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Measurement of γHV68 Infection in Mice
Published on: November 22, 2011
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Open reading frames M12/M13 jointly contribute to MHV-68 latency
Beatrix Steer1, Barbara Adler2, Heiko Adler1,3
1Institute of Asthma and Allergy Prevention, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; Member of the German Center of Lung Research (DZL), Munich, Germany.
The Journal of General Virology
|August 8, 2023
Summary
Murine gammaherpesvirus 68 (MHV-68) genes M12 and M13 have redundant functions. Deleting both M12 and M13 attenuates MHV-68 during latency, suggesting a role in gammaherpesvirus pathogenesis.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Murine gammaherpesvirus 68 (MHV-68) is a key model for studying gammaherpesvirus pathogenesis.
- The functions of MHV-68 open reading frames M12 and M13 remain uncharacterized.
Purpose of the Study:
- To investigate the roles of MHV-68 ORFs M12 and M13 in viral pathogenesis.
- To analyze the in vitro and in vivo phenotypes of MHV-68 mutants lacking M12, M13, or both.
Main Methods:
- Construction and analysis of recombinant MHV-68 with targeted mutations in M12 and M13.
- Assessment of viral replication and latency in cell culture (fibroblasts) and in vivo (mice).
Main Results:
- Single deletion mutants (M12 or M13) showed no discernible phenotype in vitro or in vivo.
- The M12/13 double mutant exhibited attenuated virulence during the latency phase in vivo, despite normal lytic growth.
- Reversion to wild-type MHV-68 restored the normal latency phenotype.
Conclusions:
- MHV-68 genes M12 and M13 likely possess redundant functions crucial for viral latency.
- These findings enhance understanding of MHV-68 pathogenesis and may offer insights into the roles of similar genes in human gammaherpesviruses like EBV and KSHV.
