HIV-1 latency remains a major problem for the eradication of viruses in infected individuals. We evaluated the
effect of MC1293 on the epigenetic change at HIV-1 LTR and the induction of the latent viruses in the latency Jurkat T
cell line. We found MC1293 can activate HIV-1 gene expression, increase the acetylation level of H3 and H4 at the nuc-1
site of HIV-1 LTR. In addition, MC1293 can synergize with prostratin to activate the HIV-1 promoter, and has relatively
lower toxicity compared to Trichostatin A (TSA). The results suggest that the acetylation of histone plays an important
role in regulating HIV-1 LTR gene expression, and MC1293 is potential drug candidate for antilatency therapies.
Keywords: HIV-1 latency, MC1293, histone deacetylase inhibitors, histone modification, HDAC, drugs, patients, LTR, induction, viruses
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