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

High-throughput screening approaches have expanded our knowledge of specific cellular cofactors involved in FLUAV infection, with many of these methods identifying host factors involved in viral entry. Gene disruption screens identified host factors involved in sialic acid metabolism utilized for attachment (Carette et al., 2009; Han et al., 2017) . Vacuolar ATPases involved in endosomal acidification and other host factors facilitating fusion and uncoating were identified through siRNA knockdown, proteomic, and overexpression screens (Banerjee et al., 2014; König et al., 2010; Lee et al., 2017; Mar et al., 2018; Yángüez et al., 2018) . These studies also revealed previously unknown steps of FLUAV particle entry such as the role of the aggresome in viral uncoating (Banerjee et al., 2014) . Frequent identification of cellular factors involved in viral entry highlights the critical role of this process during viral replication. Despite these discoveries, however, the mechanistic details of steps occurring after fusion remain poorly understood.