CD4 is a Critical Component of the Receptor for Human Herpesvirus 7: Interference with Human Immunodeficiency Virus
In this study, we demonstrate that the glycoprotein CD4, a member of the immunoglobulin superfamily, is a critical component of the receptor for human herpesvirus 7 (HHV-7), a recently discovered T-lymphotropic human herpesvirus. A selective and progressive downregulation of the surface membrane exp...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1994-04, Vol.91 (9), p.3872-3876 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Lusso, Paolo Secchiero, Paola Crowley, Richard W. Garzino-Demo, Alfredo Berneman, Zwi N. Gallo, Robert C. |
| description | In this study, we demonstrate that the glycoprotein CD4, a member of the immunoglobulin superfamily, is a critical component of the receptor for human herpesvirus 7 (HHV-7), a recently discovered T-lymphotropic human herpesvirus. A selective and progressive downregulation of the surface membrane expression of CD4 was observed in human CD4+T cells in the course of HHV-7 infection. Various murine monoclonal antibodies to CD4 and the recombinant soluble form of human CD4 caused a dose-dependent inhibition of HHV-7 infection in primary CD4+T lymphocytes. Moreover, radiolabeled HHV-7 specifically bound to cervical carcinoma cells (HeLa) expressing human CD4. A marked reciprocal interference was observed between HHV-7 and human immunodeficiency virus (HIV), the retrovirus that causes the acquired immunodeficiency syndrome and also uses CD4 as a receptor. Previous exposure of CD4+T cells to HHV-7 dramatically interfered with infection by both primary and in vitro-passaged HIV-1 isolates. Reciprocally, persistent infection with HIV-1 or treatment with the soluble form of gp120, the CD4-binding envelope glycoprotein of HIV-1, rendered CD4+T cells resistant to HHV-7 infection. These data indicate that CD4 is critically involved in the receptor mechanism for HHV-7. The antagonistic effect between HHV-7 and HIV could be exploited to devise therapeutic approaches to AIDS. |
| doi_str_mv | 10.1073/pnas.91.9.3872 |
| format | Article |
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A selective and progressive downregulation of the surface membrane expression of CD4 was observed in human CD4+T cells in the course of HHV-7 infection. Various murine monoclonal antibodies to CD4 and the recombinant soluble form of human CD4 caused a dose-dependent inhibition of HHV-7 infection in primary CD4+T lymphocytes. Moreover, radiolabeled HHV-7 specifically bound to cervical carcinoma cells (HeLa) expressing human CD4. A marked reciprocal interference was observed between HHV-7 and human immunodeficiency virus (HIV), the retrovirus that causes the acquired immunodeficiency syndrome and also uses CD4 as a receptor. Previous exposure of CD4+T cells to HHV-7 dramatically interfered with infection by both primary and in vitro-passaged HIV-1 isolates. Reciprocally, persistent infection with HIV-1 or treatment with the soluble form of gp120, the CD4-binding envelope glycoprotein of HIV-1, rendered CD4+T cells resistant to HHV-7 infection. These data indicate that CD4 is critically involved in the receptor mechanism for HHV-7. The antagonistic effect between HHV-7 and HIV could be exploited to devise therapeutic approaches to AIDS.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.91.9.3872</identifier><identifier>PMID: 7909607</identifier><identifier>CODEN: PNASA6</identifier><language>eng</language><publisher>Washington, DC: National Academy of Sciences of the United States of America</publisher><subject>AIDS/HIV ; Antigens ; Binding, Competitive ; Biological and medical sciences ; Blood ; CD4 Antigens - metabolism ; CD4-Positive T-Lymphocytes - microbiology ; Down-Regulation ; Fundamental and applied biological sciences. Psychology ; HeLa cells ; Herpes viruses ; Herpesviridae Infections - microbiology ; Herpesvirus 7, Human - metabolism ; HIV ; HIV 1 ; HIV Infections - microbiology ; HIV-1 - metabolism ; Human herpesvirus 7 ; Human immunodeficiency virus ; Humans ; Immunity (Disease) ; Infections ; Medical research ; Microbiology ; Receptors ; Receptors, Virus - metabolism ; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains ; T lymphocytes ; Viral Interference ; Virology ; Viruses</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1994-04, Vol.91 (9), p.3872-3876</ispartof><rights>Copyright 1994 The National Academy of Sciences of the United States of America</rights><rights>1994 INIST-CNRS</rights><rights>Copyright National Academy of Sciences Apr 26, 1994</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-7ed166c22e30ab2a80d09c16d523649084cd586cf39e296e387f669687c4c6d73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/91/9.