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GADD34 attenuates HIV-1 replication by viral 5'-UTR TAR RNA-mediated translational inhibition

  1. Author:
    Ishaq,Mohammad
    Marshall,Heather
    Natarajan,Ven

  2. Author Address

    Laboratory of Molecular Cell Biology, Leidos Biomedical Research Inc, Frederick National Laboratory for Cancer Research, P.O. Box B, Frederick, MD, 21702, USA. Electronic address: mishaq@mail.nih.gov., Laboratory of Molecular Cell Biology, Leidos Biomedical Research Inc, Frederick National Laboratory for Cancer Research, P.O. Box B, Frederick, MD, 21702, USA. Electronic address: Vnatarajan@mail.nih.gov.,
    1. Year: 2020
    2. Date: JAN 15
    3. Epub Date: 2019 11 15
  2. Journal: Virology
    1. 540
    2. Pages: 119-131
  4. Type of Article: Article
  5. ISSN: 0042-6822
  1. Abstract:

    Role of GADD34, a protein that is induced following cellular stress, in HIV-1 replication was investigated. GADD34 was induced during the late phase of HIV-1 infection. siRNA-knockdown of GADD34 stimulated whereas overexpression of GADD34 inhibited HIV-1 replication. GADD34 N-terminal ER-binding-helix amino acid region 1-192 alone was found to be sufficient for the inhibition of HIV-1 replication whereas protein-phosphatase -1-binding domain and eIF-2a-phosphatase activity of GADD34 were not crucial for anti-HIV-1 activity. GADD34 did not alter the HIV-1 RNA levels but reduced the viral protein expression suggesting that GADD34 interferes in HIV protein synthesis. Studies on the effect of HIV-1-5'-UTR and its mutants on a human promoter-driven luciferase expression indicated that GADD34-inhibition was mediated by 5'-UTR/TAR RNA, probably by modulating TAR RNA structure. In summary, our data support a novel function of GADD34 as a putative anti-HIV-1 restriction factor. Copyright © 2019 Elsevier Inc. All rights reserved.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.virol.2019.11.010
  3. PMID: 31778897
  4. View record in Web of Science®
  5. WOS: 000509003900013
  6. PII : S0042-6822(19)30318-6

Library Notes

  1. Fiscal Year: FY2019-2020
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