Reovirus preferentially infects the basolateral surface and is released from the apical surface of polarized human respiratory epithelial cells.

Excoffon KJ, Guglielmi KM, Wetzel JD, Gansemer ND, Campbell JA, Dermody TS, Zabner J
J Infect Dis. 2008 197 (8): 1189-97

PMID: 18419529 · PMCID: PMC2736797 · DOI:10.1086/529515

Mammalian reoviruses infect respiratory and gastrointestinal epithelia and cause disease in neonates. Junctional adhesion molecule-A (JAM-A) is a serotype-independent receptor for reovirus. JAM-A localizes to tight junctions and contributes to paracellular permeability in polarized epithelia. To investigate the mechanisms of reovirus infection of polarized epithelial cells, we assessed reovirus replication, release, and spread after apical and basolateral adsorption to primary human airway epithelial cultures. Reovirus infection of human airway epithelia was more efficient after adsorption to the basolateral surface than after adsorption to the apical surface, and it was dependent on JAM-A. Reovirus binding to carbohydrate coreceptor sialic acid inhibited apical infection, which was partially ameliorated by treatment of the cultures with neuraminidase. Despite the preference for basolateral infection, reovirus was released from the apical surface of respiratory epithelia and did not disrupt tight junctions. These results establish the existence of an infectious circuit for reovirus in polarized human respiratory epithelial cells.

MeSH Terms (19)

Animals Cell Adhesion Molecules Cell Polarity Electric Impedance Humans Immunoglobulins Immunohistochemistry L Cells Mice Microscopy, Confocal Neuraminidase Orthoreovirus, Mammalian Reassortant Viruses Receptors, Cell Surface Reoviridae Infections Respiratory Mucosa Respiratory Tract Infections Tight Junctions Virus Shedding

Connections (1)

This publication is referenced by other Labnodes entities: