Rabbit Hemorrhagic Disease

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Francisco Parra - One of the best experts on this subject based on the ideXlab platform.

  • full genomic analysis of new variant Rabbit Hemorrhagic Disease virus revealed multiple recombination events
    Journal of General Virology, 2015
    Co-Authors: Kevin P. Dalton, Francisco Parra, Ana M. Lopes, Maria J. Magalhães, Pedro J. Esteves, Edward C. Holmes, Joana Abrantes
    Abstract:

    Rabbit Hemorrhagic Disease virus (RHDV), a Lagovirus of the family Caliciviridae, causes Rabbit Hemorrhagic Disease (RHD) in the European Rabbit (Oryctolagus cuniculus). The Disease was first documented in 1984 in China and rapidly spread worldwide. In 2010, a new RHDV variant emerged, tentatively classified as ‘RHDVb’. RHDVb is characterized by affecting vaccinated Rabbits and those <2 months old, and is genetically distinct (~20 %) from older strains. To determine the evolution of RHDV, including the new variant, we generated 28 full-genome sequences from samples collected between 1994 and 2014. Phylogenetic analysis of the gene encoding the major capsid protein, VP60, indicated that all viruses sampled from 2012 to 2014 were RHDVb. Multiple recombination events were detected in the more recent RHDVb genomes, with a single major breakpoint located in the 5′ region of VP60. This breakpoint divides the genome into two regions: one that encodes the non-structural proteins and another that encodes the major and minor structural proteins, VP60 and VP10, respectively. Additional phylogenetic analysis of each region revealed two types of recombinants with distinct genomic backgrounds. Recombinants always include the structural proteins of RHDVb, with non-structural proteins from non-pathogenic lagoviruses or from pathogenic genogroup 1 strains. Our results show that in contrast to the evolutionary history of older RHDV strains, recombination plays an important role in generating diversity in the newly emerged RHDVb.

  • Full genomic analysis of new variant Rabbit Hemorrhagic Disease virus revealed multiple recombination events.
    Journal of General Virology, 2015
    Co-Authors: Ana M. Lopes, Kevin P. Dalton, Francisco Parra, Maria J. Magalhães, Pedro J. Esteves, Edward C. Holmes, Joana Abrantes
    Abstract:

    Rabbit Hemorrhagic Disease virus (RHDV), a Lagovirus of the family Caliciviridae, causes Rabbit Hemorrhagic Disease (RHD) in the European Rabbit (Oryctolagus cuniculus). The Disease was first documented in 1984 in China and rapidly spread worldwide. In 2010, a new RHDV variant emerged, tentatively classified as ‘RHDVb’. RHDVb is characterized by affecting vaccinated Rabbits and those

  • Complete genome sequence of two Rabbit Hemorrhagic Disease virus variant b isolates detected on the Iberian Peninsula
    Archives of virology, 2015
    Co-Authors: Kevin P. Dalton, Inés Nicieza, Ángel L. Álvarez, Ana M. Lopes, Pedro J. Esteves, Joana Abrantes, Francisco Parra
    Abstract:

    We report the complete genome sequences of two isolates (RHDV-N11 and CBVal16) of variant Rabbit Hemorrhagic Disease virus (RHDVb). Isolate N11 was detected in young domestic animals during a Rabbit Hemorrhagic Disease (RHD) outbreak that occurred in 2011 on a Rabbit farm in Navarra, Spain, while CBVal16 was isolated from a wild Rabbit found dead in Valpacos, Northern Portugal, a year later. The viral sequences reported show 84.8–85.1 % and 78.3–78.5 % identity to RHDVAst/89 and RCV-A1 MIC-07, representative members of the pathogenic genogroup 1 RHDV and apathogenic Rabbit calicivirus, respectively. In comparison with other RHDV isolates belonging to the previously known genogroups 1–6, RHDVb shows marked phenotypic differences, as it causes Disease preferentially in young Rabbits under 40 days of age and shows modified red blood cell agglutination profiles as well as antigenic differences that allow this variant to escape protection by the currently available vaccines.

  • Variant Rabbit Hemorrhagic Disease virus in young Rabbits, Spain.
    Emerging Infectious Diseases, 2012
    Co-Authors: Kevin P. Dalton, Inés Nicieza, Ana Balseiro, María A. Muguerza, J. M. Rosell, Rosa Casais, Ángel L. Álvarez, Francisco Parra
    Abstract:

    Outbreaks of Rabbit Hemorrhagic Disease have occurred recently in young Rabbits on farms on the Iberian Peninsula where Rabbits were previously vaccinated. Investigation identified a Rabbit Hemorrhagic Disease virus variant genetically related to apathogenic Rabbit caliciviruses. Improved antivirus strategies are needed to slow the spread of this pathogen.

