactive recombinant HIV tat and gp120 in combination for 5 days, and TER was then measured. A (lower panel). The same cells were used to evaluate paracellular permeability after 5 days of treatment, as determined by leakage of IgG (Fab’) 2 from the apical chamber to the basolateral chamber. OD, optical density. B. The same cells were immunostained for ZO-1 (green). Cell nuclei are stained in blue. C. HSV-1 at an MOI of 10 PFU per cell was added to the upper chamber of polarized cells, and culture medium was collected from the basolateral chamber after 1, 2, or 4 h. HSV-1 paracellular spread was confirmed by detection of ICP4 protein in Vero cells (green) 4 h after infection. Cell nuclei were stained with propidium iodide (red). Yellow indicates colocalization of ICP4 with the nuclear marker. D. HSV-1 paracellular spread was quantified by counting of HSV-1-infected Vero cells in 10 random microscopic fields and determining the percentage of cells positive for ICP4. A, D: Error bars indicate SEM (n = 3).

    Article Snippet: To determine HSV-1 infection, we immunostained infected cells with mouse antibodies against HSV-1 ICP4 and gB (both from Santa Cruz Biotechnology, Inc., Dallas, TX), rabbit anti-gD (HSV-1) (MyBioSource, San Diego, CA), and goat anti-HSV-1/2 antiserum (AbD Serotec, Raleigh, NC).

    Techniques: Recombinant, Permeability, Staining, Infection, Marker

    A. Polarized tonsil epithelial cells were incubated with dual X4- and R5-tropic HIV-1 SF33 for 5 days. One set of cells was exposed to UV-inactivated virions. Culture medium was changed daily to add fresh virus, and TER was measured. B. HSV-1 was added to the apical surface of polarized cells upon complete disruption of TJs at 5 days. HSV paracellular spread at 1, 2, and 4 h after incubation was examined in Vero cells grown in the basolateral chamber of filter inserts by immunostaining of ICP4 protein. HSV-1 paracellular spread was quantified by counting HSV-1-infected Vero cells, and the percentage of cells positive for ICP4 was determined. A, B: Error bars indicate SEM (n = 3).

    Journal: PLoS ONE

    Article Title: HIV-Associated Disruption of Tight and Adherens Junctions of Oral Epithelial Cells Facilitates HSV-1 Infection and Spread

    doi: 10.1371/journal.pone.0088803

    Figure Lengend Snippet: A. Polarized tonsil epithelial cells were incubated with dual X4- and R5-tropic HIV-1 SF33 for 5 days. One set of cells was exposed to UV-inactivated virions. Culture medium was changed daily to add fresh virus, and TER was measured. B. HSV-1 was added to the apical surface of polarized cells upon complete disruption of TJs at 5 days. HSV paracellular spread at 1, 2, and 4 h after incubation was examined in Vero cells grown in the basolateral chamber of filter inserts by immunostaining of ICP4 protein. HSV-1 paracellular spread was quantified by counting HSV-1-infected Vero cells, and the percentage of cells positive for ICP4 was determined. A, B: Error bars indicate SEM (n = 3).

    Article Snippet: To determine HSV-1 infection, we immunostained infected cells with mouse antibodies against HSV-1 ICP4 and gB (both from Santa Cruz Biotechnology, Inc., Dallas, TX), rabbit anti-gD (HSV-1) (MyBioSource, San Diego, CA), and goat anti-HSV-1/2 antiserum (AbD Serotec, Raleigh, NC).

    Techniques: Incubation, Immunostaining, Infection

    A. Polarized tonsil epithelial cells were coimmunostained for nectin-1 and E-cadherin. Yellow in the merged panel indicates colocalization of nectin-1 and E-cadherin. B. Polarized tonsil cells were treated with active or inactive tat and gp120 in combination for 5 days. In parallel experiments, cells were exposed to HIV-1 SF33 for 5 days. Cells were then immunostained for E-cadherin and nectin-1. C. Polarized cells were treated with active or inactive tat and gp120 in combination or with cell-free HIV-1 SF33 for 5 days. Cells were then extracted, and E-cadherin and nectin-1 were detected by Western blot assay. D. Apical or basolateral membranes of polarized epithelial cells were treated with inactive or active HIV tat and labeled with sulfo-NHS-LC-biotin. Nectin-1 was detected in the avidin-precipitated total membrane proteins by Western blot assay. E. HSV-1 gD(306t) at 20 µg/ml was added to apical or basolateral membranes of polarized epithelial cells treated with inactive or active HIV tat/gp120. After 30 min the cell surface was labeled with sulfo-NHS-LC-biotin. Proteins biotinylated at the cell surface were precipitated with streptavidin–agarose beads, and gD was detected by Western blot assay. AP, apical; BL, basolateral.

