Rotaviral diarrheal illness is one of the most common
infectious diseases in children worldwide, but our
understanding of its pathophysiology is limited. This
study examines whether the enhanced net chloride
secretion during rotavirus infection in young rabbits
may occur as a result of hypersecretion in crypt cells
that would exceed the substantial Cl- reabsorption
observed in villi. By using a rapid filtration technique,
we evaluated transport of 36Cl and D-14C glucose
across brush border membrane (BBM) vesicles
purified from villus tip and crypt cells isolated in parallel
from the entire small intestine. Rotavirus infection
impaired SGLT1-mediated Na+-D-glucose symport
activity in both villus and crypt cell BBM, hence
contributing to the massive water loss along the cryptvillus
axis. In the same BBM preparations, rotavirus
failed to stimulate the Cl- transport activities (Cl-/H+
symport, Cl-/anion exchange and voltage-activated
Cl- conductance) at the crypt level, but not at the villus
level, questioning, therefore, the origin of net chloride
secretion. We propose that the chloride carrier might
function in both normal (absorption) and reversed
(secretion) modes in villi, depending on the direction
of the chloride electrochemical gradient resulting from
rotavirus infection, agreeing with our results that
rotavirus accelerated both Cl- influx and Cl- efflux rates
across villi BBM.