Antibody escape by polyomavirus capsid mutation facilitates neurovirulence.
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ABSTRACT:
SUBMITTER: Lauver MD
PROVIDER: S-EPMC7541085 | biostudies-literature | 2020 Sep
REPOSITORIES: biostudies-literature
Publications
Antibody escape by polyomavirus capsid mutation facilitates neurovirulence.
Lauver Matthew D MD Goetschius Daniel J DJ Netherby-Winslow Colleen S CS Ayers Katelyn N KN Jin Ge G Haas Daniel G DG Frost Elizabeth L EL Cho Sung Hyun SH Bator Carol M CM Bywaters Stephanie M SM Christensen Neil D ND Hafenstein Susan L SL Lukacher Aron E AE
eLife 20200917
JCPyV polyomavirus, a member of the human virome, causes progressive multifocal leukoencephalopathy (PML), an oft-fatal demyelinating brain disease in individuals receiving immunomodulatory therapies. Mutations in the major viral capsid protein, VP1, are common in JCPyV from PML patients (JCPyV-PML) but whether they confer neurovirulence or escape from virus-neutralizing antibody (nAb) in vivo is unknown. A mouse polyomavirus (MuPyV) with a sequence-equivalent JCPyV-PML VP1 mutation replicated p ...[more]
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