Marylinda Famiglietti

TL;DR: No single in vitro cell model alone is able to capture accurately the ex vivo response characteristics of latently infected T cells from patients, indicating a critical knowledge gap that adversely affects the ability to identify promising treatment compounds and hinders the advancement of drug testing into relevant animal models and clinical trials.

TL;DR: It is shown that homeostatic proliferation, as induced by a combination of IL-2 plus IL-7, leads to partial reactivation of latent HIV-1 but is unable to reduce the size of the reservoir in vitro, and latently infected cells are able to homeostatically proliferate in the absence of viral reactivation or cell differentiation.

TL;DR: It is found that this viral expressed antisense lncRNA is involved in modulating human immunodeficiency virus gene expression and that this regulatory effect is due to an alteration in the epigenetic landscape at the viral promoter.

TL;DR: The silent/inducible phenotype appears to be associated with chromosomal position, but the molecular basis is not fully clarified and may differ among in vitro models of latency.

TL;DR: An in vitro primary cell model of HIV-1 latency is used to show that P-TEFb availability in resting memory CD4+ T cells is governed by the differential expression and phosphorylation of its subunits, in contrast to previous observations in dividing cells, where P- TEFb can be regulated by its sequestration in the 7SK RNP complex.