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...

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Veröffentlicht in:Journal of general virology 1996-10, Vol.77 (10), p.2403-2414
Hauptverfasser: Schreiber, Michael, Wachsmuth, Christoph, Muller, Harm, Hagen, Christiane, Schmitz, Herbert, van Lunzen, Jan
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container_end_page 2414
container_issue 10
container_start_page 2403
container_title Journal of general virology
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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.
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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. 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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. 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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. 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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
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