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Herpes simplex virus type 2-infected dendritic cells produce TNF-α, which enhances CCR5 expression and stimulates HIV production from adjacent infected cells
Prior HSV-2 infection enhances the acquisition of HIV-1 >3-fold. In genital herpes lesions, the superficial layers of stratified squamous epithelium are disrupted, allowing easier access of HIV-1 to Langerhans cells (LC) in the epidermis and perhaps even dendritic cells (DCs) in the outer dermis,...
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| Published in: | The Journal of immunology (1950) 2015-05, Vol.194 (9), p.4438-4445 |
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| Main Authors: | , , , , , , , , |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c374t-7d3b28db1a41e30ac9c4706a41f40678249b55ce6fd55214c92f39a2243efe4c3 |
| container_end_page | 4445 |
| container_issue | 9 |
| container_start_page | 4438 |
| container_title | The Journal of immunology (1950) |
| container_volume | 194 |
| creator | Marsden, Valerie Donaghy, Heather Bertram, Kirstie M Harman, Andrew N Nasr, Najla Keoshkerian, Elizabeth Merten, Steven Lloyd, Andrew R Cunningham, Anthony L |
| description | Prior HSV-2 infection enhances the acquisition of HIV-1 >3-fold. In genital herpes lesions, the superficial layers of stratified squamous epithelium are disrupted, allowing easier access of HIV-1 to Langerhans cells (LC) in the epidermis and perhaps even dendritic cells (DCs) in the outer dermis, as well as to lesion infiltrating activated T lymphocytes and macrophages. Therefore, we examined the effects of coinfection with HIV-1 and HSV-2 on monocyte-derived DCs (MDDC). With simultaneous coinfection, HSV-2 significantly stimulated HIV-1 DNA production 5-fold compared with HIV-1 infection alone. Because |
| doi_str_mv | 10.4049/jimmunol.1401706 |
| format | article |
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In genital herpes lesions, the superficial layers of stratified squamous epithelium are disrupted, allowing easier access of HIV-1 to Langerhans cells (LC) in the epidermis and perhaps even dendritic cells (DCs) in the outer dermis, as well as to lesion infiltrating activated T lymphocytes and macrophages. Therefore, we examined the effects of coinfection with HIV-1 and HSV-2 on monocyte-derived DCs (MDDC). With simultaneous coinfection, HSV-2 significantly stimulated HIV-1 DNA production 5-fold compared with HIV-1 infection alone. Because <1% of cells were dually infected, this was a field effect. Virus-stripped supernatants from HSV-2-infected MDDCs were shown to enhance HIV-1 infection, as measured by HIV-1-DNA and p24 Ag in MDDCs. Furthermore these supernatants markedly stimulated CCR5 expression on both MDDCs and LCs. TNF-α was by far the most prominent cytokine in the supernatant and also within HSV-2-infected MDDCs. HSV-2 infection of isolated immature epidermal LCs, but not keratinocytes, also produced TNF-α (and low levels of IFN-β). Neutralizing Ab to TNF-α and its receptor, TNF-R1, on MDDCs markedly inhibited the CCR5-stimulating effect of the supernatant. Therefore, these results suggest that HSV-2 infection of DCs in the skin during primary or recurrent genital herpes may enhance HIV-1 infection of adjacent DCs, thus contributing to acquisition of HIV-1 through herpetic lesions.