  • Molecular and antigenic characterization of Rabbit Hemorrhagic Disease virus isolated in Cuba indicates a distinct antigenic subtype
    Archives of virology, 2007
    Co-Authors: Omar Farnos, Francisco Parra, Ricardo Lleonart, D Rodrı́guez, Odaysa Valdés, M. Chiong, Jorge R. Toledo, Erlinda Fernández, Marisela Suárez
    Abstract:

    Phylogenetic analyses conducted on isolates of Rabbit Hemorrhagic Disease virus (RHDV) from throughout the world have shown well-defined genogroups comprising representative strains of the virus and antigenic variants. In this work, we have isolated and characterized RHDV from the major epizootic that occurred in Cuba in 2004–2005. Sequence analysis of the capsid protein gene and antigenic characterization of this strain has allowed its inclusion as a member of the distinct RHDVa subtype. We also found that specific antibodies directed against RHDV reference strains bound to the Cuban isolate in a competition ELISA and inhibited virus hemagglutination in vitro. This is the second report on the molecular characterization of RHDVa circulating in the American region.

Joséantonio Boga - One of the best experts on this subject based on the ideXlab platform.

  • Horizontal Transmissible Protection against Myxomatosis and Rabbit Hemorrhagic Disease by Using a Recombinant Myxoma Virus
    Journal of virology, 2000
    Co-Authors: Juan Bárcena, Francisco Parra, Joséantonio Boga, Mónica Morales, Belén Vázquez, Javier Lucientes, Albert Pagès-manté, José Manuel Sánchez-vizcaíno, Rafael Blasco, Juan María Torres
    Abstract:

    We have developed a new strategy for immunization of wild Rabbit populations against myxomatosis and Rabbit Hemorrhagic Disease (RHD) that uses recombinant viruses based on a naturally attenuated field strain of myxoma virus (MV). The recombinant viruses expressed the RHDV major capsid protein (VP60) including a linear epitope tag from the transmissible gastroenteritis virus (TGEV) nucleoprotein. Following inoculation, the recombinant viruses induced specific antibody responses against MV, RHDV, and the TGEV tag. Immunization of wild Rabbits by the subcutaneous and oral routes conferred protection against virulent RHDV and MV challenges. The recombinant viruses showed a limited horizontal transmission capacity, either by direct contact or in a flea-mediated process, promoting immunization of contact uninoculated animals.

  • Immunization with Potato Plants Expressing VP60 Protein Protects against Rabbit Hemorrhagic Disease Virus
    Journal of virology, 1999
    Co-Authors: S. Castañón, Joséantonio Boga, M. S. Marin, José M. Martín-alonso, Ricardo J. Ordás, R. Casais, Jaime M. Humara, Francisco Parra
    Abstract:

    The major structural protein VP60 of Rabbit Hemorrhagic Disease virus (RHDV) has been produced in transgenic potato plants under the control of a cauliflower mosaic virus 35S promoter or a modified 35S promoter that included two copies of a strong transcriptional enhancer. Both types of promoters allowed the production of specific mRNAs and detectable levels of recombinant VP60, which were higher for the constructs carrying the modified 35S promoter. Rabbits immunized with leaf extracts from plants carrying this modified 35S promoter showed high anti-VP60 antibody titers and were fully protected against the Hemorrhagic Disease.

  • expression of enzymatically active Rabbit Hemorrhagic Disease virus rna dependent rna polymerase in escherichia coli
    Journal of Virology, 1998
    Co-Authors: Ana Lopez Vazquez, Rosa Casais, Joséantonio Boga, J. M. Martin Alonso, Francisco Parra
    Abstract:

    The Rabbit Hemorrhagic Disease virus (RHDV) (isolate AST/89) RNA-dependent RNA-polymerase (3Dpol) coding region was expressed in Escherichia coli by using a glutathione S-transferase-based vector, which allowed milligram purification of a homogeneous enzyme with an expected molecular mass of about 58 kDa. The recombinant polypeptide exhibited rifampin- and actinomycin D-resistant, poly(A)-dependent poly(U) polymerase. The enzyme also showed RNA polymerase activity in in vitro reactions with synthetic RHDV subgenomic RNA in the presence or absence of an oligo(U) primer. Template-size products were synthesized in the oligo(U)-primed reactions, whereas in the absence of added primer, RNA products up to twice the length of the template were made. The double-length RNA products were double stranded and hybridized to both positive- and negative-sense probes.

