Detection of a new variant of rabbit haemorrhagic disease virus in France

Gall-Reculé, Ghislaine Le; Zwingelstein, F.; Boucher, Samuel; Normand, Bernadette Le; Plassiart, G.; Portejoie, Y.; Decors, Anouk; Bertagnoli, Stéphane; Guérin, Jl; Marchandeau, Stéphane

doi:10.1136/vr.d697

Cited by 187 publications

(219 citation statements)

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“…Evidence of this is the emergence of the decreasingly homogenous new strains with altered antigenic and genetic features, showing different tropism and pathogenicity for the target species. The strains detected in relatively short period of time, which demonstrate new characteristics, vide phenotypic HA-negative RHDV variant, antigenic and genetic RHDVa variants, and the new American and French RHDV variants, are examples of this phenomenon (5,6,8,17,24,27,34,36). This may be due to the effect of environment, the use of vaccination, or the process of evolution.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown the presence of the classic form of RHDV strains with an altered haemagglutination (HA) profile (phenotypic HAnegative variant), RHDV strains known as antigenic and genetic variants (RHDVa), a moderately pathogenic calicivirus (MRCV), a recently new French RHDV variant, and non-pathogenic caliciviruses (RCV, RCV-A1, Lambay, 06-11) (1,4,5,6,24,26,27,34,36). Pathogenic RHDV and RHDVa isolates belong to one serotype (2,3,10,36).…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Fitzner

2014

Bulletin of the Veterinary Institute in Pulawy

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The field outbreak of RHD that occurred late summer 2012 on a small-scale rabbit-rearing operation in Poland and the usefulness of techniques for RHD virus diagnosis are described. During the epizootic, the overall mortality rate of rabbits older than two months was 77%. Eight liver specimens collected from dead unvaccinated rabbits (aged 3-5 months) underwent virological examinations. RHDV specific antigen was detected in two out of eight liver homogenates by haemagglutination (HA) test and ELISA, one of the two being negative in HA assay. However the presence of genetic material of RHD virus was confirmed by RT-PCR and real-time RT-PCR in all liver samples tested. Based on antigen reactivity in ELISA and sequencing of PCR amplicons of the VP60 gene, the RHDVa subtype strain was identified as the cause of infection. The partial genome sequence of a field isolate (STR 2012), comprising the C-terminus of the polymerase gene and the full capsid protein gene, revealed 91% nucleotide homology to reference FRG89 RHDV isolate and 97% to strain Triptis representing the RHDVa variant. Serological evidence of an RHD outbreak in the STR rabbit-rearing operation was confirmed in a serum sample collected from an unvaccinated surviving rabbit. A cross-reactivity examination of RHDV positive serum revealed a decrease in HI titre against the STR 2012 field antigen, and a decrease in the RHDVa control antigen as compared to classic RHDV.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Fitzner

2014

Bulletin of the Veterinary Institute in Pulawy

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“…For example, a semipathogenic lagovirus (Michigan rabbit calicivirus [MRCV]) isolated in Michigan, USA, reportedly targets the liver but had a lower mortality rate (32.5%) (44,45). More recently, a new genetically distinct variant, RHDV2 (RHDVb), has emerged; it was first reported in France and Spain in 2010 (46,47). Interestingly, early reports describe this virus as moderately virulent, with case fatality rates ranging from 0% to 75% in one small study (48).…”

Section: Figmentioning

confidence: 99%

Benign Rabbit Caliciviruses Exhibit Evolutionary Dynamics Similar to Those of Their Virulent Relatives

Mahar

Nicholson

Eden

et al. 2016

J Virol

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Two closely related caliciviruses cocirculate in Australia: rabbit hemorrhagic disease virus (RHDV) and rabbit calicivirus Australia 1 (RCV-A1). RCV-A1 causes benign enteric infections in the European rabbit (Oryctolagus cuniculus) in Australia and New Zealand, while its close relative RHDV causes a highly pathogenic infection of the liver in the same host. The comparison of these viruses provides important information on the nature and trajectory of virulence evolution, particularly as highly virulent strains of RHDV may have evolved from nonpathogenic ancestors such as RCV-A1. To determine the evolution of RCV-A1 we sequenced the full-length genomes of 44 RCV-A1 samples isolated from healthy rabbits and compared key evolutionary parameters to those of its virulent relative, RHDV. Despite their marked differences in pathogenicity and tissue tropism, RCV-A1 and RHDV have evolved in a very similar manner. Both viruses have evolved at broadly similar rates, suggesting that their dynamics are largely shaped by high background mutation rates, and both exhibit occasional recombination and an evolutionary environment dominated by purifying selection. In addition, our comparative analysis revealed that there have been multiple changes in both virulence and tissue tropism in the evolutionary history of these and related viruses. Finally, these new genomic data suggest that either RCV-A1 was introduced into Australia after the introduction of myxoma virus as a biocontrol agent in 1950 or there was drastic reduction of the rabbit population, and hence of RCV-A1 genetic diversity, perhaps coincident with the emergence of myxoma virus. IMPORTANCEThe comparison of closely related viruses that differ profoundly in propensity to cause disease in their hosts offers a powerful opportunity to reveal the causes of changes in virulence and to study how such changes alter the evolutionary dynamics of these pathogens. Here we describe such a novel comparison involving two closely related RNA viruses that cocirculate in Australia, the highly virulent rabbit hemorrhagic disease virus (RHDV) and the nonpathogenic rabbit calicivirus Australia 1 (RCV-A1). Both viruses infect the European rabbit, but they differ in virulence, tissue tropism, and mechanisms of transmission. Surprisingly, and despite these fundamental differences, RCV-A1 and RHDV have evolved at very similar (high) rates and with strong purifying selection. Furthermore, candidate key mutations were identified that may play a role in virulence and/or tissue tropism and therefore warrant further investigation. R evealing the factors that determine the evolution of virulence in viruses and identifying how changes in virulence might impact viral evolutionary dynamics are key queries in the study of infectious disease evolution. Although there is a large body of work on revealing the relationship between virulence and transmissibility, most studies of virulence evolution involve the retrospective analysis of single viruses (1-4). However, the comparison of closely related...

