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Mutations in HPV18 E1^E4 Impact Virus Capsid Assembly, Infectivity Competence, and Maturation.

Authors
  • Biryukov, Jennifer1
  • Myers, Jocelyn C2
  • McLaughlin-Drubin, Margaret E3, 4
  • Griffin, Heather M5
  • Milici, Janice6
  • Doorbar, John7
  • Meyers, Craig8
  • 1 Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. [email protected]
  • 2 Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. [email protected]
  • 3 Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
  • 4 Department of Medicine, Brigham and Women's Hospital, Boston, MA 02215, USA.
  • 5 Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK. [email protected]
  • 6 Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. [email protected]
  • 7 Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK. [email protected]
  • 8 Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. [email protected]
Type
Published Article
Journal
Viruses
Publisher
MDPI AG
Publication Date
Dec 19, 2017
Volume
9
Issue
12
Identifiers
DOI: 10.3390/v9120385
PMID: 29257050
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The most highly expressed protein during the productive phase of the human papillomavirus (HPV) life cycle is E1^E4. Its full role during infection remains to be established. HPV E1^E4 is expressed during both the early and late stages of the virus life cycle and contributes to viral genome amplification. In an attempt to further outline the functions of E1^E4, and determine whether it plays a role in viral capsid assembly and viral infectivity, we examined wild-type E1^E4 as well as four E1^E4 truncation mutants. Our study revealed that HPV18 genomes containing the shortest truncated form of E1^E4, the 17/18 mutant, produced viral titers that were similar to wild-type virus and significantly higher compared to virions containing the three longer E1^E4 mutants. Additionally, the infectivity of virus containing the shortest E1^E4 mutation was equivalent to wild-type and significantly higher than the other three mutants. In contrast, infectivity was completely abrogated for virus containing the longer E1^E4 mutants, regardless of virion maturity. Taken together, our results indicate for the first time that HPV18 E1^E4 impacts capsid assembly and viral infectivity as well as virus maturation.

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