Abstract
An electron microscopic study of intestinal epithelial cells of neonatal piglets infected with transmissible gastroenteritis (TGE) virus revealed a unique parasite-host cell interaction. Entry of the TGE virus into intestinal epithelial cells of newborn piglets is mediated through a network of cytoplasmic tubules of plasmalemma origin. the tubules, called microcanaliculi, are morphologically distinct from endoplasmic reticulum and Golgi. In uninfected animals similar tubules appear to be responsible for the indiscriminate uptake of large quantities of macromolecules from colostrum during the first few days of life.
Thin-section profiles of plasmalemma invaginations resembled tubules or canals and frequently contained viral particles. TGE viral particles developed and accumulated within cytoplasmic vacuoles. Initially the vacuoles were continuous with the microcanaliculi formed by deep plasmalemma invagination. Mature viral particles were 60 to 85 mu in diameter with an electron dense doughnut-shaped nucleoid surrounded by a trilaminar membrane which resembled the vacuolar wall. Abundant evidence of viral effects was observed in absorbtive epithelial cells of the jejunum and ileum but not of the duodenum.
The ability of absorbtive intestinal epithelial cells to form deep cytoplasmic tubular invaginations is temporally related to the pathogenesis of TGE and may explain in part why pigs usually are fatally affected by TGE only during the neonatal period.
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