Mechanisms of Resistance of HIV-1 Primary Isolates to Complement-Mediated Lysis
Previous studies suggested that HIV-1 primary isolates (PI) were resistant to complement-mediated lysis (CML), while virus produced in certain T cell lines and virus taken directly from the plasma of HIV+persons were both susceptible to CML. The purpose of this study was to investigate the mechanism...
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| Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 1998-07, Vol.246 (2), p.370-378 |
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| container_title | Virology (New York, N.Y.) |
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| creator | Takefman, Daniel M. Sullivan, Brenda L. Sha, Beverly E. Spear, Gregory T. |
| description | Previous studies suggested that HIV-1 primary isolates (PI) were resistant to complement-mediated lysis (CML), while virus produced in certain T cell lines and virus taken directly from the plasma of HIV+persons were both susceptible to CML. The purpose of this study was to investigate the mechanism(s) of PI resistance. PI were resistant to CML using pooled seropositive serum as an antibody source. Additionally, PI obtained from two patients at several times over 2 years were resistant to CML using autologous antibody. PI were also resistant to CML induced by monoclonal antibodies which neutralize a broad range of PI. Resistance to CML was associated with low binding of antibody to PI but was not due to low gp120 levels. Cell-line-derived virus and PI were equally sensitive to CML induced by antibody to host-cell proteins, suggesting that PBMC do not contribute properties to virions which make them more physically resistant to CML in general but that PI resistance is restricted to CML induced by antiviral antibody. These studies show that PI are resistant to CML mediated by various antiviral antibodies and indicate that low binding of antibody to virus is an important factor contributing to resistance. |
| doi_str_mv | 10.1006/viro.1998.9205 |
| format | Article |
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These studies show that PI are resistant to CML mediated by various antiviral antibodies and indicate that low binding of antibody to virus is an important factor contributing to resistance.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1006/viro.1998.9205</identifier><identifier>PMID: 9657955</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>AIDS/HIV ; Complement System Proteins - immunology ; HIV Antibodies - immunology ; HIV Envelope Protein gp120 - immunology ; HIV Infections - immunology ; HIV Infections - virology ; HIV-1 - immunology ; HIV-1 - isolation & purification ; Humans ; Tumor Cells, Cultured</subject><ispartof>Virology (New York, N.Y.), 1998-07, Vol.246 (2), p.370-378</ispartof><rights>1998 Academic Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-d0e420bbba5abe5aa4cfcd9e423675346a421cc40cdb466540c9b36f70343ef83</citedby><cites>FETCH-LOGICAL-c410t-d0e420bbba5abe5aa4cfcd9e423675346a421cc40cdb466540c9b36f70343ef83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/viro.1998.9205$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9657955$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takefman, Daniel M.</creatorcontrib><creatorcontrib>Sullivan, Brenda L.</creatorcontrib><creatorcontrib>Sha, Beverly E.</creatorcontrib><creatorcontrib>Spear, Gregory T.</creatorcontrib><title>Mechanisms of Resistance of HIV-1 Primary Isolates to Complement-Mediated Lysis</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>Previous studies suggested that HIV-1 primary isolates (PI) were resistant to complement-mediated lysis (CML), while virus produced in certain T cell lines and virus taken directly from the plasma of HIV+persons were both susceptible to CML. The purpose of this study was to investigate the mechanism(s) of PI resistance. PI were resistant to CML using pooled seropositive serum as an antibody source. Additionally, PI obtained from two patients at several times over 2 years were resistant to CML using autologous antibody. PI were also resistant