Monocytic Cell Lines T- or + Persistent Infection of CD4 Dual Regulation of Bcl-2, Resulting in Human Immunodeficiency Virus Induces a

This work aims at characterizing the interplay between human immunodeficiency virus type 1 (HIV-1) andthe antiapoptotic cellular protein Bcl-2 responsible for a persistent infection in lymphoblastoid T (J.Jhan) ormonocytic (U937) cells. We report that the kinetics of Bcl-2 protein level during the establishment of a chronicinfection is biphasic, characterized by a transient decrease followed by restoration to the initial level. Theextent and duration of this transient decrease were inversely correlated with the basal level of Bcl-2 as shownby kinetics of Bcl-2 levels in J.Jhan or U937 clones exhibiting different levels of Bcl-2. Using these clones, wealso showed that Bcl-2 downregulates HIV-1 replication. Therefore, the cells overexpressing Bcl-2 are char-acterized by a low viral burden which, in turn, has little effect on the level of this protein. The observed bipasickinetics is the result of a dual regulation of Bcl-2 induced by HIV-1 infection itself: an upregulation at thetranscriptional level of the