Myxomatosis in Australia and Europe: A model for emerging infectious diseases

Kerr, Peter J.

doi:10.1016/j.antiviral.2012.01.009

Cited by 156 publications

(200 citation statements)

References 249 publications

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“…Comparison of stocks of the original released virus with wild isolates showed clear attenuation; newer strains were associated with a more prolonged illness, potentially benefitting MYXV transmission, which involves mosquitos and other biting arthropods (10). However, the underlying molecular basis of MYXV attenuation has hitherto remained unclear.…”

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confidence: 99%

Evolutionary clash between myxoma virus and rabbit PKR in Australia

Burgess

Mohr

2016

Proc. Natl. Acad. Sci. U.S.A.

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The success of a virus in defeating or evading cellintrinsic immune responses contributes to its virulence, pathogenesis, and host range. A central tenet of virology holds that virus and host coevolve as each adapts to survive. Rarely, however, do we have the chance to observe this principal at play in the real world. The deliberate and repeated release of myxoma virus (MYXV) to control feral European rabbits introduced into Australia provides one such exceptional opportunity. Myxoma is a member of the poxvirus family, though unlike its more famous cousin variola, the agent of small pox, is unable to infect humans and is instead limited to infection of rabbits and hares. Following the release of a MYXV reference strain into the wild that exhibited 99.8% fatality rates in laboratory rabbits, attenuated strains were recovered from the field that had begun to outcompete the virulent parental strain. In addition, the resistance of rabbits to MYXV increased (1). The underlying molecular mechanism of both rabbit resistance and MYXV attenuation, however, remained elusive. Armed with the recently compiled genome sequence of 21 myxoma field isolates, a new study by Peng et al. in PNAS reveals that genetic alterations to the MYXV M156 protein correlate with both MYXV host specificity and changes in virulence observed in the field (2). Remarkably, more than 50% of MYXV field isolates produce an M156 variant that is no longer able to antagonize the rabbit double-stranded RNA (dsRNA)-activated protein kinase PKR, a critical component of IFN-stimulated defenses that controls protein synthesis. This not only provides the first mechanistic explanation for each of these facets of myxoma biology, but also elegantly illustrates the coevolution of host innate defense and viral virulence factors since the first release of MYXV in 1950.In response to virus infection, a key arm of antiviral host defenses acts to cripple the infected cell's capacity to produce the polypeptides required for virus replication and spread. This is achieved by globally inhibiting the initiation of mRNA translation and is triggered by accumulation of dsRNA, a pathogenassociated molecular pattern produced by many different viruses during their replication cycle. Upon sensing dsRNA, host PKR, which resides in uninfected cells as an inactive, unphosphorylated monomer, becomes activated as a phosphorylated dimer bound to dsRNA (Fig. 1). The ensuing site-specific phosphorylation of the eukaryotic translation initiation factor eIF2 α-subunit prevents methionine-initiator tRNA charging of 40S small ribosome subunits, inhibiting the initiation of protein synthesis and effectively preventing virus replication (3). The extraordinary efforts and diverse molecular tactics many different viruses rely upon to counteract PKR and preserve the activity of the critical initiation factor eIF2 underscore the significant role PKR plays in host defense.To safeguard eIF2 function and effectively contain PKR, viruses frequently enlist multiple molecular strategies. MYXV is no excep...

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confidence: 99%

Evolutionary clash between myxoma virus and rabbit PKR in Australia

Burgess

Mohr

2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Disease survival results in antibodies that are passed by the mothers as maternal antibodies to the embryo, further attenuating infections and disease early in the life of juveniles [17][18][19]. In contrast to RHD, juveniles infected with MYXV have a lower chance of survival than infected adults [27]. This fundamental difference in age-dependent host-virus interactions for these two virus species could influence seasonality of disease outbreaks.…”

Section: Introductionmentioning

confidence: 99%

“…MYXV and later RHDV were released into Australia as biocontrol agents against rabbits, and both led to large reductions in rabbit populations shortly after their release (in the 1950s and 1990s, respectively). Both viruses spread quickly over large geographical areas, most likely through arthropod vectors [27,31]. While RHDV can be classified at a global scale into distinct genotypes, all genotypes identified in Australia originated from the Czech (genogroup 2) genotype [32], upon which our model is based.…”