  • Programmed cell death in the pathogenesis of Rabbit Hemorrhagic Disease.
    Archives of virology, 1998
    Co-Authors: Covadonga Alonso, Joséantonio Boga, José M. Martín-alonso, J.m. Oviedo, E. Díaz, Francisco Parra
    Abstract:

    Rabbit Hemorrhagic Disease is a rapidly lethal infection caused by a calicivirus, characterized by acute liver damage and disseminated intravascular coagulation (DIC). Following morphological criteria and using a specific in situ labeling technique, we have found that liver cell death induced upon infection is due to apoptosis, and that programmed cell death is a constant feature in Rabbits experimentally infected with RHDV. The process affected mainly hepatocytes, but also macrophages and endothelial cells presented morphologic hallmarks of apoptosis, expressing all these cell types viral antigens as determined by immunohistochemistry. The occurrence of programmed cell death was correlated with the appearance of the RHDV induced pathology in tissues by DNA fragmentation detection in situ. Hepatocyte apoptosis produced extensive parenchymal destruction causing a lethal, acute fulminant hepatitis that is characteristic of RHD. Apoptosis of intravascular monocytes and endothelial cells was observed together with fibrin thrombi in blood vessels. Since apoptotic cells are known sites of enhanced procoagulant activity, apoptosis of these cell populations might constitute a first step in the pathogenesis of DIC and a common pathway to other viral Hemorrhagic fevers. In conclusion, apoptosis in RHD may be determinant in the development of the pathogenesis of this Disease.

  • Processing of Rabbit Hemorrhagic Disease virus polyprotein.
    Journal of virology, 1996
    Co-Authors: J. M. Martin Alonso, Rosa Casais, Joséantonio Boga, Francisco Parra
    Abstract:

    Expression of Rabbit Hemorrhagic Disease virus (RHDV) cDNAs in vitro with Rabbit reticulocyte lysates and in Escherichia coli have been used to study the proteolytic processing of RHDV polyprotein encoded by ORF1. An epitope tag was used for monitoring the gene products by a specific antibody. We have identified four gene products with molecular masses of 80, 43, 73, and 60 kDa, from the amino to the carboxy terminus of the polyprotein. The amino-terminal sequences of the 43- and 73-kDa products were determined and indicated that RHDV 3C proteinase cleaved Glu-Gly peptide bonds.

Rosa Casais - One of the best experts on this subject based on the ideXlab platform.

  • Variant Rabbit Hemorrhagic Disease virus in young Rabbits, Spain.
    Emerging Infectious Diseases, 2012
    Co-Authors: Kevin P. Dalton, Inés Nicieza, Ana Balseiro, María A. Muguerza, J. M. Rosell, Rosa Casais, Ángel L. Álvarez, Francisco Parra
    Abstract:

    Outbreaks of Rabbit Hemorrhagic Disease have occurred recently in young Rabbits on farms on the Iberian Peninsula where Rabbits were previously vaccinated. Investigation identified a Rabbit Hemorrhagic Disease virus variant genetically related to apathogenic Rabbit caliciviruses. Improved antivirus strategies are needed to slow the spread of this pathogen.

  • ATP Binding and ATPase Activities Associated with Recombinant Rabbit Hemorrhagic Disease Virus 2C-Like Polypeptide
    Journal of virology, 2000
    Co-Authors: M. Soledad Marín, Rosa Casais, J. M. Martin Alonso, Francisco Parra
    Abstract:

    The carboxy-terminal region of the Rabbit Hemorrhagic Disease virus p37 polyprotein cleavage product has been expressed in Escherichia coli as a glutathione S-transferase (GST) fusion protein. The recombinant GST-Delta2C protein showed in vitro ATP-binding and ATPase activities. Site-directed mutagenesis studies of the conserved residues G(522) and T(529) in motif A, D(566) and E(567) in motif B, and K(600) in motif C were also performed. These results provide the first experimental characterization of a 2C-like ATPase activity in a member of the Caliciviridae.

