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The VSV matrix protein inhibits NF-κB and the interferon response independently in mouse L929 cells.


ABSTRACT: The matrix (M) protein of vesicular stomatitis virus (VSV) plays a key role in immune evasion. While VSV has been thought to suppress the interferon (IFN) response primarily by inhibiting host cell transcription and translation, our recent findings indicate that the M protein also targets NF-κB activation. Therefore, the M protein may utilize two distinct mechanisms to limit expression of antiviral genes, inhibiting both host gene expression and NF-κB activation. Here we characterize a recently reported mutation in the M protein [M(D52G)] of VSV isolate 22-20, which suppressed IFN mRNA and protein production despite activating NF-κB. 22-20 inhibited reporter gene expression from multiple promoters, suggesting that 22-20 suppressed the IFN response via M-mediated inhibition of host cell transcription. We propose that suppression of the IFN response and regulation of NF-κB are independent, genetically separable functions of the VSV M protein.

SUBMITTER: Marquis KA 

PROVIDER: S-EPMC7447837 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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The VSV matrix protein inhibits NF-κB and the interferon response independently in mouse L929 cells.

Marquis Kaitlin A KA   Becker Rachel L RL   Weiss Amanda N AN   Morris Matthew C MC   Ferran Maureen C MC  

Virology 20200629


The matrix (M) protein of vesicular stomatitis virus (VSV) plays a key role in immune evasion. While VSV has been thought to suppress the interferon (IFN) response primarily by inhibiting host cell transcription and translation, our recent findings indicate that the M protein also targets NF-κB activation. Therefore, the M protein may utilize two distinct mechanisms to limit expression of antiviral genes, inhibiting both host gene expression and NF-κB activation. Here we characterize a recently  ...[more]

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