@article{SchwensowDeteringPedersonetal.2017, author = {Schwensow, Nina I. and Detering, Harald and Pederson, Stephen and Mazzoni, Camila and Sinclair, Ron and Peacock, David and Kovaliski, John and Cooke, Brian and Fickel, J{\"o}rns and Sommer, Simone}, title = {Resistance to RHD virus in wild Australian rabbits}, series = {Molecular ecology}, volume = {26}, journal = {Molecular ecology}, publisher = {Wiley}, address = {Hoboken}, issn = {0962-1083}, doi = {10.1111/mec.14228}, pages = {4551 -- 4561}, year = {2017}, abstract = {Deciphering the genes involved in disease resistance is essential if we are to understand host-pathogen coevolutionary processes. The rabbit haemorrhagic disease virus (RHDV) was imported into Australia in 1995 as a biocontrol agent to manage one of the most successful and devastating invasive species, the European rabbit (Oryctolagus cuniculus). During the first outbreaks of the disease, RHDV caused mortality rates of up to 97\%. Recently, however, increased genetic resistance to RHDV has been reported. Here, we have aimed to identify genomic differences between rabbits that survived a natural infection with RHDV and those that died in the field using a genomewide next-generation sequencing (NGS) approach. We detected 72 SNPs corresponding to 133 genes associated with survival of a RHD infection. Most of the identified genes have known functions in virus infections and replication, immune responses or apoptosis, or have previously been found to be regulated during RHD. Some of the genes identified in experimental studies, however, did not seem to play a role under natural selection regimes, highlighting the importance of field studies to complement the genomic background of wildlife diseases. Our study provides a set of candidate markers as a tool for the future scanning of wild rabbits for their resistance to RHDV. This is important both for wild rabbit populations in southern Europe where RHD is regarded as a serious problem decimating the prey of endangered predator species and for assessing the success of currently planned RHDV variant biocontrol releases in Australia.}, language = {en} } @article{SchwensowMazzoniMarmesatetal.2017, author = {Schwensow, Nina and Mazzoni, Camila J. and Marmesat, Elena and Fickel, J{\"o}rns and Peacock, David and Kovaliski, John and Sinclair, Ron and Cassey, Phillip and Cooke, Brian and Sommer, Simone}, title = {High adaptive variability and virus-driven selection on major histocompatibility complex (MHC) genes in invasive wild rabbits in Australia}, series = {Biological invasions : unique international journal uniting scientists in the broad field of biological invasions}, volume = {19}, journal = {Biological invasions : unique international journal uniting scientists in the broad field of biological invasions}, publisher = {Springer}, address = {Dordrecht}, issn = {1387-3547}, doi = {10.1007/s10530-016-1329-5}, pages = {1255 -- 1271}, year = {2017}, abstract = {The rabbit haemorrhagic disease virus (RHDV) was imported into Australia in 1995 as a biocontrol agent to manage one of the most successful and devastating invasive species, the European rabbit (Oryctolagus cuniculus cuniculus). During the first disease outbreaks, RHDV caused mortality rates of up to 97\% and reduced Australian rabbit numbers to very low levels. However, recently increased genetic resistance to RHDV and strong population growth has been reported. Major histocompatibility complex (MHC) class I immune genes are important for immune responses against viruses, and a high MHC variability is thought to be crucial in adaptive processes under pathogen-driven selection. We asked whether strong population bottlenecks and presumed genetic drift would have led to low MHC variability in wild Australian rabbits, and if the retained MHC variability was enough to explain the increased resistance against RHD. Despite the past bottlenecks we found a relatively high number of MHC class I sequences distributed over 2-4 loci. We identified positive selection on putative antigen-binding sites of the MHC. We detected evidence for RHDV-driven selection as one MHC supertype was negatively associated with RHD survival, fitting expectations of frequency-dependent selection. Gene duplication and pathogen-driven selection are possible (and likely) mechanisms that maintained the adaptive potential of MHC genes in Australian rabbits. Our findings not only contribute to a better understanding of the evolution of invasive species, they are also important in the light of planned future rabbit biocontrol in Australia.}, language = {en} } @article{SchwensowCookeKovaliskietal.2014, author = {Schwensow, Nina I. and Cooke, Brian and Kovaliski, John and Sinclair, Ron and Peacock, David and Fickel, J{\"o}rns and Sommer, Simone}, title = {Rabbit haemorrhagic disease: virus persistence and adaptation in Australia}, series = {Evolutionary applications}, volume = {7}, journal = {Evolutionary applications}, number = {9}, publisher = {Wiley-Blackwell}, address = {Hoboken}, issn = {1752-4571}, doi = {10.1111/eva.12195}, pages = {1056 -- 1067}, year = {2014}, abstract = {In Australia, the rabbit haemorrhagic disease virus (RHDV) has been used since 1996 to reduce numbers of introduced European rabbits (Oryctolagus cuniculus) which have a devastating impact on the native Australian environment. RHDV causes regular, short disease outbreaks, but little is known about how the virus persists and survives between epidemics. We examined the initial spread of RHDV to show that even upon its initial spread, the virus circulated continuously on a regional scale rather than persisting at a local population level and that Australian rabbit populations are highly interconnected by virus-carrying flying vectors. Sequencing data obtained from a single rabbit population showed that the viruses that caused an epidemic each year seldom bore close genetic resemblance to those present in previous years. Together, these data suggest that RHDV survives in the Australian environment through its ability to spread amongst rabbit subpopulations. This is consistent with modelling results that indicated that in a large interconnected rabbit meta-population, RHDV should maintain high virulence, cause short, strong disease outbreaks but show low persistence in any given subpopulation. This new epidemiological framework is important for understanding virus-host co-evolution and future disease management options of pest species to secure Australia's remaining natural biodiversity.}, language = {en} }