  • expression of enzymatically active Rabbit Hemorrhagic Disease virus rna dependent rna polymerase in escherichia coli
    Journal of Virology, 1998
    Co-Authors: Ana Lopez Vazquez, Rosa Casais, Joséantonio Boga, J. M. Martin Alonso, Francisco Parra
    Abstract:

    The Rabbit Hemorrhagic Disease virus (RHDV) (isolate AST/89) RNA-dependent RNA-polymerase (3Dpol) coding region was expressed in Escherichia coli by using a glutathione S-transferase-based vector, which allowed milligram purification of a homogeneous enzyme with an expected molecular mass of about 58 kDa. The recombinant polypeptide exhibited rifampin- and actinomycin D-resistant, poly(A)-dependent poly(U) polymerase. The enzyme also showed RNA polymerase activity in in vitro reactions with synthetic RHDV subgenomic RNA in the presence or absence of an oligo(U) primer. Template-size products were synthesized in the oligo(U)-primed reactions, whereas in the absence of added primer, RNA products up to twice the length of the template were made. The double-length RNA products were double stranded and hybridized to both positive- and negative-sense probes.

  • Processing of Rabbit Hemorrhagic Disease virus polyprotein.
    Journal of virology, 1996
    Co-Authors: J. M. Martin Alonso, Rosa Casais, Joséantonio Boga, Francisco Parra
    Abstract:

    Expression of Rabbit Hemorrhagic Disease virus (RHDV) cDNAs in vitro with Rabbit reticulocyte lysates and in Escherichia coli have been used to study the proteolytic processing of RHDV polyprotein encoded by ORF1. An epitope tag was used for monitoring the gene products by a specific antibody. We have identified four gene products with molecular masses of 80, 43, 73, and 60 kDa, from the amino to the carboxy terminus of the polyprotein. The amino-terminal sequences of the 43- and 73-kDa products were determined and indicated that RHDV 3C proteinase cleaved Glu-Gly peptide bonds.

  • in vitro translation of a subgenomic mrna from purified virions of the spanish field isolate ast 89 of Rabbit Hemorrhagic Disease virus rhdv
    Virus Research, 1992
    Co-Authors: Joséantonio Boga, Rosa Casais, M. S. Marin, M A Prieto, Francisco Parra
    Abstract:

    Purified preparations of the Spanish field isolate of Rabbit Hemorrhagic Disease virus AST/89 were found to contain the plus-stranded genomic RNA of more than 7.4 kilobases (kb) and large amounts of a subgenomic mRNA of 2.4 kb. The smaller RNA was translated in vitro and shown to code for a 60 kDa protein which was immunoprecipitated using anti-RHDV as well as anti-VP60 sera.

Guangqing Liu - One of the best experts on this subject based on the ideXlab platform.

  • Viral Genome-Linked Protein (VPg) Is Essential for Translation Initiation of Rabbit Hemorrhagic Disease Virus (RHDV).
    PloS one, 2015
    Co-Authors: Jie Zhu, Binbin Wang, Qiuhong Miao, Yonggui Tan, Zongyan Chen, Huimin Guo, Guangqing Liu
    Abstract:

    Rabbit Hemorrhagic Disease virus (RHDV), the causative agent of Rabbit Hemorrhagic Disease, is an important member of the caliciviridae family. Currently, no suitable tissue culture system is available for proliferating RHDV, limiting the study of the pathogenesis of RHDV. In addition, the mechanisms underlying RHDV translation and replication are largely unknown compared with other caliciviridae viruses. The RHDV replicon recently constructed in our laboratory provides an appropriate model to study the pathogenesis of RHDV without in vitro RHDV propagation and culture. Using this RHDV replicon, we demonstrated that the viral genome-linked protein (VPg) is essential for RHDV translation in RK-13 cells for the first time. In addition, we showed that VPg interacts with eukaryotic initiation factor 4E (eIF4E) in vivo and in vitro and that eIF4E silencing inhibits RHDV translation, suggesting the interaction between VPg and eIF4E is involved in RHDV translation. Our results support the hypothesis that VPg serves as a novel cap substitute during the initiation of RHDV translation.

