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PMID: 1920621 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Inhibition of human immunodeficiency virus replication in acutely infected CD4+ cells by CD8+ cells involves a noncytotoxic mechanism.

Journal of virology ·Vol. 65 ·No. 11 ·1991-11-00 ·Pages 5921-7

Walker CM, Erickson AL, Hsueh FC, Levy JA

Abstract

The mechanism by which CD8+ T cells from human immunodeficiency virus (HIV)-infected individuals suppress HIV replication in acutely infected CD4+ T cells was investigated. Cytotoxicity was not involved, as the antiviral activity of the CD8+ cells did not correlate with the ability to lyse HIV-infected or uninfected CD4+ T cells. In addition, the frequency of HIV-infected CD4+ cells increased during coculture with CD8+ T cells even in the absence of detectable levels of virus replication. Moreover, separation of the CD4+ and CD8+ cells by a 0.4-micron-pore-size filter delayed HIV replication, indicating a role, at least in part, for a soluble factor. However, cell contact was required for optimal antiviral activity. These results extend further the observation on the mechanism of antiviral HIV activity by CD8+ cells from infected individuals. They support the conclusion that CD8+ cells can play a major role in preventing development of disease in HIV-infected individuals.

MeSH Terms
Antibodies, Monoclonal Antigens, CD/analysis CD4 Antigens/immunology CD8 Antigens/immunology Cells, Cultured Cytotoxicity, Immunologic HIV/immunology,physiology HIV Seropositivity Humans Lymphocyte Activation T-Lymphocyte Subsets/immunology Time Factors Virus Replication
Chemicals
Antibodies, Monoclonal Antigens, CD CD4 Antigens CD8 Antigens
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Walker C M
Chiron Corporation, Emeryville, California 94608.
Erickson A L
Hsueh F C
Levy J A
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
1991-11-00
Pages
5921-7
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC250255
Subset
IM
Grants
NIAID NIH HHS · R01-AI-30350 · United States
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