Evolution of microparasites in spatially and genetically structured host populations: The example of RHDV infecting rabbits

Fouchet, David; Pendu, Jacques Le; Jean, Sébastien; Guiserix, Micheline; Marchandeau, Stéphane; Pontier, Dominique

doi:10.1016/j.jtbi.2008.11.021

Cited by 14 publications

(14 citation statements)

References 60 publications

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“…Since G2 strains appear to be the first pathogenic strains that circulated when emergence of RHDV was observed, acquisition of A antigen recognition by subsequent strains could have allowed a better coverage of the ABH diversity and targeting of the less susceptible and positively selected A+B− animals. Collectively, the data suggest that HBGA diversity tends to restrict the virus transmission and therefore to protect the host population, which is in accordance with the results of the models developed by Fouchet et al [44].…”

Section: Discussionsupporting

confidence: 91%

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Gall-Reculé²,

et al. 2011

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Rabbit Hemorrhagic disease virus (RHDV), a calicivirus of the Lagovirus genus, and responsible for rabbit hemorrhagic disease (RHD), kills rabbits between 48 to 72 hours post infection with mortality rates as high as 50–90%. Caliciviruses, including noroviruses and RHDV, have been shown to bind histo-blood group antigens (HBGA) and human non-secretor individuals lacking ABH antigens in epithelia have been found to be resistant to norovirus infection. RHDV virus-like particles have previously been shown to bind the H type 2 and A antigens. In this study we present a comprehensive assessment of the strain-specific binding patterns of different RHDV isolates to HBGAs. We characterized the HBGA expression in the duodenum of wild and domestic rabbits by mass spectrometry and relative quantification of A, B and H type 2 expression. A detailed binding analysis of a range of RHDV strains, to synthetic sugars and human red blood cells, as well as to rabbit duodenum, a likely gastrointestinal site for viral entrance was performed. Enzymatic cleavage of HBGA epitopes confirmed binding specificity. Binding was observed to blood group B, A and H type 2 epitopes in a strain-dependent manner with slight differences in specificity for A, B or H epitopes allowing RHDV strains to preferentially recognize different subgroups of animals. Strains related to the earliest described RHDV outbreak were not able to bind A, whereas all other genotypes have acquired A binding. In an experimental infection study, rabbits lacking the correct HBGA ligands were resistant to lethal RHDV infection at low challenge doses. Similarly, survivors of outbreaks in wild populations showed increased frequency of weak binding phenotypes, indicating selection for host resistance depending on the strain circulating in the population. HBGAs thus act as attachment factors facilitating infection, while their polymorphism of expression could contribute to generate genetic resistance to RHDV at the population level.

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Section: Discussionsupporting

confidence: 91%

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Gall-Reculé²,

et al. 2011

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“…Other non-climatic factors have also been suggested to contribute to the variable pattern of the impact of RHD in rabbit populations such as the timing of the breeding season, the presence of a related and protective RHDV-like calicivirus in rabbit populations or the negative interaction of the myxomatosis outbreaks in the populations [reviewed in [86]]. In addition, modelling studies indicated that population dynamics and spatial structure may greatly influence disease impact and host-virus co-evolution [87,88]. …”

Section: Epidemiologymentioning

confidence: 99%

Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review

Abrantes

Loo

Pendu

et al. 2012

Vet Res

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344

452

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Rabbit haemorrhagic disease virus (RHDV) is a calicivirus of the genus Lagovirus that causes rabbit haemorrhagic disease (RHD) in adult European rabbits (Oryctolagus cuniculus). First described in China in 1984, the virus rapidly spread worldwide and is nowadays considered as endemic in several countries. In Australia and New Zealand where rabbits are pests, RHDV was purposely introduced for rabbit biocontrol. Factors that may have precipitated RHD emergence remain unclear, but non-pathogenic strains seem to pre-date the appearance of the pathogenic strains suggesting a key role for the comprehension of the virus origins. All pathogenic strains are classified within one single serotype, but two subtypes are recognised, RHDV and RHDVa. RHD causes high mortality in both domestic and wild adult animals, with individuals succumbing between 48-72 h post-infection. No other species has been reported to be fatally susceptible to RHD. The disease is characterised by acute necrotising hepatitis, but haemorrhages may also be found in other organs, in particular the lungs, heart, and kidneys due to disseminated intravascular coagulation. Resistance to the disease might be explained in part by genetically determined absence or weak expression of attachment factors, but humoral immunity is also important. Disease control in rabbitries relies mainly on vaccination and biosecurity measures. Such measures are difficult to be implemented in wild populations. More recent research has indicated that RHDV might be used as a molecular tool for therapeutic applications. Although the study of RHDV and RHD has been hampered by the lack of an appropriate cell culture system for the virus, several aspects of the replication, epizootology, epidemiology and evolution have been disclosed. This review provides a broad coverage and description of the current knowledge on the disease and the virus.

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“…For rabbit haemorrhagic disease virus, Fouchet et al. () showed that host genetic diversity could contribute to the persistence of strains with widely varying virulence, ultimately favouring less virulent strains.…”

Section: Questions That Spatial Models Have Been Used To Answermentioning

confidence: 99%

Dynamic, spatial models of parasite transmission in wildlife: Their structure, applications and remaining challenges

White

Forester

Craft

2017

Journal of Animal Ecology

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Individual differences in contact rate can arise from host, group and landscape heterogeneity and can result in different patterns of spatial spread for diseases in wildlife populations with concomitant implications for disease control in wildlife of conservation concern, livestock and humans. While dynamic disease models can provide a better understanding of the drivers of spatial spread, the effects of landscape heterogeneity have only been modelled in a few well-studied wildlife systems such as rabies and bovine tuberculosis. Such spatial models tend to be either purely theoretical with intrinsic limiting assumptions or individual-based models that are often highly species- and system-specific, limiting the breadth of their utility. Our goal was to review studies that have utilized dynamic, spatial models to answer questions about pathogen transmission in wildlife and identify key gaps in the literature. We begin by providing an overview of the main types of dynamic, spatial models (e.g., metapopulation, network, lattice, cellular automata, individual-based and continuous-space) and their relation to each other. We investigate different types of ecological questions that these models have been used to explore: pathogen invasion dynamics and range expansion, spatial heterogeneity and pathogen persistence, the implications of management and intervention strategies and the role of evolution in host-pathogen dynamics. We reviewed 168 studies that consider pathogen transmission in free-ranging wildlife and classify them by the model type employed, the focal host-pathogen system, and their overall research themes and motivation. We observed a significant focus on mammalian hosts, a few well-studied or purely theoretical pathogen systems, and a lack of studies occurring at the wildlife-public health or wildlife-livestock interfaces. Finally, we discuss challenges and future directions in the context of unprecedented human-mediated environmental change. Spatial models may provide new insights into understanding, for example, how global warming and habitat disturbance contribute to disease maintenance and emergence. Moving forward, better integration of dynamic, spatial disease models with approaches from movement ecology, landscape genetics/genomics and ecoimmunology may provide new avenues for investigation and aid in the control of zoonotic and emerging infectious diseases.

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Evolution of microparasites in spatially and genetically structured host populations: The example of RHDV infecting rabbits

Cited by 14 publications

References 60 publications

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review

Dynamic, spatial models of parasite transmission in wildlife: Their structure, applications and remaining challenges

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