Abstract
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.
Highlights
Polyomaviruses (PyVs) are ubiquitous members of both human and non-human viromes
Fourteen human polyomaviruses have been identified to date, with estimated seroprevalence rates ranging from 4–98% in the general population and seropositivity rates increasing with age [4]
This review focuses on our current understanding of JCPyV capsid protein mutations in progressive multifocal leukoencephalopathy (PML) and how they relate to disease development
Summary
First discovered in mice as an infectious oncogenic agent, polyomaviruses have since been identified in a wide variety of mammals and birds, and more recently in fish and arthropods [1,2,3]. These viruses have coevolved with their animal hosts and typically cause a lifelong asymptomatic infection with persistent viral shedding [1]. The majority of polyomavirus infections are asymptomatic, several polyomaviruses cause severe diseases in immunocompromised individuals. This review focuses on our current understanding of JCPyV capsid protein mutations in PML and how they relate to disease development
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