  • Construction and applications of Rabbit Hemorrhagic Disease virus replicon.
    PloS one, 2013
    Co-Authors: Binbin Wang, Zongyan Chen, Mingjia Zhe, Chunchun Meng, Miaotao Zhang, Guangqing Liu
    Abstract:

    The study of Rabbit Hemorrhagic Disease virus (RHDV) has long been hindered by the absence of an in vitro culture system. In this study, using RHDV as a model, a series of DNA-based reporter replicons were constructed in which the firefly luciferase (Fluc) gene was fused in-frame with the open reading frame of the replicon. In this construct, the Fluc gene was inserted where the coding region of viral structural protein was deleted and was under the control of a minimal cytomegalovirus (CMV) immediate-early promoter. Fluc activity analysis showed that these reporter replicons replicate efficiently in mammalian cells. On the basis of the replicon, 5′non-coding regions (5′NCR) and genome-linked protein (VPg) were deleted, and the effect on the expression of replicon was analyzed. The results showed that the expression level of Fluc was reduced in the absence of 5′NCR and VPg, suggesting that the 5′NCR and VPg may play an important role in replication and/or translation of RHDV. To further verify the speculation, we also constructed a replication deficient mutant (pRHDV-luc/Δ3D), and the impact of 5′NCR and VPg deletion on viral translation efficiency was analyzed, our results indicated that both VPg and 5′NCR were involved in RHDV translation.

  • Protective immune responses in Rabbits induced by a suicidal DNA vaccine of the VP60 gene of Rabbit Hemorrhagic Disease virus.
    Antiviral research, 2013
    Co-Authors: Cheng Yingjie, Zongyan Chen, Chun Meng, Guangqing Liu
    Abstract:

    Abstract A suicidal DNA vaccine based on a Semliki Forest virus (SFV) replicon was evaluated for the development of a vaccine against Rabbit Hemorrhagic Disease virus (RHDV). The VP60 gene of RHDV was cloned and inserted into pSCA1, an SFV DNA-based replicon vector. The resultant plasmid, pSCA/VP60, was transfected into BHK-21 cells, and the antigenicity of the expressed protein was confirmed using indirect immunofluorescence and a western blot assay. In addition, immunogenicity was studied in Rabbits. Fifteen Rabbits were injected intramuscularly twice with pSCA/VP60 at 2-week intervals. They were challenged with an RHDV isolate 2 weeks after the second immunization. In all cases, anti-RHDV antibodies were detected by ELISA. Additionally, the lymphocyte proliferation response was tested by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide method, and neutralizing antibodies were measured by microneutralization tests. Our results showed that RHDV-specific antibodies and an RHDV-specific cell-mediated immune response were strongly induced in Rabbits. Furthermore, all of the Rabbits were protected against challenge with wild type RHDV. In conclusion, we demonstrated that the suicidal DNA vaccine is a promising vaccine candidate that facilitates the prevention of Rabbit Hemorrhagic Disease caused by RHDV.

  • Identification of in vivo interaction between Rabbit Hemorrhagic Disease virus capsid protein and minor structural protein
    Chinese Science Bulletin, 2012
    Co-Authors: Zongwei Yang, Zongyan Chen, Tao Yun, Guangqing Liu
    Abstract:

    We investigated the ability of the Rabbit Hemorrhagic Disease virus (RHDV) capsid protein (VP60) to interact specifically with the minor structural protein VP10, using an in vivo cell-based CheckMate™ Mammalian Two-Hybrid System. RHDV VP60 protein interacted specifically with VP10. Immunofluorescence analysis and co-immunoprecipitation with specific antibodies revealed the existence of biologically important VP60/VP10 complexes. However, when VP60 was divided into two fragments, the interaction between VP60 and VP10 was impaired dramatically. These results will be helpful for further investigating the mechanism of RHDV particle assembly.

Joana Abrantes - One of the best experts on this subject based on the ideXlab platform.

  • Recombination between G2 and G6 strains of Rabbit Hemorrhagic Disease virus (RHDV) in China.
    Archives of virology, 2016
    Co-Authors: Fang Wang, Joana Abrantes, Zhiyu Fan, Yanhua Song, Yuanyuan Zuo, Pedro J. Esteves
    Abstract:

    Rabbit Hemorrhagic Disease (RHD) is an acute fatal Disease caused by the lagovirus Rabbit Hemorrhagic Disease virus (RHDV), which was first reported in 1984 in China. Genetic characterization of RHDV has demonstrated that two different genogroups (G2 and G6) are present in China. To gain a better understanding of the molecular evolution of RHDV, we searched for recombination events by analyzing all full-length RHDV capsid VP60 sequences of Chinese isolates belonging to the genogroups 2 and 6. Our results revealed a recombinant origin for the NanBu/China/2011 isolate. This recombination event occurred between G2 and G6 strains with two breakpoints located at nucleotide positions 393 and 1079 of the VP60 sequence. Phylogenetically, the NanBu/China/2011 strain clustered with genogroup G6 in the entire capsid gene sequence except in the fragment between nucleotides 394 and 1078, where it clustered with genogroup G2. As the consequences of the presence of a G2/G6 recombinant strain in China are unpredictable, the circulation of RHDV in the populations should be carefully monitored.

