RT Journal Article
SR Electronic
T1 EPS8 facilitates uncoating of influenza A virus
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 592485
DO 10.1101/592485
A1 Gloria P. Larson
A1 Vy Tran
A1 Shuǐqìng Yú
A1 Yíngyún Caì
A1 Christina A. Higgins
A1 Danielle M. Smith
A1 Steven F. Baker
A1 Sheli R. Radoshitzky
A1 Jens H. Kuhn
A1 Andrew Mehle
YR 2019
UL http://biorxiv.org/content/early/2019/03/28/592485.abstract
AB All viruses balance interactions between cellular machinery co-opted to support replication and host factors deployed to halt the infection. We used gene correlation analysis to perform an unbiased screen for host factors involved in influenza A virus (FLUAV) infection. Our screen identified the cellular factor epidermal growth factor receptor pathway substrate 8 (EPS8) as the highest confidence pro-viral candidate. Knockout and overexpression of EPS8 confirmed its importance in enhancing FLUAV infection and titers. Loss of EPS8 did not affect virion attachment, uptake, or fusion. Rather, our data show that EPS8 specifically functions during virion uncoating. EPS8 physically associated with incoming virion components, and subsequent nuclear import of released ribonucleoprotein complexes was significantly delayed in the absence of EPS8. Our study identified EPS8 as a host factor important for uncoating, a crucial step of FLUAV infection during which the interface between the virus and host is still being discovered.