Post-Transcriptional Control of Type I Interferon Induction by Porcine Reproductive and Respiratory Syndrome Virus in Its Natural Host Cells

Xiuqing Wang,Jane Christopher-Hennings

doi:10.3390/v4050725

Xiuqing Wang, Jane Christopher-Hennings

Open Access

https://doi.org/10.3390/v4050725

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Journal: Viruses	Publication Date: May 2, 2012
Citations: 57	License type: CC BY 4.0

Affiliation: South Dakota State University

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) is not only a poor inducer of type I interferon but also inhibits the efficient induction of type I interferon by porcine transmissible gastroenteritis virus (TGEV) and synthetic dsRNA molecules, Poly I:C. However, the mechanistic basis by which PRRSV interferes with the induction of type I interferon in its natural host cells remains less well defined. The purposes of this review are to summarize the key findings in supporting the post-transcriptional control of type I interferon in its natural host cells and to propose the possible role of translational control in the regulation of type I interferon induction by PRRSV.

Highlights

Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded, positive-senseRNA virus with a genome size of approximately 15 kb
Recent studies have shown that porcine monocyte-derived dendritic cells are highly susceptible to PRRSV infection in vitro [2, 3]
The nuclear factor kappa B (NF- B) pathway has been shown to contribute to the transcriptional activation of type I interferon by PRRSV [15], one study shows that NF- B is more likely related to induction of inflammatory cytokines such as TNF- and IL-6, rather than type I interferon, after influenza A virus infection and CpG ODN stimulation [9]

Summary

Introduction

Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded, positive-sense. The nuclear factor kappa B (NF- B) pathway has been shown to contribute to the transcriptional activation of type I interferon by PRRSV [15], one study shows that NF- B is more likely related to induction of inflammatory cytokines such as TNF- and IL-6, rather than type I interferon, after influenza A virus infection and CpG ODN stimulation [9]. This discrepancy may be due to the cell types and viruses used in different studies since different cell types and different viruses exhibit distinct features in the induction of type I interferon pathway. Virus replication and viral infectivity are usually not essential to the induction of type I interferon since both UV-inactivated and heat-inactivated influenza A viruses induce more abundant interferon- than their live virus counterparts [16]

Transcriptional Control of Type I Interferon by PRRSV

Post-Transcriptional and Translational Control of Type I Interferon by PRRSV

Conclusions