HIV-1 Rev downregulates Tat expression and viral replication via modulation of NAD(P)H:quinine oxidoreductase 1 (NQO1)

Sneh Lata, Amjad Ali, Vikas Sood, Rameez Raja and Akhil C. Banerjea ()
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Sneh Lata: University College of Medical Sciences and Guru Teg Bahadur Hospital
Amjad Ali: Laboratory of Virology, National Institute of Immunology
Vikas Sood: University College of Medical Sciences and Guru Teg Bahadur Hospital
Rameez Raja: Laboratory of Virology, National Institute of Immunology
Akhil C. Banerjea: Laboratory of Virology, National Institute of Immunology

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract 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. Here we report that HIV-1 Rev causes specific degradation of cytoplasmic Tat, which results in inhibition of HIV-1 replication. The nuclear export signal (NES) region of Rev is crucial for this activity but is not involved in direct interactions with Tat. Rev reduces the levels of ubiquitinated forms of Tat, which have previously been reported to be important for its transcriptional properties. Tat is stabilized in the presence of NAD(P)H: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.

Date: 2015
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DOI: 10.1038/ncomms8244

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