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Viruses. 2012 Mar;4(3):397-413. doi: 10.3390/v4030397. Epub 2012 Mar 15.

Innate immunity evasion by Dengue virus.

Author information

1
Department of Microbiology and the Global Health and Emerging Pathogens Institute (GHEPI), Mount Sinai School of Medicine, New York, NY 10029-6574, USA. juliet.morrison@mssm.edu

Abstract

For viruses to productively infect their hosts, they must evade or inhibit important elements of the innate immune system, namely the type I interferon (IFN) response, which negatively influences the subsequent development of antigen-specific adaptive immunity against those viruses. Dengue virus (DENV) can inhibit both type I IFN production and signaling in susceptible human cells, including dendritic cells (DCs). The NS2B3 protease complex of DENV functions as an antagonist of type I IFN production, and its proteolytic activity is necessary for this function. DENV also encodes proteins that antagonize type I IFN signaling, including NS2A, NS4A, NS4B and NS5 by targeting different components of this signaling pathway, such as STATs. Importantly, the ability of the NS5 protein to bind and degrade STAT2 contributes to the limited host tropism of DENV to humans and non-human primates. In this review, we will evaluate the contribution of innate immunity evasion by DENV to the pathogenesis and host tropism of this virus.

KEYWORDS:

interferon antagonism; NS2B3; NS5; STAT2 degradation

PMID:
22590678
PMCID:
PMC3347034
DOI:
10.3390/v4030397
[Indexed for MEDLINE]
Free PMC Article

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