Loss of antibody reactivity directed against the V3 domain of certain human immunodeficiency virus type 1 variants during disease progression
1 Medical Microbiology Section, Department of Virology and 2 Division of Clinical Medicine, Bernhard Nocht Institute for Tropical Medicine, D-20359 Hamburg, Germany We have previously shown that in AIDS patients a predominant species of infectious virus can be found which is not neutralized by homol...
Gespeichert in:
Veröffentlicht in: | Journal of general virology 1996-10, Vol.77 (10), p.2403-2414 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 2414 |
---|---|
container_issue | 10 |
container_start_page | 2403 |
container_title | Journal of general virology |
container_volume | 77 |
creator | Schreiber, Michael Wachsmuth, Christoph Muller, Harm Hagen, Christiane Schmitz, Herbert van Lunzen, Jan |
description | 1 Medical Microbiology Section, Department of Virology
and 2 Division of Clinical Medicine, Bernhard Nocht Institute for Tropical Medicine, D-20359 Hamburg, Germany
We have previously shown that in AIDS patients a predominant species of infectious virus can be found which is not neutralized by homologous serum. The presence of the infectious virus was associated with the lack of type-specific antibody directed against the V3 domains of these virions. In contrast to this lack of V3-specific antibody, the other V3 domains of non-infectious virions were well recognized by antibody. To determine whether the lack of a V3-specific antibody response is due to a progressive loss of antibody during human immunodeficiency virus type 1 (HIV-1) infection, we monitored the anti-V3 antibody response in 90 patients over time. Anti-V3 antibodies were monitored by a V3-specific ELISA using 21 different V3 domains as a fusion with glutathione S -transferase (GST-V3) based upon sequences from 11 HIV-1 patient isolates and 10 sequences from an HIV-1 B subtype consensus-like GST-V3 expression library. This strictly heterologous screening showed a loss of V3-specific antibodies in 20 out of the 90 patients tested. To study the in vivo relevance of these findings we analysed V3 antibody loss in two patients. This strictly autologous antibody screening was performed based upon V3 sequences of the patients' cell-free virions. In both patients the loss of a V3-specific antibody could be detected in parallel to a decline of CD4 + T cells. Moreover, the escape of a distinct V3 variant was shown to correlate closely with the loss of the V3-specific antibody.
Present address: Department of Internal Medicine, Infectious Disease Unit, University Hospital Eppendorf, Hamburg, Germany.
Received 3 April 1996;
accepted 8 July 1996. |
doi_str_mv | 10.1099/0022-1317-77-10-2403 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78483685</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>15695271</sourcerecordid><originalsourceid>FETCH-LOGICAL-c413t-afb7af1e9a63b4672cd6db10b8442893cceb12888a323b1d0bdd16a6dfe4ebae3</originalsourceid><addsrcrecordid>eNqFkcuO1DAQRS0EGpqBPwDJKyQWAb8SJ0s04jFSS2yAreVHJW3UsRvbaZSP4J9x1K0Ru1nZrrp1r1wHodeUvKdkGD4QwlhDOZWNlA0lDROEP0E7Krq2YVXwFO0eJM_Ri5x_EUKFaOUNuun7XgpJd-jvPuaM44h1KN5Et-IE2hZ_9mXFziewBRzWk_YhF1wOgH9y7OJc39uUhVS262GZdcB-npcQHYzeegh2xWeflozLegJM8VknX1MydkvyYaruGXQGfEpxSpCzj-ElejbqY4ZX1_MW_fj86fvd12b_7cv93cd9YwXlpdGjkXqkMOiOG9FJZl3nDCWmF4L1A7cWDGX1j5ozbqgjxjna6c6NIMBo4Lfo7cW3Zv9eIBc1-2zheNQB4pKV7EXPu759VEjbbmiZpFUoLkKb6kITjOqU_KzTqihRGy61sVAbCyXlVtxw1bE3V__FzOAehq58av_dpX_w0-FPxaEmCLOvIcZHVdf7n9c_efeigg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>15695271</pqid></control><display><type>article</type><title>Loss of antibody reactivity directed against the V3 domain of certain human immunodeficiency virus type 1 variants during disease progression</title><source>MEDLINE</source><source>Microbiology Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Schreiber, Michael ; Wachsmuth, Christoph ; Muller, Harm ; Hagen, Christiane ; Schmitz, Herbert ; van Lunzen, Jan</creator><creatorcontrib>Schreiber, Michael ; Wachsmuth, Christoph ; Muller, Harm ; Hagen, Christiane ; Schmitz, Herbert ; van Lunzen, Jan</creatorcontrib><description>1 Medical Microbiology Section, Department of Virology
and 2 Division of Clinical Medicine, Bernhard Nocht Institute for Tropical Medicine, D-20359 Hamburg, Germany
We have previously shown that in AIDS patients a predominant species of infectious virus can be found which is not neutralized by homologous serum. The presence of the infectious virus was associated with the lack of type-specific antibody directed against the V3 domains of these virions. In contrast to this lack of V3-specific antibody, the other V3 domains of non-infectious virions were well recognized by antibody. To determine whether the lack of a V3-specific antibody response is due to a progressive loss of antibody during human immunodeficiency virus type 1 (HIV-1) infection, we monitored the anti-V3 antibody response in 90 patients over time. Anti-V3 antibodies were monitored by a V3-specific ELISA using 21 different V3 domains as a fusion with glutathione S -transferase (GST-V3) based upon sequences from 11 HIV-1 patient isolates and 10 sequences from an HIV-1 B subtype consensus-like GST-V3 expression library. This strictly heterologous screening showed a loss of V3-specific antibodies in 20 out of the 90 patients tested. To study the in vivo relevance of these findings we analysed V3 antibody loss in two patients. This strictly autologous antibody screening was performed based upon V3 sequences of the patients' cell-free virions. In both patients the loss of a V3-specific antibody could be detected in parallel to a decline of CD4 + T cells. Moreover, the escape of a distinct V3 variant was shown to correlate closely with the loss of the V3-specific antibody.
