Rotavirus-induced structural and functional alterations in tight junctionsof polarized intestinal caco-2 cell monolayers

We provide here new insights into rotavirus (RRV) pathogenicity by showing that RRV infection promotes structural and functional injuries localized at the tight junctions (TJ) in the cell-cell junctional complex of cultured p olarized human intestinal Caco-2 cells forming monolayers, RRV infection re sulted in a progressive increase in the paracellular permeability to [H-3] mannitol as a function of the time postinfection, We observed a disorganiza tion of the TJ-associated protein occludin as a function of the time postin fection, whereas distribution of the zonula adherens associated E-cadherin was not affected. These structural and functional RRV-induced TJ injuries w ere not accompanied by alteration in cell and monolayer integrity, as asses sed by the lack of change in transepithelial membrane resistance and lactat e dehydrogenase release. Finally, using the stabilizer of actin filaments J asplakinolide, we demonstrated that the RRV-induced structural and function al alterations in TJ are independent of the RRV-induced apical F-actin rear rangements.