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TF protein of Sindbis virus antagonizes host type I interferon responses in a palmitoylation-dependent manner
Journal article   Open access   Peer reviewed

TF protein of Sindbis virus antagonizes host type I interferon responses in a palmitoylation-dependent manner

K. J. Rogers, S. Jones-Burrage, W. Maury and S. Mukhopadhyay
Virology (New York, N.Y.), Vol.542, pp.63-70
03/01/2020
DOI: 10.1016/j.virol.2020.01.001
PMCID: PMC7024065
PMID: 32056669
url
https://www.ncbi.nlm.nih.gov/pmc/articles/7024065View
Open Access

Abstract

Sindbis virus (SINV) produces the small membrane protein TF from the 6K gene via a (-1) programmed ribosomal frameshifting. While several groups have shown that TF-deficient virus exhibits reduced virulence, the mechanism(s) by which this occurs remain unknown. Here, we demonstrate a role for TF In antagonizing the host interferon response. Using wild-type and type 1 interferon receptor-deficient mice and primary cells derived from these animals, we show that TF controls the induction of the host interferon response at early times during infection. Loss of TF production leads to elevated interferon and a concurrent reduction in viral loads with a loss of pathogenicity. Palmitoylation of if has been shown to be important for particle assembly and morphology. We find that palmitoylation of TF also contributes to the ability of TF to antagonize host interferon responses as dysregulated palmitoylation of TF reduces virulence in a manner similar to loss of TF.
 Virology Life Sciences & Biomedicine Science & Technology

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