Journal
VIROLOGY
Volume 479, Issue -, Pages 75-84Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2015.01.006
Keywords
Rotavirus; Innate immunity; Interferon signaling pathway; OAS/RNase L pathway; beta-TrCP; NE-kappa B; Viral E3 ubiquitin ligase; Viral phosphodiesterase
Categories
Funding
- National Institute of Allergy and Infectious Diseases at the National Institutes of Health [Z1A AI000754, Z1A AI000788]
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The innate immune response involves a broad array of pathogen sensors that stimulate the production of interferons (IFNs) to induce an antiviral state. Rotavirus, a significant cause of childhood gastroenteritis and a member of the Reoviridae family of segmented, double-stranded RNA viruses, encodes at least two direct antagonists of host innate immunity: NSP1 and VP3. NSP1, a putative E3 ubiquitin ligase, mediates the degradation of cellular factors involved in both IFN induction and downstream signaling. VP3, the viral capping enzyme, utilizes a 2H-phosphodiesterase domain to prevent activation of the cellular oligoadenylate synthase (OAS)/RNase L pathway. Computational, molecular, and biochemical studies have provided key insights into the structural and mechanistic basis of innate immune antagonism by NSPI and VP3 of group A rotaviruses (RVA). Future studies with non-RVA isolates will be essential to understand how other rotavirus species evade host innate immune responses. Published by Elsevier Inc.
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