Bookkeeping in the secondary school

Thesis (Ed.M.)--Boston Universit

Problems in referring patients for chronic care

This item was digitized by the Internet Archive. Thesis (M.S.)--Boston Universit

Edgar Allen Poe: The dream-saga of a tragic poet

Thesis (Ed. M.)--Boston Universit

Government regulation of the milk industry

Thesis (M.B.A.)--Boston Universit

Policies and performance of SBIC's

Thesis (M.B.A.)--Boston University. Missing pages 76 and 77 in numbering onl

Editorial: ulcerative colitis submucosal fibrosis and inflammation: more than just strictures

info:eu-repo/semantics/publishedVersio

Homeostatic Proliferation Fails to Efficiently Reactivate HIV-1 Latently Infected Central Memory CD4+ T Cells

Homeostatic proliferation ensures the longevity of central memory T-cells by inducing cell proliferation in the absence of cellular differentiation or activation. This process is governed mainly by IL-7. Central memory T-cells can also be stimulated via engagement of the T-cell receptor, leading to cell proliferation but also activation and differentiation. Using an in vitro model of HIV-1 latency, we have examined in detail the effects of homeostatic proliferation on latently infected central memory T cells. We have also used antigenic stimulation via anti-CD3/anti-CD28 antibodies and established a comparison with a homeostatic proliferation stimulus, to evaluate potential differences in how either treatment affects the dynamics of latent virus populations. First, we show 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. Second, latently infected cells are able to homeostatically proliferate in the absence of viral reactivation or cell differentiation. These results indicate that IL-2 plus IL-7 may induce a detrimental effect by favoring the maintenance of the latent HIV-1 reservoir. On the other hand, antigenic stimulation efficiently reactivated latent HIV-1 in cultured central memory cells and led to depletion of the latently infected cells via virus-induced cell death