Seroconversion in an industrial unit of rabbits infected with a non‐pathogenic rabbit haemorrhagic disease‐like virus

Capucci, Lorenzo; Nardin, Alessandra; Llombart‐Bosch, Antonio

doi:10.1136/vr.140.25.647

Cited by 67 publications

(76 citation statements)

References 11 publications

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“…In other words, these RCV-like viruses have not recently given rise to RHDV. However, the circulation of these RCV-like viruses, probably in an oral-fecal cycle with a gut tropism (3,35), does explain the detection of antibodies in sera stored prior to 1984 that react with RHDV and in rabbits that had never been exposed to RHDV (3,4,21,26,27,31,32). It can be assumed that these viruses spread to Australia and New Zealand in wild and/or domestic rabbits introduced from the United Kingdom.…”

Section: Discussionmentioning

confidence: 99%

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Origin and Phylodynamics of Rabbit Hemorrhagic Disease Virus

Kerr

Kitchen

Holmes

2009

J Virol

102

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To determine the origin, phylogenetic relationships, and evolutionary dynamics of rabbit hemorrhagic disease virus (RHDV), we examined 210 partial and complete capsid gene nucleotide sequences. Using a Bayesian Markov chain Monte Carlo approach, we estimated that these sequences evolved at a rate of 3.9 ؋ 10 ؊4 to 11.9 ؋ 10 ؊4 nucleotide substitutions per site per year. This rate was consistent across subsets of data, was robust in response to recombination, and casts doubt on the provenance of viral strains isolated from the 1950s to the 1970s, which share strong sequence similarity to modern isolates. Using the same analysis, we inferred that the time to the most recent common ancestor for a joint group of RHDV and rabbit calicivirus sequences was <550 years ago and was <150 years ago for the RHDV isolates that have spread around the world since 1984. Importantly, multiple lineages of RHDV were clearly circulating before the major Chinese outbreak of 1984, a finding indicative of an early evolution of RHDV virulence. Four phylogenetic groups within RHDV were defined and analyzed separately. Each group shared a common ancestor in the mid-1960s or earlier, and each showed an expansion of populations starting before 1984. Notably, the group characterized by the antigenic variant RHDVa harbors the greatest genetic diversity, compatible with an elevated fitness. Overall, we contend that the high virulence of RHDV likely evolved once in the early part of the 20th century, well before the documented emergence of rabbit hemorrhagic disease in 1984.

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Section: Discussionmentioning

confidence: 99%

“…In some cases immunity to these viruses may provide a degree of cross-protection against virulent RHDV (3,4,7,21,27,29,31,32). Sequence data has been published for three of these avirulent viruses: from commercial rabbits in Italy (3), from wild rabbits on Lambay Island in Ireland (15), and from wild rabbits in Australia (35).…”

mentioning

confidence: 99%

Origin and Phylodynamics of Rabbit Hemorrhagic Disease Virus

Kerr

Kitchen

Holmes

2009

J Virol

102

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“…The first possibility was eliminated when it was shown that the viruses causing disease in rabbits and hares were related but distinctly different caliciviruses. The second possibility seemed more likely because antibodies that cross-reacted with RHDV were detected in rabbit sera collected in the Czech Republic 12 years before the first outbreaks (Rodak et al 1990), and Capucci et al (1994Capucci et al ( , 1997 showed that seroconversion occurred in asymptomatic rabbits in some rabbitries where RHD had never been seen.…”

Section: Origin Of the Virusmentioning

confidence: 99%

Rabbit haemorrhagic disease and the biological control of wild rabbits, Oryctolagus cuniculus, in Australia and New Zealand

Cooke¹,

Fenner²

2002

Wildl. Res.

