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Role of nitric oxide during rotavirus infection
Author(s) -
RodríguezDíaz Jesús,
Banasaz Mahanez,
Istrate Claudia,
Buesa Javier,
Lundgren Ove,
Espinoza Felix,
Sundqvist Tommy,
Rottenberg Martin,
Svensson Lennart
Publication year - 2006
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20650
Subject(s) - virology , rotavirus , nitric oxide , medicine , biology , virus , endocrinology
The pathophysiological mechanisms behind rotavirus‐induced diarrhoea still remain incomplete. Current views suggest that the non‐structural protein 4 (NSP4) of rotavirus and the enteric nervous system (ENS) participate in water secretion and diarrhoea. In the present work the role of nitric oxide (NO) in rotavirus infection and disease has been studied in vitro, mice and humans. Incubation of human intestinal epithelial cells (HT‐29) with purified NSP4 but not with infectious virus produced NO 2 /NO 3 accumulation in the incubation media. The NSP4‐induced release of NO metabolites occurred within the first minutes after the addition of the toxin. Mice infected with murine rotavirus (strain EDIM) accumulated NO 2 /NO 3 in the urine at the onset for diarrhoea. Following rotavirus infection, inducible nitric oxide synthetase (iNOS) mRNA was upregulated in ileum, but not in duodenum or jejunum of newborn pups within 5 days post‐infection. A prospective clinical study including 46 children with acute rotavirus infection and age‐matched controls concluded that rotavirus infection stimulates NO production during the course of the disease ( P < 0.001). These observations identify NO as an important mediator of host responses during rotavirus infection. J. Med. Virol. 78:979–985, 2006. © 2006 Wiley‐Liss, Inc.