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EPS8 facilitates uncoating of influenza A virus

Gloria P. Larson, Vy Tran, Shuǐqìng Yú, Yíngyún Caì, Christina A. Higgins, Danielle M. Smith, View ORCID ProfileSteven F. Baker, View ORCID ProfileSheli R. Radoshitzky, View ORCID ProfileJens H. Kuhn, View ORCID ProfileAndrew Mehle
doi: https://doi.org/10.1101/592485
Gloria P. Larson
1Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA
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Vy Tran
1Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA
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Shuǐqìng Yú
2Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infection Diseases, National Institutes of Health, Frederick, Maryland, USA
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Yíngyún Caì
2Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infection Diseases, National Institutes of Health, Frederick, Maryland, USA
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Christina A. Higgins
1Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA
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Danielle M. Smith
1Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA
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Steven F. Baker
1Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA
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  • ORCID record for Steven F. Baker
Sheli R. Radoshitzky
3Molecular and Translational Sciences Division, United States Army Medical Research Institute of Infectious Diseases, Frederick, Maryland, USA
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  • ORCID record for Sheli R. Radoshitzky
Jens H. Kuhn
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  • ORCID record for Jens H. Kuhn
Andrew Mehle
1Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA
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  • ORCID record for Andrew Mehle
  • For correspondence: amehle@wisc.edu
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SUMMARY

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.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted March 28, 2019.
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EPS8 facilitates uncoating of influenza A virus
Gloria P. Larson, Vy Tran, Shuǐqìng Yú, Yíngyún Caì, Christina A. Higgins, Danielle M. Smith, Steven F. Baker, Sheli R. Radoshitzky, Jens H. Kuhn, Andrew Mehle
bioRxiv 592485; doi: https://doi.org/10.1101/592485
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EPS8 facilitates uncoating of influenza A virus
Gloria P. Larson, Vy Tran, Shuǐqìng Yú, Yíngyún Caì, Christina A. Higgins, Danielle M. Smith, Steven F. Baker, Sheli R. Radoshitzky, Jens H. Kuhn, Andrew Mehle
bioRxiv 592485; doi: https://doi.org/10.1101/592485

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