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Published on: April 21, 2015
Myxoma virus M130R is a novel virulence factor required for lethal myxomatosis in rabbits
John W Barrett1, Steven J Werden, Fuan Wang
1Biotherapeutics Research Group, Robarts Research Institute and Department of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5K8, Canada.
Abstract:
Myxoma virus (MV) is a highly lethal, rabbit-specific poxvirus that induces a disease called myxomatosis in European rabbits. In an effort to understand the function of predicted immunomodulatory genes we have deleted various viral genes from MV and tested the ability of these knockout viruses to induce lethal myxomatosis. MV encodes a unique 15 kD cytoplasmic protein (M130R) that is expressed late (12h post infection) during infection. M130R is a non-essential gene for MV replication in rabbit, monkey or human cell lines. Construction of a targeted gene knockout virus (vMyx130KO) and infection of susceptible rabbits demonstrate that the M130R knockout virus is attenuated and that loss of M130R expression allows the rabbit host immune system to effectively respond to and control the lethal effects of MV. M130R expression is a bona fide poxviral virulence factor necessary for full and lethal development of myxomatosis.
Insights
Myxoma virus (MV) uses the M130R protein to cause lethal myxomatosis in rabbits. Deleting this gene makes the virus less harmful, allowing rabbits to fight infection.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Myxoma virus (MV) causes lethal myxomatosis in European rabbits.
- Understanding viral immunomodulatory genes is crucial for controlling MV.
- The M130R protein is a unique, late-expressed, non-essential MV gene.
Purpose of the Study:
- To investigate the role of the M130R gene in MV pathogenesis.
- To determine if M130R is a virulence factor in myxomatosis.
Main Methods:
- Constructed a targeted gene knockout virus (vMyx130KO) lacking the M130R gene.
- Infected susceptible rabbits with wild-type MV and vMyx130KO.
- Assessed the virulence and host immune response to both viral strains.
Main Results:
- The M130R knockout virus (vMyx130KO) was significantly attenuated compared to wild-type MV.
- Loss of M130R expression enabled the rabbit host immune system to control the infection.
- M130R is essential for the full lethal development of myxomatosis.
Conclusions:
- The M130R protein is a critical poxviral virulence factor.
- Targeting M130R could be a strategy for developing attenuated myxoma virus vaccines or therapeutics.
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