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Journal of Virology, March 2001, p. 2706-2709, Vol. 75, No. 6
Institute of Virology, University Hospital
Rotterdam, 3015 GE Rotterdam,1 and
Laboratory for Histocompatibility and Immunogenetics,
Bloodbank Rotterdam, 3015 CN Rotterdam,2
The Netherlands, and UMR103, CNRS bioMerieux, ENS de Lyon,
Lyon, France3
Received 10 October 2000/Accepted 8 December 2000
Early after seroconversion, macrophage-tropic human
immunodeficiency virus type 1 (HIV-1) variants are predominantly found, even when a mixture of macrophage-tropic and non-macrophage-tropic variants was transmitted. For virus contracted by sexual transmission, this is presently explained by selection at the port of entry, where
macrophages are infected and T cells are relatively rare. Here we
explore an additional mechanism to explain the selection of
macrophage-tropic variants in cases where the mucosa is bypassed during
transmission, such as blood transfusion, needle-stick accidents, or
intravenous drug abuse. With molecularly cloned primary isolates of
HIV-1 in irradiated mice that had been reconstituted with a high dose of human peripheral blood mononuclear cells, we found that a
macrophage-tropic HIV-1 clone escaped more efficiently from specific
cytotoxic T-lymphocyte (CTL) pressure than its non-macrophage-tropic counterpart. We propose that CTLs favor the selective outgrowth of
macrophage-tropic HIV-1 variants because infected macrophages are less
susceptible to CTL activity than infected T cells.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.6.2706-2709.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Macrophage Tropism of Human Immunodeficiency Virus Type 1 Facilitates In Vivo Escape from Cytotoxic T-Lymphocyte
Pressure
*
Corresponding author. Mailing address: Institute
of Virology, Erasmus Medical Centre Rotterdam, Dr. Molewaterplein
50, 3015 GE Rotterdam, The Netherlands. Phone: (31)-10-4088066. Fax:
(31)-10-4089485. E-mail: osterhaus{at}viro.fgg.eur.nl.
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