Early Stages of Rabbit Haemorrhagic Disease Virus Infection Monitored by Polymerase Chain Reaction

Guittré, Caroline; Ruvoën-Clouet, Nathalie; Barraud, Luc; Chérel, Y.; Baginski, I.; Prave, M.; Ganière, Jean‐Pierre; Trépo, Christian; Cova, Lucyna

doi:10.1111/j.1439-0450.1996.tb00294.x

Cited by 16 publications

(22 citation statements)

References 23 publications

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“…These cells could be a primary site of viral replication. This is in agreement with the fact that tracheitis is a frequent early sign of the disease (6,24,27). We were able to observe that both native and recombinant virus particles can attach to them through recognition of A or H type 2 antigens.…”

supporting

confidence: 75%

“…Death is the result of a widespread circulation dysfunction associated with disseminated intravascular coagulation and necrotizing hepatitis lesions (14,24). Large quantities of virus particles are found in several organs, especially the liver, which is considered the major site of virus replication (6,14,19,27). The viral genome consists of a single-stranded RNA of nearly 7.5 kb, packaged in a small icosahedral capsid (3,15).…”

mentioning

confidence: 99%

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Binding of Rabbit Hemorrhagic Disease Virus to Antigens of the ABH Histo-Blood Group Family

Ruvoën-Clouet

Ganière

André‐Fontaine

et al. 2000

J Virol

132

120

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The ability of rabbit hemorrhagic disease virus to agglutinate human erythrocytes and to attach to rabbit epithelial cells of the upper respiratory and digestive tracts was shown to depend on the presence of ABH blood group antigens. Indeed, agglutination was inhibited by saliva from secretor individuals but not from nonsecretors, the latter being devoid of H antigen. In addition, erythrocytes of the rare Bombay phenotype, which completely lack ABH antigens, were not agglutinated. Native viral particles from extracts of infected rabbit liver as well as virus-like particles from the recombinant virus capsid protein specifically bound to synthetic A and H type 2 blood group oligosaccharides. Both types of particles could attach to adult rabbit epithelial cells of the upper respiratory and digestive tracts. This binding paralleled that of anti-H type 2 blood group reagents and was inhibited by the H type 2-specific lectin UEA-I and polyacrylamide-conjugated H type 2 trisaccharide. Young rabbit tissues were almost devoid of A and H type 2 antigens, and only very weak binding of virus particles could be obtained on these tissues. Rabbit hemorragic disease virus (RHDV) is a noncultivablecalicivirus that infects rabbits and causes epidemics of an acute fatal hepatitis. The disease is characterized by high morbidity and mortality rates for adult animals. Death is the result of a widespread circulation dysfunction associated with disseminated intravascular coagulation and necrotizing hepatitis lesions (14, 24). Large quantities of virus particles are found in several organs, especially the liver, which is considered the major site of virus replication (6,14,19,27). The viral genome consists of a single-stranded RNA of nearly 7.5 kb, packaged in a small icosahedral capsid (3, 15). The capsid protein has an estimated molecular mass of 60 kDa (VP60) (16), and expression of the corresponding cDNA in insect cells infected with a recombinant baculovirus yields a protein that spontaneously assembles into virus-like particles (VLPs). These VLPs are both antigenically and morphologically similar to native RHDV particles (11,23). Yet very little is known about the pathogenesis of naturally occurring RHDV infections, and identification of the cellular receptor(s) used by the virus to establish infection would lead to a better understanding of the pathogenesis of RHDV.RHDV is known to agglutinate human erythrocytes (2, 25), and previous studies demonstrated that its hemagglutinin receptor on human red blood cells corresponds to a developmental antigen which is not expressed on fetal cells and is mainly carried by polyglycosylceramides (26). The glycolipid nature of the receptor on human red blood cells suggests that the carbohydrate moiety could be recognized by the virus capsid protein. Carbohydrate antigens of the histo-blood group family are developmental antigens that can be shared among various mammal species, and the presence of some of these antigens has been detected on epithelial cells of the rabbit digestive tract (1,17,21...

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supporting

confidence: 75%

mentioning

confidence: 99%

Binding of Rabbit Hemorrhagic Disease Virus to Antigens of the ABH Histo-Blood Group Family

Ruvoën-Clouet

Ganière

André‐Fontaine

et al. 2000

J Virol

132

120

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“…Specific primers ( Table 1) enabling amplification of the 3' end of the RHDV polymerase gene (POL) and the full capsid protein (VP60) gene were synthesised according to the primer sequences (4,5,15,21,22,25). The following thermal profiles were applied: 94°C for 3 min, 35 cycles of 94°C for 1 min, 55°C for 1 min, 72°C for 1 min, and a final extension at 72°C for 10 min.…”

