Disulfiram Reactivates Latent HIV-1 in a Bcl-2-Transduced Primary CD4 <sup>+</sup> T Cell Model without Inducing Global T Cell Activation
Sifei Xing(Johns Hopkins University), C. Korin Bullen(Johns Hopkins University), Neeta S. Shroff(Howard Hughes Medical Institute), Liang Shan(Johns Hopkins University), Hung‐Chih Yang(Johns Hopkins University), Jordyn Manucci(Johns Hopkins University), Shridhar Bhat(Johns Hopkins University), Hao Zhang(Johns Hopkins University), Joseph B. Margolick(Johns Hopkins University), Thomas C. Quinn(Johns Hopkins University), David M. Margolis(University of North Carolina at Chapel Hill), Janet D. Siliciano(Johns Hopkins University), Robert F. Siliciano(Howard Hughes Medical Institute)
Cited by 194Open Access
Abstract
Highly active antiretroviral therapy (HAART) can reduce plasma HIV-1 levels to below the detection limit. However, due to the latent reservoir in resting CD4(+) cells, HAART is not curative. Elimination of this reservoir is critical to curing HIV-1 infection. Agents that reactivate latent HIV-1 through nonspecific T cell activation are toxic. Here we demonstrate in a primary CD4(+) T cell model that the FDA-approved drug disulfiram reactivates latent HIV-1 without global T cell activation. The extent to which disulfiram reactivates latent HIV-1 in patient cells is unclear, but the drug alone or in combination may be useful in future eradication strategies.
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