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

We also considered the possibility that other viruses using receptor-mediated endocytosis or similar internalization pathways could be affected by EPS8. A panel of RNA viruses using diverse cellular receptors and entry mechanisms was used to infect A549 cells overexpressing EPS8 ( Figure S4 ). There were no obvious trends or associations with viral families or entry pathways. Nonetheless, these results indicate that EPS8 enhancement of infection is specific to certain viruses, and the multifunctional nature of EPS8 may impart an anti-viral function for other viruses. In summary, our gene correlation analysis identified both pro-and antiviral host factors with a functional impact on early stages of FLUAV replication without requiring artificial manipulation of the cellular environment. Through interrogation of early steps of FLUAV infection, we established EPS8 as an novel cofactor facilitating FLUAV uncoating. Infectious Disease Award from the Burroughs Wellcome Fund. This work was also supported in part The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It . https://doi.org/10.1101/592485 doi: bioRxiv preprint EPS8 facilitates uncoating of influenza A virus 10 Larson, Tran, et al.