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Journal of Virology, July 2001, p. 6173-6182, Vol. 75, No. 13
AIDS Vaccine Program1 and
Intramural Research Support Program,2
SAIC-Frederick, National Cancer Institute at Frederick, Frederick,
Maryland 21702-1201
Received 14 December 2000/Accepted 6 April 2001
Human immunodeficiency virus (HIV) infection results in a
functional impairment of CD4+ T cells long before a
quantitative decline in circulating CD4+ T cells is
evident. The mechanism(s) responsible for this functional unresponsiveness and eventual depletion of CD4+ T cells
remains unclear. Both direct effects of cytopathic infection of
CD4+ cells and indirect effects in which uninfected
"bystander" cells are functionally compromised or killed have been
implicated as contributing to the immunopathogenesis of HIV infection.
Because T-cell receptor engagement of major histocompatibility complex (MHC) molecules in the absence of costimulation mediated via CD28 binding to CD80 (B7-1) or CD86 (B7-2) can lead to anergy or apoptosis, we determined whether HIV type 1 (HIV-1) virions incorporated MHC class
I (MHC-I), MHC-II, CD80, or CD86. Microvesicles produced from matched
uninfected cells were also evaluated. HIV infection increased MHC-II
expression on T- and B-cell lines, macrophages, and peripheral blood
mononclear cells (PBMC) but did not significantly alter the expression
of CD80 or CD86. HIV virions derived from all MHC-II-positive cell
types incorporated high levels of MHC-II, and both virions and
microvesicles preferentially incorporated CD86 compared to CD80. CD45,
expressed at high levels on cells, was identified as a protein present
at high levels on microvesicles but was not detected on HIV-1 virions.
Virion-associated, host cell-derived molecules impacted the ability of
noninfectious HIV virions to trigger death in freshly isolated PBMC.
These results demonstrate the preferential incorporation or exclusion
of host cell proteins by budding HIV-1 virions and suggest that host
cell proteins present on HIV-1 virions may contribute to the overall pathogenesis of HIV-1 infection.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.13.6173-6182.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Differential Incorporation of CD45, CD80 (B7-1), CD86 (B7-2), and
Major Histocompatibility Complex Class I and II Molecules into
Human Immunodeficiency Virus Type 1 Virions and Microvesicles:
Implications for Viral Pathogenesis and Immune Regulation
*
Corresponding author: Mailing address: Retroviral
Pathogenesis Laboratory, AIDS Vaccine Program, SAIC-Frederick, National Cancer Institute at Frederick, Building 535, Fifth Floor, Frederick, MD
21702-1201. Phone: (301) 846-5019. Fax: (301) 846-5588. E-mail: lifson{at}avpaxp1.ncifcrf.gov.
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