J Virol, June 1998, p. 4633-4642, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
The Picower Institute for Medical Research, Manhasset, New York 110301; Institute of Virology, Slovak Academy of Sciences, Bratislava, Slovakia2; and MGN Medical Research Laboratories, Setauket, New York 117333
Received 26 November 1997/Accepted 3 March 1998
The human immunodeficiency virus type 1 (HIV-1) laboratory strains
adapted to T-cell lines, as well as most syncytium-inducing primary
isolates, replicate poorly in macrophages, which, beside CD4+ T lymphocytes, are major targets of HIV-1. In the
present work, we used a semiquantitative PCR-based technique to study
viral entry into cells, kinetics of reverse transcription, and
translocation of the viral DNA into the nucleus of macrophages infected
with different HIV-1 strains. Our results demonstrate that
T-lymphotropic strains efficiently enter macrophages. Entry was
inhibited by a monoclonal antibody against CD4 and by stromal
cell-derived factor 1
, a natural ligand of CXCR4, suggesting that
both CD4 and CXCR4 act as receptors on macrophages for HIV-1
T-lymphotropic strains. Analysis of the kinetics of reverse
transcription and nuclear import revealed that the most pronounced
differences between T-lymphotropic and macrophagetropic strains
occurred at the level of nuclear translocation of viral DNA, although a
delay in reverse transcription was also observed. These results suggest
that postentry steps are critical for restricted replication of
T-lymphotropic HIV-1 strains in macrophages.
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