Abstract:
Autophagy plays a protective role during many viral and bacterial infections. Predictably, evolution has led to several viruses developing mechanisms by which to evade the inhibitory effects of the pathway. However, one family of viruses, the picornaviruses, has gone one step further, by actively exploiting autophagy. Using mice in which Atg5 has been conditionally deleted in pancreatic acinar cells, we have studied the outcome of infection by coxsackievirus B3 (CVB3), a member of the enterovirus genus and picornavirus family. Two key findings emerged: disruption of autophagy (1) dramatically compromised virus replication in vivo, and (2) significantly limited pancreatic disease.
Autophagic Punctum to:
M Alirezaei, CT Flynn, MR Wood, JL Whitton. Pancreatic acinar cell-specific autophagy disruption reduces coxsackievirus replication and pathogenesis in vivo. Cell Host Microbe 2012; 11: 298-305
PMID: 22423969 DOI: 10.1016/j.chom.2012.01.014
Received: March 14, 2012; Accepted: March 26, 2012; Published Online: June 1, 2012