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Defective interfering virus particles modulate virulence.

D R Cave, F M Hendrickson, A S Huang

    Journal of Virology
    |August 1, 1985
    PubMed
    Summary
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    Defective interfering (DI) particles influence vesicular stomatitis virus (VSV) virulence in mice by inducing cyclic virus growth, not gradual accumulation. This VSV cycling pattern has implications for disease diagnostics and transmission.

    Area of Science:

    • Virology
    • Immunology
    • Infectious Diseases

    Background:

    • Defective interfering (DI) particles are variants of viruses that require a standard homologous virus for replication.
    • DI particles are known to modulate viral infections, but their precise role in initiating cyclic virus growth in vivo remains unclear.

    Purpose of the Study:

    • To investigate whether DI particles modulate vesicular stomatitis virus (VSV) virulence by initiating a cyclic pattern of virus growth in vivo.
    • To determine the relationship between VSV and DI particle loads and the development of disease symptoms in infected mice.

    Main Methods:

    • Adult mice were intranasally inoculated with VSV, with or without DI particles.
    • Viral loads, presence of VSV and DI RNA, and disease progression (paralysis, mortality) were monitored.

    Related Experiment Videos

  • Infectivity measurements and RNA hybridization were used to quantify virus and DI particle presence in mouse brains.

    • Main Results:

    • VSV infection alone led to paralysis in most mice between days 7-9.
    • Coinfection with DI particles altered paralysis onset and severity, but protection was not predictable by particle ratios or amounts.
    • Infectivity measurements revealed a reproducible VSV cycling pattern in mouse brains with a periodicity of approximately 5 days.
    • DI RNA was detected in coinfected mice, indicating ongoing interaction between standard VSV and DI particles.

    Conclusions:

    • VSV exhibits cyclic growth patterns in vivo, influenced by the presence of DI particles.
    • This viral cycling, occurring before a full immune response, has potential implications for viral diagnostics and disease transmission.
    • The dynamic interaction between VSV and DI particles suggests a complex host-virus relationship beyond initial replication sites.