Location: Foreign Animal Disease ResearchTitle: Cytokine mRNA expression in foot-and-mouth disease virus (FMDV) persistently infected bovine pharynx cultures: effect of IFNgamma on replication of persistent virus) Author
Submitted to: American Society for Virology Meeting
Publication Type: Abstract only
Publication Acceptance Date: 6/1/2009
Publication Date: 7/10/2009
Citation: O'Donnell, V., Smoliga, G.R., Pacheco Tobin, J., Baxt, B., Rodriguez, L.L. 2009. Cytokine mRNA expression in foot-and-mouth disease virus (FMDV) persistently infected bovine pharynx cultures: effect of IFNgamma on replication of persistent virus. American Society for Virology Meeting. Paper No. W36-9: P. 178. Interpretive Summary:
Technical Abstract: Foot-and-mouth disease virus (FMDV), a member of the family Picornaviridae, genus Aphtovirus, causes a highly contagious disease in livestock. Following acute infection in ruminants, up to 50% of both vaccinated and non-vaccinated animals become persistently infected asymptomatic carriers with low-level excretion of virus from the oral-nasal pharynx. In order to understand the persistence mechanisms at the molecular level, we previously developed and established an FMDV persistently infected primary cell culture derived from bovine oral-nasal pharyngeal tissues. The persistent culture continues to harbor FMDV without showing evident cytophatic effect for up to 22 passages. In this study, mRNA expression of a number of cytokines was measured in the FMDV persistently infected culture and compared to an acutely infected bovine pharynx culture. Down regulation of IL-1B, IL-2, IL-12 and IFNalpha was observed in FMDV persistently infected pharynx cultures but not in acutely infected cells. Previous reports suggest that IFNgamma plays a role in establishment and maintenance of persistence in cattle. We examined the effect of IFNgamma on FMDV replication in persistently infected bovine pharynx cultures. Interestingly, treatment with IFNgamma restricted FDMV replication and even cured the persistent culture, suggesting that a cytokine-mediated mechanism may be involved in the maintenance of persistence.