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J. Exp. Med.,
Volume 187, Number 10, May 18, 1998 1689-1697
By
From the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Bethesda, Maryland 20892
It remains controversial whether human T lymphotropic virus type I (HTLV-I) coinfection
leads to more rapid progression of human immunodeficiency virus (HIV) disease in dually infected individuals. To investigate whether HTLV-I infection of certain cells can modulate
HIV-1 infection of surrounding cells, primary CD4+ T cells were treated with cell-free supernatants from HTLV-I-infected MT-2 cell cultures. The primary CD4+ T cells became resistant to macrophage (M)-tropic HIV-1 but highly susceptible to T cell (T)-tropic HIV-1. The
CC chemokines RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein (MIP)-1
, and MIP-1
in the MT-2 cell supernatants were
identified as the major suppressive factors for M-tropic HIV-1 as well as the enhancers of
T-tropic HIV-1 infection, whereas soluble Tax protein increased susceptibility to both M- and
T-tropic HIV-1. The effect of Tax or CC chemokines on T-tropic HIV-1 was mediated, at
least in part, by increasing HIV Env-mediated fusogenicity. Our data suggest that the net effect of HTLV-I coinfection in HIV-infected individuals favors the transition from M- to T-tropic
HIV phenotype, which is generally indicative of progressive HIV disease.
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