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Journal of Virology, December 1998, p. 10165-10170, Vol. 72, No. 12
Department of
Medicine1 and
Immunogenetics and
Transplantation Laboratory, Department of
Surgery,2 School of Medicine, University of
California, San Francisco, San Francisco, California 94143-1270
Received 14 July 1998/Accepted 1 September 1998
CD8+ T cells from human immunodeficiency virus
(HIV)-infected individuals can suppress HIV replication in cultured
CD4+ cells by a noncytotoxic mechanism. Efficient
suppression of HIV replication (>90% reduction) does not require HLA
class I or class II histocompatibility between the effector
CD8+ T cells and the infected target CD4+ T
cells. However, maximal control of HIV production occurs when the
CD8+ effector cells and CD4+ target cells are
syngeneic. In some cases, more than 20-fold fewer syngeneic
CD8+ T cells were required to achieve the same degree of
HIV inhibition as HLA-mismatched CD8+ T cells. The
increased antiviral activity seen in the syngeneic setting did not map
exclusively to either the HLA class I or class II locus. These findings
suggest that genetic compatibility (potentially, but not necessarily,
at the HLA class I and class II loci) regulates CD8+ T-cell
noncytotoxic antiviral activity against infected CD4+ T cells.
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
HLA Compatibility Requirements for
CD8+-T-Cell-Mediated Suppression of Human
Immunodeficiency Virus Replication
and
*
Corresponding author. Mailing address: Department of
Medicine, School of Medicine, University of California, San Francisco, San Francisco, CA 94143-1270. Phone: (415) 476-4071. Fax: (415) 476-8365. E-mail: jalevy{at}itsa.ucsf.edu.
Present address: Xoma Corporation, Berkeley, CA 94170.
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