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2364553$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2364553$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4245244$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7909607$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lusso, Paolo</creatorcontrib><creatorcontrib>Secchiero, Paola</creatorcontrib><creatorcontrib>Crowley, Richard W.</creatorcontrib><creatorcontrib>Garzino-Demo, Alfredo</creatorcontrib><creatorcontrib>Berneman, Zwi N.</creatorcontrib><creatorcontrib>Gallo, Robert C.</creatorcontrib><title>CD4 is a Critical Component of the Receptor for Human Herpesvirus 7: Interference with Human Immunodeficiency Virus</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>In this study, we demonstrate that the glycoprotein CD4, a member of the immunoglobulin superfamily, is a critical component of the receptor for human herpesvirus 7 (HHV-7), a recently discovered T-lymphotropic human herpesvirus. A selective and progressive downregulation of the surface membrane expression of CD4 was observed in human CD4+T cells in the course of HHV-7 infection. Various murine monoclonal antibodies to CD4 and the recombinant soluble form of human CD4 caused a dose-dependent inhibition of HHV-7 infection in primary CD4+T lymphocytes. Moreover, radiolabeled HHV-7 specifically bound to cervical carcinoma cells (HeLa) expressing human CD4. A marked reciprocal interference was observed between HHV-7 and human immunodeficiency virus (HIV), the retrovirus that causes the acquired immunodeficiency syndrome and also uses CD4 as a receptor. Previous exposure of CD4+T cells to HHV-7 dramatically interfered with infection by both primary and in vitro-passaged HIV-1 isolates. Reciprocally, persistent infection with HIV-1 or treatment with the soluble form of gp120, the CD4-binding envelope glycoprotein of HIV-1, rendered CD4+T cells resistant to HHV-7 infection. These data indicate that CD4 is critically involved in the receptor mechanism for HHV-7. The antagonistic effect between HHV-7 and HIV could be exploited to devise therapeutic approaches to AIDS.</description><subject>AIDS/HIV</subject><subject>Antigens</subject><subject>Binding, Competitive</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>CD4 Antigens - metabolism</subject><subject>CD4-Positive T-Lymphocytes - microbiology</subject><subject>Down-Regulation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>HeLa cells</subject><subject>Herpes viruses</subject><subject>Herpesviridae Infections - microbiology</subject><subject>Herpesvirus 7, Human - metabolism</subject><subject>HIV</subject><subject>HIV 1</subject><subject>HIV Infections - microbiology</subject><subject>HIV-1 - metabolism</subject><subject>Human herpesvirus 7</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Immunity (Disease)</subject><subject>Infections</subject><subject>Medical research</subject><subject>Microbiology</subject><subject>Receptors</subject><subject>Receptors, Virus - metabolism</subject><subject>Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains</subject><subject>T lymphocytes</subject><subject>Viral Interference</subject><subject>Virology</subject><subject>Viruses</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkkuP0zAUhSMEGsrAlhVIFkKza_ErdozYoPBopZGQELC1PM4NdZXYGTuZx7_HUUtVWMDC8uJ89_oen1sUzwleESzZm8GbtFJkpVaskvRBsSBYkaXgCj8sFhhTuaw45Y-LJyntMMaqrPBZcSYVVgLLRZHqDxy5hAyqoxudNR2qQz8ED35EoUXjFtBXsDCMIaI2n_XUG4_WEAdINy5OCcm3aONHiC1E8BbQrRu3B2zT95MPDbTOuqzdox9zxdPiUWu6BM8O93nx_dPHb_V6efnl86Z-f7m0JefjUkJDhLCUAsPmipoKN1hZIpqSstlfxW1TVsK2TAFVArL_VgglKmm5FY1k58W7fd9huuqhsdlSNJ0eoutNvNfBOP2n4t1W_ww3mjNR8Vx-cSiP4XqCNOreJQtdZzyEKWkpuCgZwf8FiVBMkopm8NVf4C5M0ec_0BQTJhiT89SrPWRjSClCexyYYD1HrufItSJa6TnyXPDy1OYRP2Sc9dcH3aScbxuNty4dsbwdJeX8pM3c_rd6-szFv3TdTl03wt2YwRd7cJfy0hzJObSyZOwX1G3Vcw</recordid><startdate>19940426</startdate><enddate>19940426</enddate><creator>Lusso, Paolo</creator><creator>Secchiero, Paola</creator><creator>Crowley, Richard W.</creator><creator>Garzino-Demo, Alfredo</creator><creator>Berneman, Zwi N.</creator><creator>Gallo, Robert C.