Abstract
quinine oxidoreductase 1 (NQO1), and potent degradation of Tat is induced by dicoumarol, an NQO1 inhibitor. Furthermore, Rev causes specific reduction in the levels of endogenous NQO1. Thus, we propose that Rev is able to induce degradation of Tat indirectly by downregulating NQO1 levels. Our findings have implications in HIV-1 gene expression and latency.
Highlights
HIV-1 gene expression and replication largely depend on the regulatory proteins Tat and Rev, but it is unclear how the intracellular levels of these viral proteins are regulated after infection
By a series of experiments we show that Rev leads to marked reduction in HIV-1 gene expression, which correlated with the decrease in intracellular levels of Tat
HIV-1 latency arises when the intracellular levels of the regulatory protein Tat falls below a critical threshold level
Summary
HIV-1 gene expression and replication largely depend on the regulatory proteins Tat and Rev, but it is unclear how the intracellular levels of these viral proteins are regulated after infection. Tat and Rev proteins are able to shuttle between the nucleus and cytoplasm and potentially perform functions in both of these cellular compartments[6,7,8,9] Both Tat and Rev extensively exploit various cellular factors to govern viral gene expression[10,11]. We observed that NQO1 stabilizes Tat protein in a dose-dependent manner and the inhibitor of NQO1, dicoumarol, potently induces degradation of the Tat protein and inhibits HIV-1 replication. Rev downmodulates the expression of NQO1 in a dose-dependent manner These observations have very significant implications with respect to controlling HIV-1 gene expression and latency
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