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Mutations in HPV18 E1^E4 Impact Virus Capsid Assembly, Infectivity Competence, and Maturation
Jennifer Biryukov1, Jocelyn C Myers2, Margaret E McLaughlin-Drubin3,4
1Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. jenbiryukov@gmail.com.
Viruses
|December 20, 2017
Summary
The human papillomavirus (HPV) E1^E4 protein is crucial for viral infection. Shorter E1^E4 forms enhance viral capsid assembly and infectivity, while longer forms abrogate these processes.
Area of Science:
- Virology
- Molecular Biology
- Infectious Diseases
Background:
- The human papillomavirus (HPV) E1^E4 protein is highly expressed during the productive phase of the viral life cycle.
- Its precise functions in viral infection, including capsid assembly and infectivity, require further elucidation.
- HPV E1^E4 is involved in viral genome amplification and expressed throughout the virus life cycle.
Purpose of the Study:
- To investigate the role of HPV18 E1^E4 in viral capsid assembly and infectivity.
- To analyze the impact of E1^E4 truncation mutants on viral titers and infectivity.
Main Methods:
- Examination of wild-type HPV18 E1^E4 and four E1^E4 truncation mutants.
- Quantification of viral titers and infectivity assays for different E1^E4 variants.
Main Results:
- The shortest E1^E4 mutant (17/18) produced viral titers comparable to wild-type HPV.
- Infectivity of the 17/18 mutant was equivalent to wild-type, significantly higher than longer mutants.
- Longer E1^E4 mutants completely abrogated viral infectivity, irrespective of virion maturity.
Conclusions:
- HPV18 E1^E4 plays a significant role in viral capsid assembly and infectivity.
- Truncation length of E1^E4 critically influences viral infectivity and maturation.
- These findings provide new insights into HPV pathogenesis and viral replication strategies.
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