Cell-culture propagation of porcine enteric calicivirus mediated by intestinal contents is dependent on the cyclic AMP signaling pathway.

Enteric caliciviruses are emerging pathogens in humans and animals, but they do not replicate in cell culture except for the porcine enteric calicivirus (PEC) Cowden strain. The PEC Cowden strain grows in pig kidney (LLC-PK) cells, but only in the presence of intestinal contents (IC) from uninfected gnotobiotic pigs in the medium. In this study, we investigated the relationship between IC and growth of Cowden PEC. Pretreatment of cells or the virus with IC or transfection of viral RNA into cells did not induce virus growth unless the medium was supplemented with IC. Among modulators of cell signal transduction, the G protein uncoupler, suramin, adenylate cyclase (AC) inhibitor, MDL-12,330A, and the cAMP-dependent protein kinase (PKA) inhibitor, N-(2-[bromocinnamulamino]ethyl)-5-isoquinolinesulfonamide (NBEI) inhibited the effect of IC on virus growth for up to 72 h. These data indicate that PEC virus replication may be dependent on an initial cAMP signaling pathway induced by IC.