JCPyV VP1 Mutations in Progressive Multifocal Leukoencephalopathy: Altering Tropism or Mediating Immune Evasion?
| Autor: | Lauver, Matthew D., Lukacher, Aron E. |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Progressive multifocal leukoencephalopathy (PML)
persistent infection viruses Leukoencephalopathy Progressive Multifocal polyomavirus lcsh:QR1-502 virus diseases Review VP1 biochemical phenomena metabolism and nutrition JCPyV Virus Replication JC Virus Host Specificity lcsh:Microbiology Mice Viral Tropism Capsid Mutation Animals Humans Capsid Proteins antibody escape MuPyV Immune Evasion |
| Zdroj: | Viruses, Vol 12, Iss 1156, p 1156 (2020) Viruses |
| ISSN: | 1999-4915 |
| Popis: | Polyomaviruses are ubiquitous human pathogens that cause lifelong, asymptomatic infections in healthy individuals. Although these viruses are restrained by an intact immune system, immunocompromised individuals are at risk for developing severe diseases driven by resurgent viral replication. In particular, loss of immune control over JC polyomavirus can lead to the development of the demyelinating brain disease progressive multifocal leukoencephalopathy (PML). Viral isolates from PML patients frequently carry point mutations in the major capsid protein, VP1, which mediates virion binding to cellular glycan receptors. Because polyomaviruses are non-enveloped, VP1 is also the target of the host's neutralizing antibody response. Thus, VP1 mutations could affect tropism and/or recognition by polyomavirus-specific antibodies. How these mutations predispose susceptible individuals to PML and other JCPyV-associated CNS diseases remains to be fully elucidated. Here, we review the current understanding of polyomavirus capsid mutations and their effects on viral tropism, immune evasion, and virulence. |
| Databáze: | OpenAIRE |
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