JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lewis, J.
Right arrow Articles by McKeating, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lewis, J.
Right arrow Articles by McKeating, J. A.

Journal of Virology, November 1998, p. 8943-8951, Vol. 72, No. 11
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Development of a Neutralizing Antibody Response during Acute Primary Human Immunodeficiency Virus Type 1 Infection and the Emergence of Antigenic Variants

J. Lewis,1 P. Balfe,2,* C. Arnold,3 S. Kaye,2 R. S. Tedder,2 and J. A. McKeating1

School of Animal and Microbial Sciences, University of Reading, Reading RG6 2AJ,1 Department of Virology, The Windeyer Institute of Medical Sciences, UCLMS, London W1P 6DB,2 and Virus Reference Laboratory, CPHL, Colindale, London NW9 5HT,3 United Kingdom

Received 8 May 1998/Accepted 4 August 1998

We monitored the primary humoral response to human immunodeficiency virus type 1 infection and showed that, in addition to antibodies to p24 and gp41, antigens which form the basis of most diagnostic assays, the response included a significant antibody response directed to the gp120 region of the infecting viral quasispecies. When tested in a recombinant virus neutralization assay, these antibodies were capable of inhibiting viral growth. We found the primary viral quasispecies to solely utilize the CCR-5 chemokine receptor; however, recombinant viruses differed in their cytopathology and in their sensitivity to beta -chemokine inhibition of viral growth. Sequence analysis of the gp120 open reading frames showed that amino acid changes in the C1 (Dright-arrowG at position 62) and C4 (Vright-arrowA at position 430) regions accounted for the phenotypic differences. These data demonstrate that early in infection, polymorphism exists in envelope glycoprotein coreceptor interactions and imply that therapeutic strategies targeted at this step in the viral life cycle may lead to rapid resistance.

* Corresponding author. Mailing address: Department of Virology, The Windeyer Institute of Medical Sciences, UCLMS, 46 Cleveland St., London W1P 6DB, United Kingdom. Phone: 44 171 504 9490. Fax: 44 171 580 5896. E-mail: p.balfe{at}ucl.ac.uk.

Journal of Virology, November 1998, p. 8943-8951, Vol. 72, No. 11
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 1998 by the American Society for Microbiology. All rights reserved.