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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-1β 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.
Key Words: HIV • HTLV-I • Tax • chemokines • chemokine receptors
H. Moriuchi and M. Moriuchi contributed equally to this project, which M. Moriuchi performed for the partial fulfillment of the requirements of the PhD program of the Department of Microbiology at Howard University, Washington, DC.
Abbreviations used: GST, glutathione S-transferase; HCMV, human cytomegalovirus; HTLV-I, human T lymphotropic virus type I; MIP, macrophage inflammatory protein; MOI, multiplicity of infection; RANTES, regulated on activation, normal T cell expressed and secreted; RT, reverse transcriptase; rVV, recombinant vaccinia virus.
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