As2O3 synergistically reactivate latent HIV-1 by induction of NF-κB

Pengfei Wang, Xiying Qu, Xiaohui Wang, Lin Liu, Xiaoli Zhu, Hanxian Zeng, Huanzhang Zhu
Antiviral Research 2013 October 25
None of the current agents can safely and effectively eliminate latent HIV-1 reservoirs, meaning that there is a major barrier to the final cure of AIDS. Arsenic trioxide (As2O3), a drug used to treat acute promyelocytic leukemia (APL), was reported to affect the transcription factors and pathways involved in modulating HIV-1 expression. However, little is known about the effect and molecular basis of As2O3 in inducing HIV-1 expression in latently infected cells. Using the Jurkat T cell model of HIV-1 latency, we found that As2O3 activated latent HIV-1 replication with a similar potency to valproic acid (VPA) and did so in a dose- and time-dependent manner. We also found that As2O3 synergistically reactivated latent HIV-1 transcription with prostratin, tumor necrosis factor alpha (TNF-α) or VPA. Moreover, we provide evidence indicating that As2O3-induced HIV-1 activation involves the nuclear factor kappa B (NF-κB) signaling pathway. In conclusion, we have found that As2O3 can synergistically reactivate latent HIV-1 with other activators, which may provide a new tool to unravel the mechanisms of virus latency and reactivation.

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