Present address: Department of Internal Medicine, Infectious Disease Unit, University Hospital Eppendorf, Hamburg, Germany.
Received 3 April 1996;
accepted 8 July 1996.</description><identifier>ISSN: 0022-1317</identifier><identifier>EISSN: 1465-2099</identifier><identifier>DOI: 10.1099/0022-1317-77-10-2403</identifier><identifier>PMID: 8887471</identifier><language>eng</language><publisher>England: Soc General Microbiol</publisher><subject>AIDS/HIV ; Amino Acid Sequence ; Antibodies, Heterophile ; Antibody Specificity ; Base Sequence ; Disease Progression ; DNA, Viral ; Genetic Variation ; HIV Antibodies - blood ; HIV Antibodies - immunology ; HIV Envelope Protein gp120 - chemistry ; HIV Envelope Protein gp120 - genetics ; HIV Envelope Protein gp120 - immunology ; HIV Infections - blood ; HIV Infections - immunology ; HIV-1 - genetics ; HIV-1 - immunology ; human immunodeficiency virus 1 ; Humans ; Male ; Molecular Sequence Data ; Peptide Fragments - chemistry ; Peptide Fragments - genetics ; Peptide Fragments - immunology ; Recombinant Fusion Proteins - chemistry ; Recombinant Fusion Proteins - genetics ; Recombinant Fusion Proteins - immunology</subject><ispartof>Journal of general virology, 1996-10, Vol.77 (10), p.2403-2414</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-afb7af1e9a63b4672cd6db10b8442893cceb12888a323b1d0bdd16a6dfe4ebae3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,3735,3736,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8887471$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schreiber, Michael</creatorcontrib><creatorcontrib>Wachsmuth, Christoph</creatorcontrib><creatorcontrib>Muller, Harm</creatorcontrib><creatorcontrib>Hagen, Christiane</creatorcontrib><creatorcontrib>Schmitz, Herbert</creatorcontrib><creatorcontrib>van Lunzen, Jan</creatorcontrib><title>Loss of antibody reactivity directed against the V3 domain of certain human immunodeficiency virus type 1 variants during disease progression</title><title>Journal of general virology</title><addtitle>J Gen Virol</addtitle><description>1 Medical Microbiology Section, Department of Virology
and 2 Division of Clinical Medicine, Bernhard Nocht Institute for Tropical Medicine, D-20359 Hamburg, Germany
We have previously shown that in AIDS patients a predominant species of infectious virus can be found which is not neutralized by homologous serum. The presence of the infectious virus was associated with the lack of type-specific antibody directed against the V3 domains of these virions. In contrast to this lack of V3-specific antibody, the other V3 domains of non-infectious virions were well recognized by antibody. To determine whether the lack of a V3-specific antibody response is due to a progressive loss of antibody during human immunodeficiency virus type 1 (HIV-1) infection, we monitored the anti-V3 antibody response in 90 patients over time. Anti-V3 antibodies were monitored by a V3-specific ELISA using 21 different V3 domains as a fusion with glutathione S -transferase (GST-V3) based upon sequences from 11 HIV-1 patient isolates and 10 sequences from an HIV-1 B subtype consensus-like GST-V3 expression library. This strictly heterologous screening showed a loss of V3-specific antibodies in 20 out of the 90 patients tested. To study the in vivo relevance of these findings we analysed V3 antibody loss in two patients. This strictly autologous antibody screening was performed based upon V3 sequences of the patients' cell-free virions. In both patients the loss of a V3-specific antibody could be detected in parallel to a decline of CD4 + T cells. Moreover, the escape of a distinct V3 variant was shown to correlate closely with the loss of the V3-specific antibody.
