Prospects for virally vectored immunocontraception in the control of wild house mice (Mus domesticus)
Alec J. Redwood A C D , Lee M. Smith A C , Megan L. Lloyd A C , Lyn A. Hinds B C , Christopher M. Hardy B C and Geoffrey R. Shellam A CA Discipline of Microbiology and Immunology, School of Biomedical, Biomolecular and Chemical Sciences, M502, The University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia.
B CSIRO Entomology, GPO Box 1700, Canberra, ACT 2601, Australia.
C Invasive Animals Cooperative Research Centre, 3D1 University of Canberra, ACT 2601, Australia.
D Corresponding author. Email: aredwood@cyllene.uwa.edu.au
Wildlife Research 34(7) 530-539 https://doi.org/10.1071/WR07041
Submitted: 7 April 2007 Accepted: 11 July 2007 Published: 13 December 2007
Abstract
The wild house mouse (Mus domesticus) is not native to Australia and was introduced from Europe with early settlement. It undergoes periodic population explosions or plagues, which place significant economic and social burdens on agricultural communities. Present control mechanisms rely on improvements to farm hygiene and the use of rodenticides. This review covers over a decade of work on the use of virally vectored immunocontraception (VVIC) as an adjunct method of controlling mouse populations. Two viral vectors, ectromelia virus (ECTV) and murine cytomegalovirus (MCMV) have been tested as potential VVIC vectors: MCMV has been the most widely studied vector because it is endemic to Australia; ECTV less so because its use would have required the introduction of a new pathogen into the Australian environment. Issues such as efficacy, antigen choice, resistance, transmission, species specificity and safety of VVIC are discussed. In broad terms, both vectors when expressing murine zona pellucida 3 (mZP3) induced long-term infertility in most directly inoculated female mice. Whereas innate and acquired resistance to MCMV may be a barrier to VVIC, the most significant barrier appears to be the attenuation seen in MCMV-based vectors. This attenuation is likely to prevent sufficient transmission for broad-scale use. Should this issue be overcome, VVIC has the potential to contribute to the control of house mouse populations in Australia.
Acknowledgements
Many colleagues have contributed to this research endeavour over the last decade: in particular, we thank Hugh Tyndale-Biscoe, Grant Singleton and Roger Pech who questioned, motivated and encouraged everyone to address key questions in field and laboratory studies. Equally, the work would not have been completed without the enthusiasm and able assistance of numerous field and laboratory technicians and students – thank you! The authors also thank various agencies for funding support: the Biological Control of Vertebrate Pest Populations Cooperative Research Centre, the Invasive Animals Cooperative Research Centre, the Pest Animal Control Cooperative Research Centre, the Australian Grains Research Development Corporation, the Australian Government Biotechnology Innovation Fund, the Western Australian Government, Department of Industry and Resources through the Centres of Excellence in Science and Innovation Program, the National Health and Medical Research Council of Australia and the Australian Research Council.
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