Section: Methodsmentioning

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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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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“…This single-stranded nonenvelope RNA virus has a 7.5-kb genome and a 2.2 kb subgenome well packaged in a 27 to 35 nm (in diameter) icosahedral capsid with a major structural protein of about 60 kDa (VP60), and 10 peripheral cup-shaped depressions [12,20]. The ability to agglutinate human erythrocytes of group O, A, B and AB were reported [12,15,20].Detection by reverse transcriptase-polymerase chain reaction (RT-PCR) in a rabbit inoculation model showed that the RHDV RNA was present as early as 18 hr post inoculation (HPI) in the liver and spleen, whereas thymus, kidney, tonsil and lymph node were found to be positive after more than 26 HPI [21] or 36 HPI [9]. Liver was considered to be the major organ for RHDV replication [8,10].…”

mentioning

confidence: 99%

“…Detection by reverse transcriptase-polymerase chain reaction (RT-PCR) in a rabbit inoculation model showed that the RHDV RNA was present as early as 18 hr post inoculation (HPI) in the liver and spleen, whereas thymus, kidney, tonsil and lymph node were found to be positive after more than 26 HPI [21] or 36 HPI [9]. Liver was considered to be the major organ for RHDV replication [8,10].…”

mentioning

confidence: 99%

Impairment of Renal Function and Electrolyte Balance in Rabbit Hemoorhagic Disease

Chen

Chou

Liu

et al. 2008

The Journal of Veterinary Medical Science

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ABSTRACT. Rabbit hemorrhagic disease virus (RHDV) induced viral fulminant hepatitis in adult rabbits. We investigated the damage of renal function and electrolyte balance in experimentally infected rabbit by measuring the related serum parameters to elucidate the pathogenesis of RHDV as an index for medical treatment. Nineteen New Zealand White rabbits, ten females and nine males, were each intramuscularly inoculated with 0.5 ml 50% rabbit lethal dose (RLD 50 ) rabbit hemorrhagic disease virus. Blood samples were collected at 0 hr post inoculation (HPI) and every 6 hr from 18 HPI repeatedly through 66 HPI. After virus inoculation, serum blood urea nitrogen (BUN), creatinine (CREA) and sodium (Na + ) were elevated to a highly significant level (p<0.0001), whereas serum potassium (K + ) was moderately elevated to a significant level (p<0.05). Hypoglycemia developed highly significantly (p<0.0001). Serum chloride ion (Cl -) was the only parameter which did not change significantly (p=0.077). No significant sexual difference was observed among these parameters. Renal insufficiency progressed from 36 hr, as indicated by the increases in BUN and CREA; significant changes in electrolytes resulting in the increased osmolality of extracellular fluid that induced flow disturbance which consequently destroy the homeostasis in cells. Therefore, the later impairments in renal function and electrolyte balance might be an important threat for rabbits which might have survived from acute fulminant hepatitis in RHD. KEY WORDS: electrolyte balance, rabbit hemorrhagic disease virus, renal insufficiency, serum.J. Vet. Med. Sci. 70(9): 951-958, 2008 Rabbit hemorrhagic disease (RHD) was first reported in 1984 in the People's Republic of China [12] and widespread worldwide to Europe, Australia, Mexico, North Africa and New Zealand in the following years. In 1994, RHD was first recognized in Taiwan by Dr. Y. S. Lu through serological tests and was characterized by hemagglutination, electron microscopic examination, viral protein analysis and RT-PCR in 1998 [20]. The characteristic pathological signs for RHD were hemorrhages in the respiratory system, liver, spleen, cardiac muscle, and occasionally in the kidneys. Incubation period in rabbits is 2 to 3 days, morbidity approaches 100%, and mortality is sometimes over 90% in adults. The high morbidity and mortality rates have made RHD a big threat for rabbit industry and also a biological control tool for wild rabbit population. The causative virus, rabbit hemorrhagic disease virus (RHDV), was classified into the family Caliciviridae. This single-stranded nonenvelope RNA virus has a 7.5-kb genome and a 2.2 kb subgenome well packaged in a 27 to 35 nm (in diameter) icosahedral capsid with a major structural protein of about 60 kDa (VP60), and 10 peripheral cup-shaped depressions [12,20]. The ability to agglutinate human erythrocytes of group O, A, B and AB were reported [12,15,20].Detection by reverse transcriptase-polymerase chain reaction (RT-PCR) in a rabbit inoculation model showed t...

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Early Stages of Rabbit Haemorrhagic Disease Virus Infection Monitored by Polymerase Chain Reaction

Cited by 16 publications

References 23 publications

Binding of Rabbit Hemorrhagic Disease Virus to Antigens of the ABH Histo-Blood Group Family

Binding of Rabbit Hemorrhagic Disease Virus to Antigens of the ABH Histo-Blood Group Family

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Impairment of Renal Function and Electrolyte Balance in Rabbit Hemoorhagic Disease

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