Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Gen Virol. 2012 Apr;93(Pt 4):797-806. doi: 10.1099/vir.0.038281-0. Epub 2011 Dec 28.

Early activation of the host complement system is required to restrict central nervous system invasion and limit neuropathology during Venezuelan equine encephalitis virus infection.

Author information

  • 1Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, NC 27599, USA. brookecb@niaid.nih.gov

Abstract

Venezuelan equine encephalitis virus (VEEV) is a mosquito-borne RNA virus of the genus Alphavirus, family Togaviridae, that is responsible for sporadic outbreaks in human and equid populations in Central and South America. In order to ascertain the role that complement plays in resolving VEEV-induced disease, complement-deficient C3(-/-) mice were infected with a VEEV mutant (V3533) that caused mild, transient disease in immunocompetent mice. In the absence of a functional complement system, peripheral inoculation with V3533 induced much more severe encephalitis. This enhanced pathology was associated with a delay in clearance of infectious virus from the serum and more rapid invasion of the central nervous system in C3(-/-) mice. If V3533 was inoculated directly into the brain, however, disease outcome in C3(-/-) and wild-type mice was identical. These findings indicate that complement-dependent enhancement of peripheral virus clearance is critical for protecting against the development of severe VEEV-induced encephalitis.

PMID:
22205717
[PubMed - indexed for MEDLINE]
PMCID:
PMC3542714
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Ingenta plc Icon for PubMed Central
    Loading ...
    Write to the Help Desk