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1401706</identifier><identifier>PMID: 25840914</identifier><language>eng</language><publisher>United States</publisher><subject>Coinfection ; Culture Media, Conditioned - metabolism ; Cytokines - biosynthesis ; Dendritic Cells - immunology ; Dendritic Cells - metabolism ; Dendritic Cells - virology ; Gene Expression Regulation ; Herpes Genitalis - genetics ; Herpes Genitalis - immunology ; Herpes Genitalis - metabolism ; Herpes simplex virus 2 ; Herpesvirus 2, Human - physiology ; Herpesvirus 2, Human - radiation effects ; HIV Infections - genetics ; HIV Infections - immunology ; HIV Infections - metabolism ; HIV Infections - virology ; HIV-1 - physiology ; Human immunodeficiency virus ; Human immunodeficiency virus 1 ; Humans ; Models, Biological ; Receptors, CCR5 - genetics ; Receptors, CCR5 - metabolism ; Tumor Necrosis Factor-alpha - metabolism ; Up-Regulation ; Virus Replication</subject><ispartof>The Journal of immunology (1950), 2015-05, Vol.194 (9), p.4438-4445</ispartof><rights>Copyright © 2015 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c374t-7d3b28db1a41e30ac9c4706a41f40678249b55ce6fd55214c92f39a2243efe4c3</citedby><cites>FETCH-LOGICAL-c374t-7d3b28db1a41e30ac9c4706a41f40678249b55ce6fd55214c92f39a2243efe4c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25840914$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marsden, Valerie</creatorcontrib><creatorcontrib>Donaghy, Heather</creatorcontrib><creatorcontrib>Bertram, Kirstie M</creatorcontrib><creatorcontrib>Harman, Andrew N</creatorcontrib><creatorcontrib>Nasr, Najla</creatorcontrib><creatorcontrib>Keoshkerian, Elizabeth</creatorcontrib><creatorcontrib>Merten, Steven</creatorcontrib><creatorcontrib>Lloyd, Andrew R</creatorcontrib><creatorcontrib>Cunningham, Anthony L</creatorcontrib><title>Herpes simplex virus type 2-infected dendritic cells produce TNF-α, which enhances CCR5 expression and stimulates HIV production from adjacent infected cells</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Prior HSV-2 infection enhances the acquisition of HIV-1 >3-fold. In genital herpes lesions, the superficial layers of stratified squamous epithelium are disrupted, allowing easier access of HIV-1 to Langerhans cells (LC) in the epidermis and perhaps even dendritic cells (DCs) in the outer dermis, as well as to lesion infiltrating activated T lymphocytes and macrophages. Therefore, we examined the effects of coinfection with HIV-1 and HSV-2 on monocyte-derived DCs (MDDC). With simultaneous coinfection, HSV-2 significantly stimulated HIV-1 DNA production 5-fold compared with HIV-1 infection alone. Because <1% of cells were dually infected, this was a field effect. Virus-stripped supernatants from HSV-2-infected MDDCs were shown to enhance HIV-1 infection, as measured by HIV-1-DNA and p24 Ag in MDDCs. Furthermore these supernatants markedly stimulated CCR5 expression on both MDDCs and LCs. TNF-α was by far the most prominent cytokine in the supernatant and also within HSV-2-infected MDDCs. HSV-2 infection of isolated immature epidermal LCs, but not keratinocytes, also produced TNF-α (and low levels of IFN-β). Neutralizing Ab to TNF-α and its receptor, TNF-R1, on MDDCs markedly inhibited the CCR5-stimulating effect of the supernatant. Therefore, these results suggest that HSV-2 infection of DCs in the skin during primary or recurrent genital herpes may enhance HIV-1 infection of adjacent DCs, thus contributing to acquisition of HIV-1 through herpetic lesions.</description><subject>Coinfection</subject><subject>Culture Media, Conditioned - metabolism</subject><subject>Cytokines - biosynthesis</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - metabolism</subject><subject>Dendritic Cells - virology</subject><subject>Gene Expression Regulation</subject><subject>Herpes Genitalis - genetics</subject><subject>Herpes Genitalis - immunology</subject><subject>Herpes Genitalis - metabolism</subject><subject>Herpes simplex virus 2</subject><subject>Herpesvirus 2, Human - physiology</subject><subject>Herpesvirus 2, Human - radiation effects</subject><subject>HIV Infections - genetics</subject><subject>HIV Infections - immunology</subject><subject>HIV Infections - metabolism</subject><subject>HIV Infections - virology</subject><subject>HIV-1 - physiology</subject><subject>Human immunodeficiency virus</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Models, Biological</subject><subject>Receptors, CCR5 - genetics</subject><subject>Receptors, CCR5 - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Up-Regulation</subject><subject>Virus Replication</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNqFUc1O4zAQthCIdrt754R85EBg7DhOckTVQpGqRULANXLtieoqcYLtsPAyvAMvss-06VJ63dNoNN-f5iPkhMGFAFFebmzbDq5rLpgAloM8IFOWZZBICfKQTAE4T1gu8wn5FsIGACRwcUwmPCsElExMyfsCfY-BBtv2Db7SF-uHQONbj5Qn1tWoIxpq0Blvo9VUY9ME2vvODBrpw6_r5M_HOf29tnpN0a2V06PYfH6fUXztPYZgO0eVMzRE2w6NiuN5cfu0U4jba-27liqzURpdpHvPf07fyVGtmoA_dnNGHq9_PswXyfLu5nZ-tUx0mouY5CZd8cKsmBIMU1C61GJ8x7jVAmRecFGuskyjrE2WcSZ0yeu0VJyLFGsUOp2Rs0_dMdfzgCFWrQ3bBMphN4SKFVDkDKCA_0NlLjiwMt1C4ROqfReCx7rqvW2Vf6sYVNsCq68Cq12BI-V0pz6sWjR7wldj6V9IsJsC</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Marsden, Valerie</creator><creator>Donaghy, Heather</creator><creator>Bertram, Kirstie M</creator><creator>Harman, Andrew N</creator><creator>Nasr, Najla</creator><creator>Keoshkerian, Elizabeth</creator><creator>Merten, Steven</creator><creator>Lloyd, Andrew R</creator><creator>Cunningham, Anthony L</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20150501</creationdate><title>Herpes simplex virus type 2-infected dendritic cells produce TNF-α, which enhances CCR5 expression and stimulates HIV production from adjacent infected cells</title><author>Marsden, Valerie ; 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In genital herpes lesions, the superficial layers of stratified squamous epithelium are disrupted, allowing easier access of HIV-1 to Langerhans cells (LC) in the epidermis and perhaps even dendritic cells (DCs) in the outer dermis, as well as to lesion infiltrating activated T lymphocytes and macrophages. Therefore, we examined the effects of coinfection with HIV-1 and HSV-2 on monocyte-derived DCs (MDDC). With simultaneous coinfection, HSV-2 significantly stimulated HIV-1 DNA production 5-fold compared with HIV-1 infection alone. Because <1% of cells were dually infected, this was a field effect. Virus-stripped supernatants from HSV-2-infected MDDCs were shown to enhance HIV-1 infection, as measured by HIV-1-DNA and p24 Ag in MDDCs. Furthermore these supernatants markedly stimulated CCR5 expression on both MDDCs and LCs. TNF-α was by far the most prominent cytokine in the supernatant and also within HSV-2-infected MDDCs. 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| identifier | ISSN: 0022-1767 |
| ispartof | The Journal of immunology (1950), 2015-05, Vol.194 (9), p.4438-4445 |
| issn | 0022-1767 1550-6606 |
| language | eng |
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| source | Electronic Journals Library |
| subjects | Coinfection Culture Media, Conditioned - metabolism Cytokines - biosynthesis Dendritic Cells - immunology Dendritic Cells - metabolism Dendritic Cells - virology Gene Expression Regulation Herpes Genitalis - genetics Herpes Genitalis - immunology Herpes Genitalis - metabolism Herpes simplex virus 2 Herpesvirus 2, Human - physiology Herpesvirus 2, Human - radiation effects HIV Infections - genetics HIV Infections - immunology HIV Infections - metabolism HIV Infections - virology HIV-1 - physiology Human immunodeficiency virus Human immunodeficiency virus 1 Humans Models, Biological Receptors, CCR5 - genetics Receptors, CCR5 - metabolism Tumor Necrosis Factor-alpha - metabolism Up-Regulation Virus Replication |
| title | Herpes simplex virus type 2-infected dendritic cells produce TNF-α, which enhances CCR5 expression and stimulates HIV production from adjacent infected cells |
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