    Journal: PLoS ONE

    Article Title: HIV-Associated Disruption of Tight and Adherens Junctions of Oral Epithelial Cells Facilitates HSV-1 Infection and Spread

    doi: 10.1371/journal.pone.0088803

    Figure Lengend Snippet: A. Polarized tonsil epithelial cells were coimmunostained for nectin-1 and E-cadherin. Yellow in the merged panel indicates colocalization of nectin-1 and E-cadherin. B. Polarized tonsil cells were treated with active or inactive tat and gp120 in combination for 5 days. In parallel experiments, cells were exposed to HIV-1 SF33 for 5 days. Cells were then immunostained for E-cadherin and nectin-1. C. Polarized cells were treated with active or inactive tat and gp120 in combination or with cell-free HIV-1 SF33 for 5 days. Cells were then extracted, and E-cadherin and nectin-1 were detected by Western blot assay. D. Apical or basolateral membranes of polarized epithelial cells were treated with inactive or active HIV tat and labeled with sulfo-NHS-LC-biotin. Nectin-1 was detected in the avidin-precipitated total membrane proteins by Western blot assay. E. HSV-1 gD(306t) at 20 µg/ml was added to apical or basolateral membranes of polarized epithelial cells treated with inactive or active HIV tat/gp120. After 30 min the cell surface was labeled with sulfo-NHS-LC-biotin. Proteins biotinylated at the cell surface were precipitated with streptavidin–agarose beads, and gD was detected by Western blot assay. AP, apical; BL, basolateral.

    Article Snippet: To determine HSV-1 infection, we immunostained infected cells with mouse antibodies against HSV-1 ICP4 and gB (both from Santa Cruz Biotechnology, Inc., Dallas, TX), rabbit anti-gD (HSV-1) (MyBioSource, San Diego, CA), and goat anti-HSV-1/2 antiserum (AbD Serotec, Raleigh, NC).

    Techniques: Western Blot, Labeling, Avidin-Biotin Assay

    A. Polarized tonsil cells were treated with HIV tat/gp120 or HIV virions for 5 days and infected with HSV-1. After 24 h, cells were fixed and immunostained using anti-HSV-1 gB antibodies (red). Cell nuclei are stained in blue. B. HSV-1 infection was quantitatively evaluated, and the percentage of cells positive for gB was determined. Error bars indicate SEM. C. Cells were incubated with antibodies against nectin-1 for 1 h and then infected with HSV-1. Cells were fixed after 24 h, HSV-1 infection was confirmed by detection of goat anti-HSV-1 immune serum, and the number of infected cells was counted. ab, cells incubated with antibodies. c, control cells without antibodies. Error bars indicate SEM. *P<0.01, **P<0.001, all compared with the control group.

    Journal: PLoS ONE

    Article Title: HIV-Associated Disruption of Tight and Adherens Junctions of Oral Epithelial Cells Facilitates HSV-1 Infection and Spread

    doi: 10.1371/journal.pone.0088803

    Figure Lengend Snippet: A. Polarized tonsil cells were treated with HIV tat/gp120 or HIV virions for 5 days and infected with HSV-1. After 24 h, cells were fixed and immunostained using anti-HSV-1 gB antibodies (red). Cell nuclei are stained in blue. B. HSV-1 infection was quantitatively evaluated, and the percentage of cells positive for gB was determined. Error bars indicate SEM. C. Cells were incubated with antibodies against nectin-1 for 1 h and then infected with HSV-1. Cells were fixed after 24 h, HSV-1 infection was confirmed by detection of goat anti-HSV-1 immune serum, and the number of infected cells was counted. ab, cells incubated with antibodies. c, control cells without antibodies. Error bars indicate SEM. *P<0.01, **P<0.001, all compared with the control group.

    Article Snippet: To determine HSV-1 infection, we immunostained infected cells with mouse antibodies against HSV-1 ICP4 and gB (both from Santa Cruz Biotechnology, Inc., Dallas, TX), rabbit anti-gD (HSV-1) (MyBioSource, San Diego, CA), and goat anti-HSV-1/2 antiserum (AbD Serotec, Raleigh, NC).

    Techniques: Infection, Staining, Incubation

    A. Polarized tonsil cells were treated with active or inactive tat/gp120 and HIV virions for 5 days. Disrupted cells were infected with HSV-1 at 0.01 PFU per cell from basolateral membranes of polarized cells. After 3 days, cells were fixed and immunostained using goat anti-HSV immune serum (green). Cell nuclei are stained in red. Yellow represents colocalization of HSV proteins and nuclei. B. (upper panel) Plaque numbers were counted from 3 independent filter inserts and data are presented as the average number of HSV-infected plaques per insert. (lower panel) Cell-to-cell spread of HSV-1 was quantitatively evaluated by counting HSV-infected cells in the plaques. Results are presented as the average number of HSV-infected cells per plaque. Error bars indicate SEM. C. Polarized cells were infected with HSV-1. After 4 h, antibodies to nectin-1 and gD were added separately and in combination. Cell medium was changed daily to add fresh antibodies. Cells were fixed and immunostained for HSV-1, and the plaque numbers (upper panel) and the number of HSV-1-positive cells in plaques were counted (lower panel). Error bars indicate SEM. *P<0.05, *P<0.01, **P<0.001, all compared with the control group.

