Rabbit hemorrhagic disease: A review with special reference to its epizootiology

Mitro, Susanna D.; Krauss, H

doi:10.1007/bf00463093

Cited by 67 publications

(39 citation statements)

References 9 publications

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“…RHD kills more than 90% of adult rabbits 24-72 hours after their experimental inoculation with calicivirus (Ohlinger et al 1990;Shien et al 2000). The viral agent replicates in the liver, and induces a fulminant necrotic hepatitis that kills the animals (Marcato et al 1991;Mitro and Krauss 1993;Ferreira et al 2006a, b). Current views on the natural history of RHD are focused on the fulminant liver disease triggered by the virus (Ferreira et al 2006a, b).…”

Section: Introductionmentioning

confidence: 96%

Early acute depletion of lymphocytes in calicivirus-infected adult rabbits

et al. 2010

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Rabbit Haemorrhagic Disease (RHD) is a lethal infection caused by calicivirus that kills 90% of the infected adult rabbits within 3 days. The calicivirus replicates in the liver and causes a fulminant hepatitis. Most studies on the pathology of RHD have been focused on the fulminant liver disease. This may not be the only mechanism in the pathogenesis of RHD: calicivirus infection may also induce leukopenia in the infected adult rabbits. We show now by flow cytometry analysis that the calicivirus induces an early decrease in B and T cells, in both spleen and liver. The depletion of B and T cells was associated with apoptosis labelled by annexin V. These changes occurred in rabbits before they showed enzymatic evidence of liver damage and persisted after liver transaminase values were very high. We conclude that depletion of lymphocytes caused by the calicivirus infection precedes or attends liver damage. The relative contribution of this lymphocyte depletion for the pathogenesis of the fatal calicivirus infection of rabbits remains to be investigated.

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Section: Introductionmentioning

confidence: 96%

Early acute depletion of lymphocytes in calicivirus-infected adult rabbits

et al. 2010

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“…The origin and evolution of RHDV and its relationship to other caliciviruses, are of particular scientific interest [3,12,[25][26][27][28][29]. Two main hypotheses exist to explain the origin and the emergence of new RHDV variants: 1) evolution from pre-existing nonpathogenic viruses circulating in European leporids and 2) a species jump [30].…”

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confidence: 99%

Comparative analysis of rabbit hemorrhagic disease virus strains originating from outbreaks in the Russian Federation

et al. 2016

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Since the first introduction of rabbit hemorrhagic disease (RHD) in 1986, disease outbreaks have been continuously reported in different regions of Russia. Despite extensive vaccination, sporadic RHD cases are still reported. Here, we examine eleven RHDV strains originating from disease outbreaks occurring between 2003 and 2012 and one widely used vaccine strain. Notable phenotypic and genetic heterogeneity among RHDV strains was observed. The RHDV strains Tambov-2010, Perm-2010, Manihino-09 showed different hemagglutinating activity (HA) at 4 °C and room temperature. While all RHDV field strains were identified as hemagglutinating virulent viruses of the RHDVa variant, the vaccine strain was assigned as a "classical" RHDV. These data indicate that since 2003, RHDVa has become the predominant variant circulating in Russia.

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“…Two years later, rabbit hemorrhagic disease was also observed in New Zealand (14). The etiological agent was identified as a calicivirus (10), a positive-sense, singlestranded RNA virus which is antigenically related to European brown hare syndrome virus (12,16). The complete genome of the virus has been elucidated for the German isolate (9) and shown to comprise a single-stranded, positive-sense RNA genome of 7,437 nucleotides (nt).…”

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confidence: 99%

Recovery of Infectious Rabbit Hemorrhagic Disease Virus from Rabbits after Direct Inoculation with In Vitro-Transcribed RNA

Liu

Zhang

Zheng

et al. 2006

J Virol

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We report the first full-length infectious clone of strain JX/CHA/97 of rabbit hemorrhagic disease virus (RHDV). The transcripts from the full-length cDNA clones were infectious when they were directly injected into rabbits. The sequence of the virus recovered from the rabbits was identical to that of the injected RNA transcripts. The cDNA clone was engineered to contain one silent nucleotide change to create an EcoRV site (A to T at nucleotide 2908). The genetic marker was retained in the recovered progeny virus. The transfection of RNA transcripts into RK-13 cells resulted in the synthesis of viral antigens, indicating that the cDNA clones were replication competent. This stable infectious molecular clone should be an important tool for developing a better understanding of the molecular biology and pathogenesis of RHDV.

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Rabbit hemorrhagic disease: A review with special reference to its epizootiology

Cited by 67 publications

References 9 publications

Early acute depletion of lymphocytes in calicivirus-infected adult rabbits

Early acute depletion of lymphocytes in calicivirus-infected adult rabbits

Comparative analysis of rabbit hemorrhagic disease virus strains originating from outbreaks in the Russian Federation

Recovery of Infectious Rabbit Hemorrhagic Disease Virus from Rabbits after Direct Inoculation with In Vitro-Transcribed RNA

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