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MHV68 complement regulatory protein facilitates MHV68 replication in primary macrophages in a complement independent manner. Virology 2010 Jan 20;396(2):323-8

Date

11/17/2009

Pubmed ID

19910013

Pubmed Central ID

PMC2805278

DOI

10.1016/j.virol.2009.10.030

Scopus ID

2-s2.0-70749112365   7 Citations

Abstract

Murine gammaherpesvirus-68 (MHV68) is genetically related to human Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus and provides a tractable model to study gammaherpesvirus-host interactions in vivo and in vitro. The MHV68-encoded v-RCA product inhibits murine complement activation and shares sequence homology with other virus and host regulators of complement activation. Here we show that v-RCA is required for efficient MHV68 replication in primary murine macrophages, but not in murine embryonic fibroblasts. v-RCA-deficient MHV68 mutant viruses display defects in viral DNA synthesis in infected macrophages. Importantly, attenuated growth of v-RCA mutant viruses is not rescued in macrophages lacking critical components of the complement system including C3, indicating that the macrophage-specific role of v-RCA in MHV68 replication is complement-independent. This contrasts with the situation in vivo in which attenuated neurovirulence of v-RCA mutant viruses is rescued in C3-deficient mice. This study shows a novel, complement independent cell-type-specific function of a gammaherpesvirus RCA protein.

Author List

Tarakanova VL, Molleston JM, Goodwin M, Virgin HW 4th

Author

Vera Tarakanova PhD Associate Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Cell Line
Complement Activation
Complement C3
DNA, Viral
Fibroblasts
Gammaherpesvirinae
Host-Pathogen Interactions
Humans
Macrophages
Mice
Mice, Inbred C57BL
Reverse Transcriptase Polymerase Chain Reaction
Virus Replication
jenkins-FCD Prod-482 91ad8a360b6da540234915ea01ff80e38bfdb40a