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Rotavirus

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Gastroenteritis

3. Introduction

Rotavirus is a genus of double-stranded RNA virus in the family Reoviridae. Rotavirus is a leading cause of severe acute gastroenteritis (severe diarrhoea) in infants and young children, with over 95% of these children infected by the time they are 5 years old. The most severe cases occur among infants and young children between 6 months and 24 months of age. By the age of five, nearly every child in the world has been infected with rotavirus at least once. However, with each infection, immunity develops, subsequent infections are less severe,[3] and adults are rarely affected. There are seven species of this virus, referred to as A, B, C, D, E, F and G. Rotavirus A, the most common, causes more than 90% of infections in humans (Wiki: Rotavirus).

4. Microbial Pathogenesis

Rotavirus is transmitted by the faecal-oral route and possibly by the respiratory route. The diarrhoea is caused by multiple activities of the virus. Malabsorption occurs because of the destruction of gut enterocytes. The toxic rotavirus protein NSP4 induces age- and calcium ion-dependent chloride secretion, and disrupts SGLT1 transporter-mediated reabsorption of water. A recurrence of mild diarrhoea often follows the reintroduction of milk into the child's diet, due to bacterial fermentation of the disaccharide lactose in the gut (Wiki: Rotavirus).

5. Host Ranges and Animal Models

In addition to humans, rotaviruses infect and cause diarrhoea in young animals. They have been shown to infect mammals (for example, apes, cattle, pigs, sheep, rats,, cats, and dogs, mice, horses, rabbits) and birds (chickens and turkeys). These rotaviruses are a potential reservoir for genetic exchange with human rotaviruses. There is evidence that animal rotaviruses can infect humans, either by direct transmission of the virus or by contributing one or several RNA segments to reassortants with human strains (Wiki: Rotavirus).

6. Host Protective Immunity

Protective immune responses against rotavirus infections have been correlated with production of rotavirusspecific fecal IgA in vivo in human and porcine studies
as well as in mice (Herrmann et al., 1999).

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