Viruses 2009, 1(3), 1035-1056; doi:10.3390/v1031035
Review

Rotavirus Antagonism of the Innate Immune Response

Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 50 South Drive MSC 8026, Room 6314, Bethesda, MD 20892-8026, USA
* Author to whom correspondence should be addressed.
Received: 14 September 2009; in revised form: 5 November 2009 / Accepted: 20 November 2009 / Published: 24 November 2009
(This article belongs to the Special Issue Interferon Antiviral Response and Viral Evasion)
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Abstract: Rotavirus is a primary cause of severe dehydrating gastroenteritis in infants and young children. The virus is sensitive to the antiviral effects triggered by the interferon (IFN)-signaling pathway, an important component of the host cell innate immune response. To counteract these effects, rotavirus encodes a nonstructural protein (NSP1) that induces the degradation of proteins involved in regulating IFN expression, such as members of the IFN regulatory factor (IRF) family. In some instances, NSP1 also subverts IFN expression by causing the degradation of a component of the E3 ubiquitin ligase complex responsible for activating NF-κB. By antagonizing multiple components of the IFN-induction pathway, NSP1 aids viral spread and contributes to rotavirus pathogenesis.
Keywords: rotavirus; NSP1; interferon regulatory factor; IRF

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MDPI and ACS Style

Arnold, M.M.; Patton, J.T. Rotavirus Antagonism of the Innate Immune Response. Viruses 2009, 1, 1035-1056.

AMA Style

Arnold MM, Patton JT. Rotavirus Antagonism of the Innate Immune Response. Viruses. 2009; 1(3):1035-1056.

Chicago/Turabian Style

Arnold, Michelle M.; Patton, John T. 2009. "Rotavirus Antagonism of the Innate Immune Response." Viruses 1, no. 3: 1035-1056.

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