HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules
It is well documented that a wide range of host-derived cell surface constituents is inserted within HIV type 1 (HIV-1) and located on the exterior of the virion. Although no virus-associated protein of host origin has been shown to be absolutely required for virus replication, studies have revealed...
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Veröffentlicht in: | The Journal of immunology (1950) 2005-04, Vol.174 (8), p.4779-4788 |
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creator | Roy, Jocelyn Martin, Genevieve Giguere, Jean-Francois Belanger, Dave Petrin, Myriam Tremblay, Michel J |
description | It is well documented that a wide range of host-derived cell surface constituents is inserted within HIV type 1 (HIV-1) and located on the exterior of the virion. Although no virus-associated protein of host origin has been shown to be absolutely required for virus replication, studies have revealed that many of these proteins are functional and can affect several steps of the virus life cycle. In this study, we found that HIV-1 acquires peptide-loaded class II MHC (MHC-II) and the costimulatory CD86 molecules from the host cell. Moreover, we present evidence that virions bearing such peptide-loaded MHC-II and CD86 proteins can lead to activation of the transcription factors NF-kappa B and NF-AT in an Ag-specific human T cell line. A linear correlation was found between activation of NF-kappa B and the amount of peptide-loaded MHC-II molecules inserted within HIV-1. Finally, transcription of unintegrated and integrated HIV-1 DNA was promoted upon exposure of peptide-specific human T cells to viruses bearing both peptide-loaded MHC-II and CD86 proteins. These data suggest that HIV-1 can operate as an APC depending on the nature of virus-anchored host cell membrane components. It can be proposed that HIV-1 can manipulate one of its primary targets through the process of incorporation of host-derived proteins. |
doi_str_mv | 10.4049/jimmunol.174.8.4779 |
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Although no virus-associated protein of host origin has been shown to be absolutely required for virus replication, studies have revealed that many of these proteins are functional and can affect several steps of the virus life cycle. In this study, we found that HIV-1 acquires peptide-loaded class II MHC (MHC-II) and the costimulatory CD86 molecules from the host cell. Moreover, we present evidence that virions bearing such peptide-loaded MHC-II and CD86 proteins can lead to activation of the transcription factors NF-kappa B and NF-AT in an Ag-specific human T cell line. A linear correlation was found between activation of NF-kappa B and the amount of peptide-loaded MHC-II molecules inserted within HIV-1. Finally, transcription of unintegrated and integrated HIV-1 DNA was promoted upon exposure of peptide-specific human T cells to viruses bearing both peptide-loaded MHC-II and CD86 proteins. These data suggest that HIV-1 can operate as an APC depending on the nature of virus-anchored host cell membrane components. 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Although no virus-associated protein of host origin has been shown to be absolutely required for virus replication, studies have revealed that many of these proteins are functional and can affect several steps of the virus life cycle. In this study, we found that HIV-1 acquires peptide-loaded class II MHC (MHC-II) and the costimulatory CD86 molecules from the host cell. Moreover, we present evidence that virions bearing such peptide-loaded MHC-II and CD86 proteins can lead to activation of the transcription factors NF-kappa B and NF-AT in an Ag-specific human T cell line. A linear correlation was found between activation of NF-kappa B and the amount of peptide-loaded MHC-II molecules inserted within HIV-1. Finally, transcription of unintegrated and integrated HIV-1 DNA was promoted upon exposure of peptide-specific human T cells to viruses bearing both peptide-loaded MHC-II and CD86 proteins. These data suggest that HIV-1 can operate as an APC depending on the nature of virus-anchored host cell membrane components. It can be proposed that HIV-1 can manipulate one of its primary targets through the process of incorporation of host-derived proteins.