Abstract

Viruses possess many strategies to impair host cellular responses to infection. Nuclear export of host messenger RNAs (mRNA) that encode antiviral factors is critical for antiviral protein production and control of viral infections. Several viruses have evolved sophisticated strategies to inhibit nuclear export of host mRNAs, including targeting mRNA export factors and nucleoporins to compromise their roles in nucleo-cytoplasmic trafficking of cellular mRNA. Here, we present a review of research focused on suppression of host mRNA nuclear export by viruses, including influenza A virus and vesicular stomatitis virus, and the impact of this viral suppression on host antiviral responses.

Highlights

  • Nucleo-cytoplasmic trafficking of proteins and RNA is critical for proper cellular functions and survival

  • Regulation of cellular innate immune responses to pathogens occurs at multiple levels, including at the level of nucleo-cytoplasmic trafficking, whereby nuclear export of messenger RNAs (mRNA) encoding cellular defense proteins is critical for a host response to pathogen invasion

  • These results suggested that the rotavirus-induced nuclear export block of poly(A) mRNA was responsible for the inhibition of host translation during infection

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Summary

Introduction

Nucleo-cytoplasmic trafficking of proteins and RNA is critical for proper cellular functions and survival. DNA and RNA viruses alike are susceptible to IFN-induced cellular responses; they employ many strategies to block host up-regulation of antiviral response genes, including inhibition of both host transcription and post-transcriptional steps, which involves mRNA nuclear export and translation. These two nuclear export receptors are manipulated by many DNA and RNA viruses to promote viral mRNA export and/or inhibit host mRNA trafficking. VSV M protein interacts with Rae and Nup, resulting in mRNA nuclear export block This complex may be involved in transcription inhibition of a subset of genes. Nuclear budding of these DFz2C granules contained an RNA transcript encoding a protein that localizes to the NMJ, and nuclear envelope budding may be a mechanism used to deliver mRNAs to distinct cellular sites for translation so that particular proteins are localized to areas where they carry out their functions. Whether viruses utilize this pathway for nuclear export is currently unknown

Viral Mechanisms to Exploit Nuclear Export Receptors
Influenza Virus Inhibits Host mRNA Processing and Nuclear Export
Vesiculoviruses and mRNA Nuclear Export Inhibition
Picornaviruses Disrupt Nucleo-Cytoplasmic Trafficking
Rotavirus Inhibits Host mRNA Nuclear Export
Inhibition of Nucleo-Cytoplasmic Trafficking by DNA Viruses
Conclusions and Future Perspectives
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