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The paramyxoviruses simian virus 5 and mumps virus recruit host cell CD46 to evade complement-mediated neutralization

John B Johnson1, Ken Grant, Griffith D Parks

  • 1Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1064, USA.

Journal of Virology
|May 22, 2009
PubMed

Insights

Simian virus 5 (SV5) and mumps virus (MuV) evade the complement system by incorporating CD46, a complement regulator, into their viral particles. This incorporation helps viruses resist neutralization by host immune responses.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • The complement system is a crucial part of innate immunity that viruses encounter.
  • Previous studies showed simian virus 5 (SV5) acquires complement C3 fragments upon interaction with human serum.
  • The presence of inactive C3b on SV5 virions suggests potential complement evasion mechanisms.

Purpose of the Study:

  • To investigate the role of virion-associated complement regulators in SV5 and mumps virus (MuV) complement evasion.
  • To determine if SV5 and MuV incorporate complement regulatory proteins into progeny virions.
  • To elucidate the mechanism by which these viruses resist complement-mediated neutralization.

Main Methods:

  • Purification of SV5 and MuV virions from different cell lines (A549, CHO, engineered CHO-CD46).
  • Analysis of virion-associated proteins using Western blot and gradient centrifugation.
  • In vitro complement cleavage assays using purified complement components and virions.
  • Neutralization assays using human serum to assess viral resistance.

Main Results:

  • SV5 virions derived from human cells contained CD46, a complement regulator, and exhibited C3b cofactor activity for factor I-mediated cleavage.
  • SV5 produced in CD46-deficient cells lacked this cofactor activity, while virions from CD46-overexpressing cells showed enhanced activity.
  • Both SV5 and MuV incorporating CD46 demonstrated increased resistance to complement-mediated neutralization by human serum.

Conclusions:

  • Rubulaviruses SV5 and MuV utilize CD46 as a mechanism to evade the host complement system.
  • Incorporation of cell surface complement inhibitors into progeny virions limits complement-mediated neutralization.
  • This strategy allows viruses to successfully navigate innate immune defenses during infection.

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