Section: Study System: Rabbits In Australiamentioning

confidence: 99%

“…Infected rabbits were assumed to recover from disease with recovery rates (g V ) of adults (more than 90 days old) sampled across a range of possible values. We modelled recovery rates of juveniles (less than or equal to 90 days old) with logistic logit-link regression models to account for increasing susceptibility of juveniles to clinical RHD [18] and increasing recovery rates for myxomatosis [27]. For this, we assumed the decrease in juvenile recovery rates from RHD to follow a continuous decrease from 100% after the insusceptibility period towards a rate of recovery typical for adults, which we determined by sampling values of the regression slope a Juv,RHD of a logistic model.…”

Section: Coupling Of Individual-based Epidemiological and Demographicmentioning

confidence: 99%

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Timing and severity of immunizing diseases in rabbits is controlled by seasonal matching of host and pathogen dynamics

Wells

Brook

Lacy

et al. 2015

J. R. Soc. Interface.

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Infectious diseases can exert a strong influence on the dynamics of host populations, but it remains unclear why such disease-mediated control only occurs under particular environmental conditions. We used 16 years of detailed field data on invasive European rabbits (Oryctolagus cuniculus) in Australia, linked to individual-based stochastic models and Bayesian approximations, to test whether (i) mortality associated with rabbit haemorrhagic disease (RHD) is driven primarily by seasonal matches/mismatches between demographic rates and epidemiological dynamics and (ii) delayed infection (arising from insusceptibility and maternal antibodies in juveniles) are important factors in determining disease severity and local population persistence of rabbits. We found that both the timing of reproduction and exposure to viruses drove recurrent seasonal epidemics of RHD. Protection conferred by insusceptibility and maternal antibodies controlled seasonal disease outbreaks by delaying infection; this could have also allowed escape from disease. The persistence of local populations was a stochastic outcome of recovery rates from both RHD and myxomatosis. If susceptibility to RHD is delayed, myxomatosis will have a pronounced effect on population extirpation when the two viruses coexist. This has important implications for wildlife management, because it is likely that such seasonal interplay and disease dynamics has a strong effect on long-term population viability for many species.

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“…In European rabbits, the virus causes the disease myxomatosis. Infected rabbits develop skin tumours and usually die within 8-12 days [12]. This virus was intentionally released in Australia and France in the 1950s and led to dramatic reductions of rabbit populations in these countries and other European nations.…”

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Cats, Rabbits, Birds, and Viruses, Oh My! Modelling the Conservative Implications of a Complex Virus Release in a Predator-Prey System

Soucy¹

2017

SIURO

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Abstract. Mathematical models have proven useful in planning conservation efforts for threatened species. In this paper, we develop a model based on the Macquarie Island ecosystem, where native seabirds were threatened by invasive pest species. In particular, European rabbits (Oryctolagus cuniculus) destroyed seabird nesting sites, while feral cats (Felis catus) preferentially hunted rabbits but also consumed seabirds. Management strategies included releasing a rabbit-killing disease and shooting feral cats. We investigate the interactions between species in the ecosystem as well as conservation practices using analytical techniques such as the basic reproductive ratio (R 0 ) and partial rank correlation coefficient analysis. The results of this study reveal that the important factors to disease establishment change depending on the ecological interactions present in the system. Additionally, we show that the interaction between disease and predation sometimes produces surprising outcomes. Overall, the results of the study demonstrate the need for mathematical modelling in the conservation process in order to anticipate the complex responses of an ecosystem to management practices. We conclude with a brief list of considerations for conservation planners dealing with ecologically complex systems in the future.

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Myxomatosis in Australia and Europe: A model for emerging infectious diseases

Cited by 156 publications

References 249 publications

Evolutionary clash between myxoma virus and rabbit PKR in Australia

Evolutionary clash between myxoma virus and rabbit PKR in Australia

Timing and severity of immunizing diseases in rabbits is controlled by seasonal matching of host and pathogen dynamics

Cats, Rabbits, Birds, and Viruses, Oh My! Modelling the Conservative Implications of a Complex Virus Release in a Predator-Prey System

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