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Review
. 2013 Dec 30:347:f7204.
doi: 10.1136/bmj.f7204.

Diagnosis, management, and prevention of rotavirus gastroenteritis in children

Affiliations
Review

Diagnosis, management, and prevention of rotavirus gastroenteritis in children

Umesh D Parashar et al. BMJ. .
No abstract available

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Conflict of interest statement

Competing interests: We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: UDP and GK—none. EASN has participated in vaccine and disease surveillance studies funded by GlaxoSmithKline and Pfizer.

Figures

Fig 1
Fig 1
World Health Organization estimates of rotavirus mortality (deaths/100 000 children under 5 years of age) by country in 2008. Reproduced, with permission, from Lancet Infectious Diseases
Fig 2
Fig 2
Mechanisms of rotavirus pathogenesis. Most information on rotavirus pathogenesis is derived from small animal models. Infection leads to attachment of the rotavirus to enterocytes (1), uncoating of the virus (2), followed by transcription and translation of viral proteins (3). This leads to the formation of a viroplasm, from which double layered particles assemble (4) and acquire outer coat proteins to form triple layered mature particles, which are shed by a non-classical secretory pathway (5). The viral enterotoxin non-structural protein 4 (NSP4; red triangles) is also released with the mature virions. NSP4 induces the release of intracellular calcium (Ca2+) (6) from the endoplasmic reticulum (ER) and disrupts tight junctions (7), resulting in paracellular leakage of fluid and electrolytes. NSP4 can act on crypt cells to induce chloride (Cl−) secretion directly (8) or through the enteric nervous system (ENS) (9), both of which draw water into the lumen. A decrease in brush border enzymes induced by infection (10) results in accumulation of sugars in the lumen and osmotic fluid loss. Destruction of intestinal cells later in infection results in loss of surface area and a malabsorptive diarrhea (11)

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