Role of the Herpes Simplex Virus CVSC Proteins at the Capsid Portal Vertex

Author:

Huet Alexis1,Huffman Jamie B.2,Conway James F.1ORCID,Homa Fred L.2ORCID

Affiliation:

1. Department of Structural Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

2. Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

Abstract

Herpes simplex virus 1 (HSV-1) is the causative agent of several pathologies ranging in severity from the common cold sore to life-threatening encephalitic infection. A critical step during productive HSV-1 infection is the cleavage and packaging of replicated, concatemeric viral DNA into preformed capsids. A key knowledge gap is how the capsid engages the replicated viral genome and the subsequent packaging of a unit-length HSV genome. Here, biochemical and structural studies focused on the unique portal vertex of wild-type HSV and packaging mutants provide insights into the mechanism of HSV genome packaging. The significance of our research is in identifying the portal proteins pUL6 and pUL17 as key viral factors for engaging the terminase complex with the capsid and the subsequent cleavage, packaging, and stable incorporation of the viral genome in the HSV-1 capsid.

Funder

HHS | NIH | National Institute of Allergy and Infectious Diseases

HHS | NIH | NIH Office of the Director

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

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