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Published byRafael Gómez Cano Modified over 6 years ago
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No-Go’ing Back: Co-opting RVB-2 to Control HIV-1 Gene Expression and Immune Response
Valerie Le Sage, Alessandro Cinti, Andrew J. Mouland Trends in Microbiology Volume 23, Issue 10, Pages (October 2015) DOI: /j.tim Copyright © 2015 Elsevier Ltd Terms and Conditions
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Figure 1 A Schematic Model of HIV-1 Gag Expression Regulated by the Host Factor RVB-2. Export of the viral genomic mRNA (gag mRNA) from the nucleus (top right) results in the translation of the Gag structural protein, which is regulated by the proportion of RVB-2 and the C-terminal domain of envelope (EnvCTD) (yellow circles) in the cytoplasm. The expression of Gag is sufficient to produce ‘bald’, non-infectious virus particles, which occurs upon depletion of RVB-2 and in the absence of sufficient quantities of the Env protein as shown in (A). A fine balance in Gag expression is orchestrated by RVB-2 (B) through an interaction between the host protein and the nascent matrix (MA) domain of Gag (red circles) and the 5′ untranslated region (UTR) of the target gag mRNA. These binding events lead to translational stalling that blocks Gag protein expression and initiates no-go mRNA decay through the recruitment of eRF1/Pelota resulting in gag mRNA cleavage. (C) Upon reaching a threshold of Env protein, the EnvCTD competes with RVB-2 for binding to MA and allows Gag synthesis to proceed and assembly of infectious HIV-1 virions. Trends in Microbiology , DOI: ( /j.tim ) Copyright © 2015 Elsevier Ltd Terms and Conditions
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