EPS8 facilitates uncoating of influenza A virus

Gloria P. Larson; Vy Tran; Shuiqìng Yú; Yíngyún Caì; Christina A. Higgins; Danielle M. Smith; Steven F. Baker; Sheli R. Radoshitzky; Jens H. Kuhn; Andrew Mehle

Although cells lacking EPS8 have decreased FLUAV gene expression, that was not the case during FLUBV infection. FLUAV and FLUBV are structurally similar, and it is tempting to generalize that the replication cycle is largely the same for the two viruses. Like FLUAV, FLUBV utilizes receptormediated endocytosis for entry (Shaw and Palese, 2013) . Acidification of the FLUBV virion interior is facilitated by viral membrane protein and proton pump BM2, a FLUAV M2 homolog (Mould et al., 2003) . FLUBV undergoes uncoating after fusion of viral and endosomal membranes, but many of the details of FLUBV uptake and uncoating are still unknown. Interestingly, cellular immune responses to FLUBV infection differ from those to FLUAV infection (Jiang et al., 2016; Mäkelä et al., 2015) . Therefore, it is possible that host processes involved in other steps of FLUBV infection also differ, as suggested by the discordant importance of EPS8 for FLUAV and FLUBV.