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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Critical role of complement and viral evasion of complement in acute, persistent, and latent gamma-herpesvirus

Sharookh B Kapadia1, Beth Levine, Samuel H Speck

  • 1Department of Immunology and Pathology, Department of Molecular Microbiology, Washington University School of Medicine, Box 8118, 660 South Euclid Avenue, St. Louis, MO 63110, USA.

Immunity
|August 28, 2002
PubMed

Insights

Murine gamma-herpesvirus 68 (gammaHV68) uses a protein to evade complement during acute infection. However, complement factor C3 remains crucial for controlling viral latency, highlighting complement

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Gamma-herpesviruses possess immune evasion proteins targeting host complement.
  • Regulators of complement activation (RCA) are viral homologs involved in immune evasion.

Purpose of the Study:

  • To investigate the roles of complement factor C3 and gammaHV68 RCA in viral pathogenesis.
  • To understand the interplay between gammaHV68 RCA, complement, and host immune responses.

Main Methods:

  • Utilizing knockout mouse models (e.g., IFNgammaR(-/-)) and viral genetic manipulation (deletion mutants).
  • Assessing viral virulence during acute central nervous system (CNS) infection and persistent replication.
  • Evaluating the impact on viral latency.

Main Results:

  • Deletion of gammaHV68 RCA reduced virulence in acute CNS infection, an effect reversed by host C3 deletion.
  • gammaHV68 RCA is vital for persistent viral replication and virulence in IFNgammaR(-/-) mice.
  • C3 influences viral latency, but gammaHV68 RCA does not counteract this role.

Conclusions:

  • Complement serves as a critical host defense against gamma-herpesvirus.
  • Gamma-herpesviruses have evolved strategies to evade complement-mediated responses during acute infection.
  • These viral immune evasion strategies are less effective against complement during latent infection.

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