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147 Reduced Cell Susceptibility to HIV-1 Infection
in Vietnamese Exposed Uninfected Intravenous Drug-Users
T. X. Lien1, L. T. Tram1, N. V. Ngai2, A. David3, P. Versmisse3, D. Perez-Bercoff3, J.-Y. Follézou4, I. Theodorou5, D. Scott-Algara3, F. Barré-Sinoussi*3, and G. Pancino3
1Inst. Pasteur and 2Hosp. Binh-Trieu, Ho Chi Minh City, Vietnam; 3Inst. Pasteur, Paris, France; 4Hosp. Paul Brousse, Villejuif, France; and 5Hosp. Pitié-Salpêtrière, Paris, France
Background: We previously identified a population of highly HIV-exposed uninfected individuals (EUs) among intravascular drug users (IVDUs) in Ho Chi Minh City, Vietnam. Thirty-four EUs from the cohort of IVDUs were included in a study that aims to identify immune factors related to this protection against HIV-1 infection. Twenty-three low risk uninfected voluntary blood donors were enrolled as a control group.
Methods: Peripheral blood lymphocyte subsets and activation markers were analyzed by flow cytometry. Peripheral blood mononuclear cells (PBMC) or CD4+ cell susceptibility to HIV infection was evaluated by infecting PHA-activated cells with 3 HIV-1 isolates (a primary Vietnamese isolate, HIV-1 132W, the R5 HIV-1 BaL, and the X4 HIV-1 NL-4.3).
Results: No significant differences in lymphocyte phenotypes between EU and the control group were observed. Reduced susceptibility to at least 1 of the 3 viruses was observed with the PBMC of 16 of 34 EUs tested but only 2 of 23 controls. In some cases, the resistance to HIV-1 was associated with a restriction of virus replication in CD4+ cells. In other cases, HIV-1 infection of target cells was inhibited by CD8+ lymphocytes. Only in some of these last cases, high levels of secreted beta-chemokines were found and could account for HIV-1 suppression.
Conclusions: Our data indicated that a low susceptibility of PBMC to HIV-1 infection correlates with protection against HIV-1 in EU IVDUs. Different mechanisms appear involved in the reduction of cell susceptibility to HIV-1 infection, which may contribute to a natural protection against HIV in vivo: a refractory state of CD4+ cells to HIV-1, beta-chemokine, or other T CD8+ suppressive factors. These mechanisms might have to be considered to elaborate efficient immunotherapeutical and vaccinal strategies, in addition to adaptive immunity.
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