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“…Until recently, only one serotype was circulating (20); however, it seems possible that a new serotype (termed RHDVb or RHDV2) has emerged (7,9,15,21). Significantly, the original RHDV vaccine has been reported to have low or no efficacy against RHDVb (7,8).…”

Section: Discussionmentioning

confidence: 99%

“…A vaccine for RHDV was introduced in the 1990s (6), and this provided good coverage for the strains circulating at that time and up until recently (reviewed in reference 5). However, atypical RHD outbreaks in vaccinated rabbits and with high mortalities in young rabbits appear to be changing the epidemiological panorama of this disease, which coincided with the emergence and spread of a new variant RHDV (7)(8)(9).…”

mentioning

confidence: 99%

Structural Analysis of a Rabbit Hemorrhagic Disease Virus Binding to Histo-Blood Group Antigens

Leuthold

Dalton

Hansman

2015

J Virol

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Rabbit hemorrhagic disease virus (RHDV) is a member of the Caliciviridae family (Lagovirus genus). RHDV is highly contagious and attaches to epithelial cells in the digestive or respiratory tract, leading to massive lesions with high mortality rates. A new variant of RHDV (termed RHDVb) recently has emerged, and previously vaccinated rabbits appear to have little protection against this new strain. Similar to human norovirus (Caliciviridae, Norovirus genus), RHDV binds histo-blood group antigens (HBGAs), and this is thought to be important for infection. Here, we report the HBGA binding site on the RHDVb capsid-protruding domain (P domain) using X-ray crystallography. The HBGA binding pocket was located in a negatively charged patch on the side of the P domain and at a dimeric interface. Residues from both monomers contributed to the HBGA binding and involved a network of direct hydrogen bonds and water-mediated interactions. An amino acid sequence alignment of different RHDV strains indicated that the residues directly interacting with the ABH-fucose of the HBGAs (Asp472, Asn474, and Ser479) were highly conserved. This result suggested that different RHDV strains also could bind HBGAs at the equivalent pocket. Moreover, several HBGA binding characteristics between RHDVb and human genogroup II norovirus were similar, which indicated a possible convergent evolution of HBGA binding interactions. Further structural studies with other RHDV strains are needed in order to better understand the HBGA binding mechanisms among the diverse RHDV strains. IMPORTANCEWe identified, for the first time, the HBGA binding site on an RHDVb P domain using X-ray crystallography. Our results showed that RHDVb and human genogroup II noroviruses had similar HBGA binding interactions. Recently, it was discovered that synthetic HBGAs or HBGA-expressing enteric bacteria could enhance human genogroup II norovirus infection in B cells. Considering that RHDVb and genogroup II norovirus similarly interacted with HBGAs, it may be possible that a comparable cell culture system also could work with RHDVb. Taken together, these new findings will extend our understanding of calicivirus HBGA interactions and may help to elucidate the specific roles of HBGAs in calicivirus infections. Rabbit hemorrhagic disease (RHD) was first reported in China in 1984 (1), and the etiological agent, rabbit hemorrhagic disease virus (RHDV; Caliciviridae family, Lagovirus genus), was identified subsequently (2-4). RHDV is highly contagious and is endemic in several countries with wild rabbit populations. The virus attaches to epithelial cells in the digestive or respiratory tract and can lead to massive lesions in the liver, trachea, and lungs of adult rabbits. High mortality rates in the range of 90% can lead to a drastic decimation of rabbit populations (reviewed in reference 5), which is an ecological threat and economic burden. A vaccine for RHDV was introduced in the 1990s (6), and this provided good coverage for the strains circulating at that time and ...

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Detection of a new variant of rabbit haemorrhagic disease virus in France

Cited by 187 publications

References 3 publications

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Benign Rabbit Caliciviruses Exhibit Evolutionary Dynamics Similar to Those of Their Virulent Relatives

Structural Analysis of a Rabbit Hemorrhagic Disease Virus Binding to Histo-Blood Group Antigens

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