to CML induced by monoclonal antibodies which neutralize a broad range of PI. Resistance to CML was associated with low binding of antibody to PI but was not due to low gp120 levels. Cell-line-derived virus and PI were equally sensitive to CML induced by antibody to host-cell proteins, suggesting that PBMC do not contribute properties to virions which make them more physically resistant to CML in general but that PI resistance is restricted to CML induced by antiviral antibody. These studies show that PI are resistant to CML mediated by various antiviral antibodies and indicate that low binding of antibody to virus is an important factor contributing to resistance.</description><subject>AIDS/HIV</subject><subject>Complement System Proteins - immunology</subject><subject>HIV Antibodies - immunology</subject><subject>HIV Envelope Protein gp120 - immunology</subject><subject>HIV Infections - immunology</subject><subject>HIV Infections - virology</subject><subject>HIV-1 - immunology</subject><subject>HIV-1 - isolation & purification</subject><subject>Humans</subject><subject>Tumor Cells, Cultured</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1LwzAYxoMoc06v3oSevLUmbZI2RxnqBhsTUa8hTd9ipG1m0g3235va4U08vV_P-8DzQ-ia4IRgzO_2xtmECFEkIsXsBE0JFjzGGSWnaIoxTWNepOk5uvD-E4c5z_EETQRnuWBsijZr0B-qM771ka2jF_DG96rTMEyL5XtMomdnWuUO0dLbRvXgo95Gc9tuG2ih6-M1VCasq2h1CL-X6KxWjYerY52ht8eH1_kiXm2elvP7VawpwX1cYaApLstSMVUCU4rqWlciLDOes4xyRVOiNcW6KinnLDSizHidh2AZ1EU2Q7ej79bZrx34XrbGa2ga1YHdeVn8ZE3Jv0LCqeCEsCBMRqF21nsHtdyOwSXBckAtB9RyQC0H1OHh5ui8K1uofuVHtuFejHcIHPYGnPTaQEBbGQe6l5U1f1l_A6W8jRk</recordid><startdate>19980705</startdate><enddate>19980705</enddate><creator>Takefman, Daniel M.</creator><creator>Sullivan, Brenda L.</creator><creator>Sha, Beverly E.</creator><creator>Spear, Gregory T.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19980705</creationdate><title>Mechanisms of Resistance of HIV-1 Primary Isolates to Complement-Mediated Lysis</title><author>Takefman, Daniel M. ; Sullivan, Brenda L. ; Sha, Beverly E. ; Spear, Gregory T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-d0e420bbba5abe5aa4cfcd9e423675346a421cc40cdb466540c9b36f70343ef83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>AIDS/HIV</topic><topic>Complement System Proteins - immunology</topic><topic>HIV Antibodies - immunology</topic><topic>HIV Envelope Protein gp120 - immunology</topic><topic>HIV Infections - immunology</topic><topic>HIV Infections - virology</topic><topic>HIV-1 - immunology</topic><topic>HIV-1 - isolation & purification</topic><topic>Humans</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takefman, Daniel M.</creatorcontrib><creatorcontrib>Sullivan, Brenda L.</creatorcontrib><creatorcontrib>Sha, Beverly E.</creatorcontrib><creatorcontrib>Spear, Gregory T.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takefman, Daniel M.</au><au>Sullivan, Brenda L.</au><au>Sha, Beverly E.</au><au>Spear, Gregory T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of Resistance of HIV-1 Primary Isolates to Complement-Mediated Lysis</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>1998-07-05</date><risdate>1998</risdate><volume>246</volume><issue>2</issue><spage>370</spage><epage>378</epage><pages>370-378</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>Previous studies suggested that HIV-1 primary isolates (PI) were resistant to complement-mediated lysis (CML), while virus produced in certain T cell lines and virus taken directly from the plasma of HIV+persons were both susceptible to CML. 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| ispartof | Virology (New York, N.Y.), 1998-07, Vol.246 (2), p.370-378 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals |
| subjects | AIDS/HIV Complement System Proteins - immunology HIV Antibodies - immunology HIV Envelope Protein gp120 - immunology HIV Infections - immunology HIV Infections - virology HIV-1 - immunology HIV-1 - isolation & purification Humans Tumor Cells, Cultured |
| title | Mechanisms of Resistance of HIV-1 Primary Isolates to Complement-Mediated Lysis |
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