123

124

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This review considers the history of the discovery of the rabbit haemorrhagic disease virus (RHDV) and its spread throughout the world in domestic and wild rabbits, which led eventually to its deliberate release into Australia and New Zealand for the control of a major pest, the introduced wild rabbit. The physical and genetic structure of RHDV is now well understood, and its pathogenic effects are also well known. The epidemiology of rabbit haemorrhagic disease (RHD) has been clearly documented in the field in European countries, Australia and New Zealand. Since its initial spread through largely naïve populations of wild rabbits it has established a pattern of mainly annual epizootics in most areas. The timing of epizootics is dependent on climatic variables that determine when rabbits reproduce and the appearance of new, susceptible rabbits in the population. The activity of RHDV is also influenced by climatic extremes that presumably affect its persistence and the behaviour of insect vectors, and evidence is growing that pre-existing RHDV-like viruses in some parts of Australia may interact with RHDV, reducing its effectiveness. The timing of epizootics is further modified by the resistance to RHD shown by young rabbits below 5 weeks of age and the presence of protective maternal antibodies that also protect against fatal RHD. RHD has reduced rabbit abundance, particularly in dry regions, but rabbits in cooler, high-rainfall areas have been able to maintain their populations. In Australia and New Zealand, RHD has raised the prospects for managing rabbits in low rainfall areas and brought substantial economic and environmental benefits.

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“…Such non-pathogenic strains are also suspected to occur in Australia and New Zealand, where RHD was introduced in 1995 and 1997, respectively as a control agent of rabbit populations [14,27,29,32]. The only known non-pathogenic calicivirus closely related to RHDV, called Rabbit calicivirus (RCV), was identified in the intestine of domestic rabbits in Italy [7,8]. RCV can be distinguished from the RHDV by its tissue tropism, viral titre and the sequence of the capsid protein.…”

Section: Introductionmentioning

confidence: 99%

Serological evidence for a non-protective RHDV-like virus

et al. 2005

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-The data were recorded during a Rabbit haemorrhagic disease outbreak that occurred in France in 2001 in a wild population of rabbits that we have been monitoring since 2000. These data suggested the existence of non-protective antibodies due to a putative RHDV-like virus. Twentyone blood and 22 liver samples were taken from the 26 corpses of recently dead rabbits that were found. RHDV was found in all liver samples. A first screening for RHD antibodies, carried out using an ELISA based on the detection of VP60-RHDV antigen, showed that 20 of the rabbits were seropositive. Moreover, we determined antibody titres for 13 of these 20 seropositive samples. All were ≥ 1/400. Such titres normally indicate antibody levels sufficient to confer protection to all known RHDV or RHDV-like strains. For 16 samples, we determined whether these rabbits had died of a chronic or an acute form of the disease, by employing monoclonal antibody (Mabs) -based differential ELISA. All had died of an acute form of RHD. Because the antibodies detected by this VP60-ELISA test are known to appear 5-6 days after infection and since acute RHD generally kills the rabbits 2-3 days after infection, we assumed that the detected antibodies must have been present before the exposure to the virus that killed these rabbits. A second detection of antibodies was made with Mabs that are specific for RHDV. The results were negative, showing that the antibodies detected with the VP60 ELISA test were not specific for RHDV. We sequenced a portion of the VP60 gene of viruses isolated in 17 rabbits. All RHDV isolates were very similar to the RHDV strains commonly isolated in France during this period, suggesting that this viral strain was not a putative variant that is not neutralised by antibodies. Therefore we conclude that the detected antibodies were probably due to a RHDV-like virus that induces the production of detectable but non-protective antibodies.

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Seroconversion in an industrial unit of rabbits infected with a non‐pathogenic rabbit haemorrhagic disease‐like virus

Cited by 67 publications

References 11 publications

Origin and Phylodynamics of Rabbit Hemorrhagic Disease Virus

Origin and Phylodynamics of Rabbit Hemorrhagic Disease Virus

Rabbit haemorrhagic disease and the biological control of wild rabbits, Oryctolagus cuniculus, in Australia and New Zealand

Serological evidence for a non-protective RHDV-like virus

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