</description><subject>Antigen-Presenting Cells - immunology</subject><subject>Antigen-Presenting Cells - virology</subject><subject>Antigens, CD - metabolism</subject><subject>B7-2 Antigen</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>CD4-Positive T-Lymphocytes - virology</subject><subject>Cell Line</subject><subject>Genome, Viral</subject><subject>HIV-1 - genetics</subject><subject>HIV-1 - immunology</subject><subject>HIV-1 - pathogenicity</subject><subject>HIV-1 - physiology</subject><subject>HLA-DR Antigens - metabolism</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Secretory Vesicles - immunology</subject><subject>Secretory Vesicles - metabolism</subject><subject>Secretory Vesicles - virology</subject><subject>Transcription, Genetic</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9r3DAQxUVoabZJP0Gg6NSevJWs_8fFSbuBLQ1lyVUo1rirIK8cy2bJt4_NbkhuPc0w_N5jeA-hK0qWnHDz4zG07bhPcUkVX-olV8qcoQUVghRSEvkBLQgpy4Iqqc7R55wfCSGSlPwTOqdCU64IW6C4vr3H2-cOMMWV2-NVPWCX8bzdVXjs0nx6GkMOQ5j2pk8tHnaA1ykPuIIYcWrwHXRD8FBskvPg8XqzKq7_Th4eV9da4t8pQj1GyJfoY-Nihi-neYG2P2-21brY_Pl1W602Rc0pHQqtG2MI4zWRpnFUPBjuBWXSMM0aYFKAKw1I7b3ixLnGQS2YBgJAvDOaXaBvR9uuT08j5MG2IdfTr24PacxWKkW55uK_4BSsKbkoJ5AdwbpPOffQ2K4PreufLSV2LsO-ljFrrLZzGZPq68l-fGjBv2lO6U_A9yOwC_92h9CDza2LccKpPRwO76xeACXqkkY</recordid><startdate>20050415</startdate><enddate>20050415</enddate><creator>Roy, Jocelyn</creator><creator>Martin, Genevieve</creator><creator>Giguere, Jean-Francois</creator><creator>Belanger, Dave</creator><creator>Petrin, Myriam</creator><creator>Tremblay, Michel J</creator><general>Am Assoc Immnol</general><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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20050415</creationdate><title>HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules</title><author>Roy, Jocelyn ; Martin, Genevieve ; Giguere, Jean-Francois ; Belanger, Dave ; Petrin, Myriam ; Tremblay, Michel J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-88f99034c069fa15b94d51369383fe365ea29e68dd740aafaec538e0ee0da983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Antigen-Presenting Cells - immunology</topic><topic>Antigen-Presenting Cells - virology</topic><topic>Antigens, CD - metabolism</topic><topic>B7-2 Antigen</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>CD4-Positive T-Lymphocytes - virology</topic><topic>Cell Line</topic><topic>Genome, Viral</topic><topic>HIV-1 - genetics</topic><topic>HIV-1 - immunology</topic><topic>HIV-1 - pathogenicity</topic><topic>HIV-1 - physiology</topic><topic>HLA-DR Antigens - metabolism</topic><topic>Human immunodeficiency virus 1</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Secretory Vesicles - immunology</topic><topic>Secretory Vesicles - metabolism</topic><topic>Secretory Vesicles - virology</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roy, Jocelyn</creatorcontrib><creatorcontrib>Martin, Genevieve</creatorcontrib><creatorcontrib>Giguere, Jean-Francois</creatorcontrib><creatorcontrib>Belanger, Dave</creatorcontrib><creatorcontrib>Petrin, Myriam</creatorcontrib><creatorcontrib>Tremblay, Michel J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roy, Jocelyn</au><au>Martin, Genevieve</au><au>Giguere, Jean-Francois</au><au>Belanger, Dave</au><au>Petrin, Myriam</au><au>Tremblay, Michel J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2005-04-15</date><risdate>2005</risdate><volume>174</volume><issue>8</issue><spage>4779</spage><epage>4788</epage><pages>4779-4788</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>It is well documented that a wide range of host-derived cell surface constituents is inserted within HIV type 1 (HIV-1) and located on the exterior of the virion. Although no virus-associated protein of host origin has been shown to be absolutely required for virus replication, studies have revealed that many of these proteins are functional and can affect several steps of the virus life cycle. In this study, we found that HIV-1 acquires peptide-loaded class II MHC (MHC-II) and the costimulatory CD86 molecules from the host cell. Moreover, we present evidence that virions bearing such peptide-loaded MHC-II and CD86 proteins can lead to activation of the transcription factors NF-kappa B and NF-AT in an Ag-specific human T cell line. A linear correlation was found between activation of NF-kappa B and the amount of peptide-loaded MHC-II molecules inserted within HIV-1. Finally, transcription of unintegrated and integrated HIV-1 DNA was promoted upon exposure of peptide-specific human T cells to viruses bearing both peptide-loaded MHC-II and CD86 proteins. 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subjects | Antigen-Presenting Cells - immunology Antigen-Presenting Cells - virology Antigens, CD - metabolism B7-2 Antigen CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism CD4-Positive T-Lymphocytes - virology Cell Line Genome, Viral HIV-1 - genetics HIV-1 - immunology HIV-1 - pathogenicity HIV-1 - physiology HLA-DR Antigens - metabolism Human immunodeficiency virus 1 Humans In Vitro Techniques Membrane Glycoproteins - metabolism NF-kappa B - metabolism Secretory Vesicles - immunology Secretory Vesicles - metabolism Secretory Vesicles - virology Transcription, Genetic |
title | HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules |
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