Present address: Department of Internal Medicine, Infectious Disease Unit, University Hospital Eppendorf, Hamburg, Germany.
Received 3 April 1996;
accepted 8 July 1996.</description><subject>AIDS/HIV</subject><subject>Amino Acid Sequence</subject><subject>Antibodies, Heterophile</subject><subject>Antibody Specificity</subject><subject>Base Sequence</subject><subject>Disease Progression</subject><subject>DNA, Viral</subject><subject>Genetic Variation</subject><subject>HIV Antibodies - blood</subject><subject>HIV Antibodies - immunology</subject><subject>HIV Envelope Protein gp120 - chemistry</subject><subject>HIV Envelope Protein gp120 - genetics</subject><subject>HIV Envelope Protein gp120 - immunology</subject><subject>HIV Infections - blood</subject><subject>HIV Infections - immunology</subject><subject>HIV-1 - genetics</subject><subject>HIV-1 - immunology</subject><subject>human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Male</subject><subject>Molecular Sequence Data</subject><subject>Peptide Fragments - chemistry</subject><subject>Peptide Fragments - genetics</subject><subject>Peptide Fragments - immunology</subject><subject>Recombinant Fusion Proteins - chemistry</subject><subject>Recombinant Fusion Proteins - genetics</subject><subject>Recombinant Fusion Proteins - immunology</subject><issn>0022-1317</issn><issn>1465-2099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcuO1DAQRS0EGpqBPwDJKyQWAb8SJ0s04jFSS2yAreVHJW3UsRvbaZSP4J9x1K0Ru1nZrrp1r1wHodeUvKdkGD4QwlhDOZWNlA0lDROEP0E7Krq2YVXwFO0eJM_Ri5x_EUKFaOUNuun7XgpJd-jvPuaM44h1KN5Et-IE2hZ_9mXFziewBRzWk_YhF1wOgH9y7OJc39uUhVS262GZdcB-npcQHYzeegh2xWeflozLegJM8VknX1MydkvyYaruGXQGfEpxSpCzj-ElejbqY4ZX1_MW_fj86fvd12b_7cv93cd9YwXlpdGjkXqkMOiOG9FJZl3nDCWmF4L1A7cWDGX1j5ozbqgjxjna6c6NIMBo4Lfo7cW3Zv9eIBc1-2zheNQB4pKV7EXPu759VEjbbmiZpFUoLkKb6kITjOqU_KzTqihRGy61sVAbCyXlVtxw1bE3V__FzOAehq58av_dpX_w0-FPxaEmCLOvIcZHVdf7n9c_efeigg</recordid><startdate>19961001</startdate><enddate>19961001</enddate><creator>Schreiber, Michael</creator><creator>Wachsmuth, Christoph</creator><creator>Muller, Harm</creator><creator>Hagen, Christiane</creator><creator>Schmitz, Herbert</creator><creator>van Lunzen, Jan</creator><general>Soc General Microbiol</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>19961001</creationdate><title>Loss of antibody reactivity directed against the V3 domain of certain human immunodeficiency virus type 1 variants during disease progression</title><author>Schreiber, Michael ; Wachsmuth, Christoph ; Muller, Harm ; Hagen, Christiane ; Schmitz, Herbert ; van Lunzen, Jan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-afb7af1e9a63b4672cd6db10b8442893cceb12888a323b1d0bdd16a6dfe4ebae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>AIDS/HIV</topic><topic>Amino Acid Sequence</topic><topic>Antibodies, Heterophile</topic><topic>Antibody Specificity</topic><topic>Base Sequence</topic><topic>Disease Progression</topic><topic>DNA, Viral</topic><topic>Genetic Variation</topic><topic>HIV Antibodies - blood</topic><topic>HIV Antibodies - immunology</topic><topic>HIV Envelope Protein gp120 - chemistry</topic><topic>HIV Envelope Protein gp120 - genetics</topic><topic>HIV Envelope Protein gp120 - immunology</topic><topic>HIV Infections - blood</topic><topic>HIV Infections - immunology</topic><topic>HIV-1 - genetics</topic><topic>HIV-1 - immunology</topic><topic>human immunodeficiency virus 1</topic><topic>Humans</topic><topic>Male</topic><topic>Molecular Sequence Data</topic><topic>Peptide Fragments - chemistry</topic><topic>Peptide Fragments - genetics</topic><topic>Peptide Fragments - immunology</topic><topic>Recombinant Fusion Proteins - chemistry</topic><topic>Recombinant Fusion Proteins - genetics</topic><topic>Recombinant Fusion Proteins - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schreiber, Michael</creatorcontrib><creatorcontrib>Wachsmuth, Christoph</creatorcontrib><creatorcontrib>Muller, Harm</creatorcontrib><creatorcontrib>Hagen, Christiane</creatorcontrib><creatorcontrib>Schmitz, Herbert</creatorcontrib><creatorcontrib>van Lunzen, Jan</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>Journal of general virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schreiber, Michael</au><au>Wachsmuth, Christoph</au><au>Muller, Harm</au><au>Hagen, Christiane</au><au>Schmitz, Herbert</au><au>van Lunzen, Jan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of antibody reactivity directed against the V3 domain of certain human immunodeficiency virus type 1 variants during disease progression</atitle><jtitle>Journal of general virology</jtitle><addtitle>J Gen Virol</addtitle><date>1996-10-01</date><risdate>1996</risdate><volume>77</volume><issue>10</issue><spage>2403</spage><epage>2414</epage><pages>2403-2414</pages><issn>0022-1317</issn><eissn>1465-2099</eissn><abstract>1 Medical Microbiology Section, Department of Virology
