Mink enteritis virus infection induced cell cycle arrest and autophagy for its replication.

Mink enteritis virus (MEV) is an important pathogen causing mink viral enteritis. The mechanisms of cell cycle arrest induced by MEV infection and the roles of autophagy in MEV replication remain unclear. In this study, the roles of MEV NS1 protein in inducing cell cycle arrest were investigated, using the in vitro CRFK cell models.

Stimulation of lipopolysaccharide from Pseudomonas aeruginosa following H9N2 IAV infection exacerbates inflammatory responses of alveolar macrophages and decreases virus replication.

H9N2 IAV infection contributed to P. aeruginosa coinfection, causing severe hemorrhagic pneumonia in mink. In this study, the in vitro alveolar macrophage models were developed to investigate the innate immune responses to P.