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1 Department of Integrative Biology, University of Texas at Houston Medical School, Houston 77030; and 2 Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030
Rotaviral infection in neonatal animals and
young children leads to acute self-limiting diarrhea, but infected
adults are mainly asymptomatic. Recently, significant in-roads have
been made into our understanding of this disease: both viral infection and virally manufactured nonstructural protein (NSP)4 evoke
intracellular Ca2+ ([Ca2+]i)
mobilization in native and transformed gastrointestinal epithelial cells. In neonatal mouse pup mucosa models,
[Ca2+]i elevation leads to age-dependent
halide ion movement across the plasma membrane, transepithelial
Cl
secretion, and, unlike many microbial enterotoxins,
initial cyclic nucleotide independence to secretory diarrhea.
Similarities between rotavirus infection and NSP4 function suggest that
NSP4 is responsible for these enterotoxigenic effects. NSP4-mediated
[Ca2+]i mobilization may further facilitate
diarrhea by signaling through other Ca2+-sensitive cellular
processes (cation channels, ion and solute transporters) to potentiate
fluid secretion while curtailing fluid absorption. Apart from these
direct actions in the mucosa at the onset of diarrhea, innate
host-mediated defense mechanisms, triggered by either or both viral
replication and NSP4-induced [Ca 2+]i
mobilization, sustain the diarrheal response. This secondary component
appears to involve the enteric nervous system and may be cyclic
nucleotide dependent. Both phases of diarrhea occur in the absence of
significant inflammation. Thus age-dependent rotaviral disease
represents an excellent experimental paradigm for understanding a
noninflammatory diarrhea.
ion transport; virus-induced diarrhea
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