</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><scope>IQODW</scope><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19940426</creationdate><title>CD4 is a Critical Component of the Receptor for Human Herpesvirus 7: Interference with Human Immunodeficiency Virus</title><author>Lusso, Paolo ; Secchiero, Paola ; Crowley, Richard W. ; Garzino-Demo, Alfredo ; Berneman, Zwi N. ; Gallo, Robert C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-7ed166c22e30ab2a80d09c16d523649084cd586cf39e296e387f669687c4c6d73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>AIDS/HIV</topic><topic>Antigens</topic><topic>Binding, Competitive</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>CD4 Antigens - metabolism</topic><topic>CD4-Positive T-Lymphocytes - microbiology</topic><topic>Down-Regulation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>HeLa cells</topic><topic>Herpes viruses</topic><topic>Herpesviridae Infections - microbiology</topic><topic>Herpesvirus 7, Human - metabolism</topic><topic>HIV</topic><topic>HIV 1</topic><topic>HIV Infections - microbiology</topic><topic>HIV-1 - metabolism</topic><topic>Human herpesvirus 7</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Immunity (Disease)</topic><topic>Infections</topic><topic>Medical research</topic><topic>Microbiology</topic><topic>Receptors</topic><topic>Receptors, Virus - metabolism</topic><topic>Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains</topic><topic>T lymphocytes</topic><topic>Viral Interference</topic><topic>Virology</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lusso, Paolo</creatorcontrib><creatorcontrib>Secchiero, Paola</creatorcontrib><creatorcontrib>Crowley, Richard W.</creatorcontrib><creatorcontrib>Garzino-Demo, Alfredo</creatorcontrib><creatorcontrib>Berneman, Zwi N.</creatorcontrib><creatorcontrib>Gallo, Robert C.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lusso, Paolo</au><au>Secchiero, Paola</au><au>Crowley, Richard W.</au><au>Garzino-Demo, Alfredo</au><au>Berneman, Zwi N.</au><au>Gallo, Robert C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD4 is a Critical Component of the Receptor for Human Herpesvirus 7: Interference with Human Immunodeficiency Virus</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1994-04-26</date><risdate>1994</risdate><volume>91</volume><issue>9</issue><spage>3872</spage><epage>3876</epage><pages>3872-3876</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><coden>PNASA6</coden><abstract>In this study, we demonstrate that the glycoprotein CD4, a member of the immunoglobulin superfamily, is a critical component of the receptor for human herpesvirus 7 (HHV-7), a recently discovered T-lymphotropic human herpesvirus. A selective and progressive downregulation of the surface membrane expression of CD4 was observed in human CD4+T cells in the course of HHV-7 infection. Various murine monoclonal antibodies to CD4 and the recombinant soluble form of human CD4 caused a dose-dependent inhibition of HHV-7 infection in primary CD4+T lymphocytes. Moreover, radiolabeled HHV-7 specifically bound to cervical carcinoma cells (HeLa) expressing human CD4. A marked reciprocal interference was observed between HHV-7 and human immunodeficiency virus (HIV), the retrovirus that causes the acquired immunodeficiency syndrome and also uses CD4 as a receptor. Previous exposure of CD4+T cells to HHV-7 dramatically interfered with infection by both primary and in vitro-passaged HIV-1 isolates. Reciprocally, persistent infection with HIV-1 or treatment with the soluble form of gp120, the CD4-binding envelope glycoprotein of HIV-1, rendered CD4+T cells resistant to HHV-7 infection. These data indicate that CD4 is critically involved in the receptor mechanism for HHV-7. The antagonistic effect between HHV-7 and HIV could be exploited to devise therapeutic approaches to AIDS.</abstract><cop>Washington, DC</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>7909607</pmid><doi>10.1073/pnas.91.9.3872</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 1994-04, Vol.91 (9), p.3872-3876 |
| issn | 0027-8424 1091-6490 |
| language | eng |
| recordid | cdi_pubmed_primary_7909607 |
| source | MEDLINE; JSTOR Archive Collection A-Z Listing; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | AIDS/HIV Antigens Binding, Competitive Biological and medical sciences Blood CD4 Antigens - metabolism CD4-Positive T-Lymphocytes - microbiology Down-Regulation Fundamental and applied biological sciences. Psychology HeLa cells Herpes viruses Herpesviridae Infections - microbiology Herpesvirus 7, Human - metabolism HIV HIV 1 HIV Infections - microbiology HIV-1 - metabolism Human herpesvirus 7 Human immunodeficiency virus Humans Immunity (Disease) Infections Medical research Microbiology Receptors Receptors, Virus - metabolism Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains T lymphocytes Viral Interference Virology Viruses |
| title | CD4 is a Critical Component of the Receptor for Human Herpesvirus 7: Interference with Human Immunodeficiency Virus |
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