    Journal: PLoS ONE

    Article Title: HIV-Associated Disruption of Tight and Adherens Junctions of Oral Epithelial Cells Facilitates HSV-1 Infection and Spread

    doi: 10.1371/journal.pone.0088803

    Figure Lengend Snippet: A. Polarized tonsil cells were treated with active or inactive tat/gp120 and HIV virions for 5 days. Disrupted cells were infected with HSV-1 at 0.01 PFU per cell from basolateral membranes of polarized cells. After 3 days, cells were fixed and immunostained using goat anti-HSV immune serum (green). Cell nuclei are stained in red. Yellow represents colocalization of HSV proteins and nuclei. B. (upper panel) Plaque numbers were counted from 3 independent filter inserts and data are presented as the average number of HSV-infected plaques per insert. (lower panel) Cell-to-cell spread of HSV-1 was quantitatively evaluated by counting HSV-infected cells in the plaques. Results are presented as the average number of HSV-infected cells per plaque. Error bars indicate SEM. C. Polarized cells were infected with HSV-1. After 4 h, antibodies to nectin-1 and gD were added separately and in combination. Cell medium was changed daily to add fresh antibodies. Cells were fixed and immunostained for HSV-1, and the plaque numbers (upper panel) and the number of HSV-1-positive cells in plaques were counted (lower panel). Error bars indicate SEM. *P<0.05, *P<0.01, **P<0.001, all compared with the control group.

    Article Snippet: To determine HSV-1 infection, we immunostained infected cells with mouse antibodies against HSV-1 ICP4 and gB (both from Santa Cruz Biotechnology, Inc., Dallas, TX), rabbit anti-gD (HSV-1) (MyBioSource, San Diego, CA), and goat anti-HSV-1/2 antiserum (AbD Serotec, Raleigh, NC).

    Techniques: Infection, Staining

    The oral mucosal epithelium consists of stratified squamous epithelial cells. Each layer of epithelial cells forms lateral intercellular junctional complexes, including AJs and TJs. HSV-1 gD receptor nectin-1 is sequestered within the intact AJs area of lateral membranes of epithelial cells (left panel). HIV-induced disruption of AJs exposes nectin-1 from its sequestered areas (right panel), which binds to HSV gD and thereby promotes HSV infection and cell-to-cell spread within the oral epithelium. HIV-induced disruption of TJs leads to paracellular spread of HSV virions, which may facilitate penetration of virus from the apical to the basolateral direction into the deeper part of the epithelium, and from the basolateral to the apical direction leading to release of virus into saliva. Thus, HIV-induced disruption of epithelial junctions may facilitate the spread of HSV-1 infection within the mucosal epithelium, leading to the rapid progression of HSV-mediated mucosal lesions and ulcers.

    Journal: PLoS ONE

    Article Title: HIV-Associated Disruption of Tight and Adherens Junctions of Oral Epithelial Cells Facilitates HSV-1 Infection and Spread

    doi: 10.1371/journal.pone.0088803

    Figure Lengend Snippet: The oral mucosal epithelium consists of stratified squamous epithelial cells. Each layer of epithelial cells forms lateral intercellular junctional complexes, including AJs and TJs. HSV-1 gD receptor nectin-1 is sequestered within the intact AJs area of lateral membranes of epithelial cells (left panel). HIV-induced disruption of AJs exposes nectin-1 from its sequestered areas (right panel), which binds to HSV gD and thereby promotes HSV infection and cell-to-cell spread within the oral epithelium. HIV-induced disruption of TJs leads to paracellular spread of HSV virions, which may facilitate penetration of virus from the apical to the basolateral direction into the deeper part of the epithelium, and from the basolateral to the apical direction leading to release of virus into saliva. Thus, HIV-induced disruption of epithelial junctions may facilitate the spread of HSV-1 infection within the mucosal epithelium, leading to the rapid progression of HSV-mediated mucosal lesions and ulcers.

    Article Snippet: To determine HSV-1 infection, we immunostained infected cells with mouse antibodies against HSV-1 ICP4 and gB (both from Santa Cruz Biotechnology, Inc., Dallas, TX), rabbit anti-gD (HSV-1) (MyBioSource, San Diego, CA), and goat anti-HSV-1/2 antiserum (AbD Serotec, Raleigh, NC).

    Techniques: Infection