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Role of nitric oxide during rotavirus infection.

Artikel i vetenskaplig tidskrift
Författare Jesús Rodríguez-Díaz
Mahanez Banasaz
Claudia Istrate
Javier Buesa
Ove Lundgren
Felix Espinoza
Tommy Sundqvist
Martin Rottenberg
Lennart Svensson
Publicerad i Journal of medical virology
Volym 78
Nummer/häfte 7
Sidor 979-85
ISSN 0146-6615
Publiceringsår 2006
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 979-85
Språk en
Länkar dx.doi.org/10.1002/jmv.20650
Ämnesord Animals, Animals, Newborn, Base Sequence, Case-Control Studies, Cell Line, Gastroenteritis, etiology, metabolism, Glycoproteins, toxicity, Humans, Infant, Mice, Mice, Inbred BALB C, Nitric Oxide, metabolism, Nitric Oxide Synthase Type II, genetics, Prospective Studies, RNA, Messenger, genetics, metabolism, Rotavirus, pathogenicity, Rotavirus Infections, etiology, metabolism, Toxins, Biological, toxicity, Viral Nonstructural Proteins, toxicity
Ämneskategorier Fysiologi, Mikrobiologi inom det medicinska området

Sammanfattning

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 NO2/NO3 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 NO2/NO3 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.

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