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

Department

Research

Document Type

Article

Publication Title

Virology

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.

First Page

117

Last Page

123

DOI

10.1016/j.virol.2020.06.013

Volume

548

Publication Date

9-1-2020

Medical Subject Headings

Animals; Cell Line; Gene Expression Regulation; Host-Pathogen Interactions; Humans; Interferon-beta (genetics, immunology); Mice; NF-kappa B (genetics, immunology); Vesicular Stomatitis (genetics, immunology, virology); Vesicular stomatitis Indiana virus (genetics, immunology, physiology); Viral Matrix Proteins (genetics, immunology)

PubMed ID

32838932

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