Human rhinovirus attenuates the type I interferon response by disrupting activation of interferon regulatory factor 3.

Journal of Virology
Tao PengKurt E Gustin

Abstract

The type I interferon (IFN) response requires the coordinated activation of the latent transcription factors NF-kappaB, interferon regulatory factor 3 (IRF-3), and ATF-2, which in turn activate transcription from the IFN-beta promoter. Synthesis and subsequent secretion of IFN-beta activate the Jak/STAT signaling pathway, resulting in the transcriptional induction of the full spectrum of antiviral gene products. We utilized high-density microarrays to examine the transcriptional response to rhinovirus type 14 (RV14) infection in HeLa cells, with particular emphasis on the type I interferon response and production of IFN-beta. We found that, although RV14 infection results in altered levels of a wide variety of host mRNAs, induction of IFN-beta mRNA or activation of the Jak/STAT pathway is not seen. Prior work has shown, and our results have confirmed, that NF-kappaB and ATF-2 are activated following infection. Since many viruses are known to target IRF-3 to inhibit the induction of IFN-beta mRNA, we analyzed the status of IRF-3 in infected cells. IRF-3 was translocated to the nucleus and phosphorylated in RV14-infected cells. Despite this apparent activation, very little homodimerization of IRF-3 was evident following infection...Continue Reading

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Citations

Oct 24, 2009·Cell Biochemistry and Biophysics·Qiu-Li ChenZhong-Tian Qi
Oct 24, 2007·Nature Immunology·Craig R Roy, Edward S Mocarski
Apr 27, 2007·Journal of Virology·Jessica K Roth-CrossSusan R Weiss
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Jun 8, 2018·Current Opinion in Allergy and Clinical Immunology·Natalia Blanca-LopezMiguel Blanca
Oct 4, 2006·International Archives of Allergy and Immunology·Stefanie KirchbergerJohannes Stockl

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