and 2 Division of Clinical Medicine, Bernhard Nocht Institute for Tropical Medicine, D-20359 Hamburg, Germany
We have previously shown that in AIDS patients a predominant species of infectious virus can be found which is not neutralized by homologous serum. The presence of the infectious virus was associated with the lack of type-specific antibody directed against the V3 domains of these virions. In contrast to this lack of V3-specific antibody, the other V3 domains of non-infectious virions were well recognized by antibody. To determine whether the lack of a V3-specific antibody response is due to a progressive loss of antibody during human immunodeficiency virus type 1 (HIV-1) infection, we monitored the anti-V3 antibody response in 90 patients over time. Anti-V3 antibodies were monitored by a V3-specific ELISA using 21 different V3 domains as a fusion with glutathione S -transferase (GST-V3) based upon sequences from 11 HIV-1 patient isolates and 10 sequences from an HIV-1 B subtype consensus-like GST-V3 expression library. This strictly heterologous screening showed a loss of V3-specific antibodies in 20 out of the 90 patients tested. To study the in vivo relevance of these findings we analysed V3 antibody loss in two patients. This strictly autologous antibody screening was performed based upon V3 sequences of the patients' cell-free virions. In both patients the loss of a V3-specific antibody could be detected in parallel to a decline of CD4 + T cells. Moreover, the escape of a distinct V3 variant was shown to correlate closely with the loss of the V3-specific antibody.
Present address: Department of Internal Medicine, Infectious Disease Unit, University Hospital Eppendorf, Hamburg, Germany.
Received 3 April 1996;
accepted 8 July 1996.</abstract><cop>England</cop><pub>Soc General Microbiol</pub><pmid>8887471</pmid><doi>10.1099/0022-1317-77-10-2403</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0022-1317 |
ispartof | Journal of general virology, 1996-10, Vol.77 (10), p.2403-2414 |
issn | 0022-1317 1465-2099 |
language | eng |
recordid | cdi_proquest_miscellaneous_78483685 |
source | MEDLINE; Microbiology Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | AIDS/HIV Amino Acid Sequence Antibodies, Heterophile Antibody Specificity Base Sequence Disease Progression DNA, Viral Genetic Variation HIV Antibodies - blood HIV Antibodies - immunology HIV Envelope Protein gp120 - chemistry HIV Envelope Protein gp120 - genetics HIV Envelope Protein gp120 - immunology HIV Infections - blood HIV Infections - immunology HIV-1 - genetics HIV-1 - immunology human immunodeficiency virus 1 Humans Male Molecular Sequence Data Peptide Fragments - chemistry Peptide Fragments - genetics Peptide Fragments - immunology Recombinant Fusion Proteins - chemistry Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - immunology |
title | Loss of antibody reactivity directed against the V3 domain of certain human immunodeficiency virus type 1 variants during disease progression |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T01%3A02%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Loss%20of%20antibody%20reactivity%20directed%20against%20the%20V3%20domain%20of%20certain%20human%20immunodeficiency%20virus%20type%201%20variants%20during%20disease%20progression&rft.jtitle=Journal%20of%20general%20virology&rft.au=Schreiber,%20Michael&rft.date=1996-10-01&rft.volume=77&rft.issue=10&rft.spage=2403&rft.epage=2414&rft.pages=2403-2414&rft.issn=0022-1317&rft.eissn=1465-2099&rft_id=info:doi/10.1099/0022-1317-77-10-2403&rft_dat=%3Cproquest_cross%3E15695271%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=15695271&rft_id=info:pmid/8887471&rfr_iscdi=true |