  • Full genomic analysis of new variant Rabbit Hemorrhagic Disease virus revealed multiple recombination events.
    Journal of General Virology, 2015
    Co-Authors: Ana M. Lopes, Kevin P. Dalton, Francisco Parra, Maria J. Magalhães, Pedro J. Esteves, Edward C. Holmes, Joana Abrantes
    Abstract:

    Rabbit Hemorrhagic Disease virus (RHDV), a Lagovirus of the family Caliciviridae, causes Rabbit Hemorrhagic Disease (RHD) in the European Rabbit (Oryctolagus cuniculus). The Disease was first documented in 1984 in China and rapidly spread worldwide. In 2010, a new RHDV variant emerged, tentatively classified as ‘RHDVb’. RHDVb is characterized by affecting vaccinated Rabbits and those

  • full genomic analysis of new variant Rabbit Hemorrhagic Disease virus revealed multiple recombination events
    Journal of General Virology, 2015
    Co-Authors: Kevin P. Dalton, Francisco Parra, Ana M. Lopes, Maria J. Magalhães, Pedro J. Esteves, Edward C. Holmes, Joana Abrantes
    Abstract:

    Rabbit Hemorrhagic Disease virus (RHDV), a Lagovirus of the family Caliciviridae, causes Rabbit Hemorrhagic Disease (RHD) in the European Rabbit (Oryctolagus cuniculus). The Disease was first documented in 1984 in China and rapidly spread worldwide. In 2010, a new RHDV variant emerged, tentatively classified as ‘RHDVb’. RHDVb is characterized by affecting vaccinated Rabbits and those <2 months old, and is genetically distinct (~20 %) from older strains. To determine the evolution of RHDV, including the new variant, we generated 28 full-genome sequences from samples collected between 1994 and 2014. Phylogenetic analysis of the gene encoding the major capsid protein, VP60, indicated that all viruses sampled from 2012 to 2014 were RHDVb. Multiple recombination events were detected in the more recent RHDVb genomes, with a single major breakpoint located in the 5′ region of VP60. This breakpoint divides the genome into two regions: one that encodes the non-structural proteins and another that encodes the major and minor structural proteins, VP60 and VP10, respectively. Additional phylogenetic analysis of each region revealed two types of recombinants with distinct genomic backgrounds. Recombinants always include the structural proteins of RHDVb, with non-structural proteins from non-pathogenic lagoviruses or from pathogenic genogroup 1 strains. Our results show that in contrast to the evolutionary history of older RHDV strains, recombination plays an important role in generating diversity in the newly emerged RHDVb.

  • Complete genome sequence of two Rabbit Hemorrhagic Disease virus variant b isolates detected on the Iberian Peninsula
    Archives of virology, 2015
    Co-Authors: Kevin P. Dalton, Inés Nicieza, Ángel L. Álvarez, Ana M. Lopes, Pedro J. Esteves, Joana Abrantes, Francisco Parra
    Abstract:

    We report the complete genome sequences of two isolates (RHDV-N11 and CBVal16) of variant Rabbit Hemorrhagic Disease virus (RHDVb). Isolate N11 was detected in young domestic animals during a Rabbit Hemorrhagic Disease (RHD) outbreak that occurred in 2011 on a Rabbit farm in Navarra, Spain, while CBVal16 was isolated from a wild Rabbit found dead in Valpacos, Northern Portugal, a year later. The viral sequences reported show 84.8–85.1 % and 78.3–78.5 % identity to RHDVAst/89 and RCV-A1 MIC-07, representative members of the pathogenic genogroup 1 RHDV and apathogenic Rabbit calicivirus, respectively. In comparison with other RHDV isolates belonging to the previously known genogroups 1–6, RHDVb shows marked phenotypic differences, as it causes Disease preferentially in young Rabbits under 40 days of age and shows modified red blood cell agglutination profiles as well as antigenic differences that allow this variant to escape protection by the currently available vaccines.

  • Rabbit Hemorrhagic Disease Virus Detected in Pico, Azores, Portugal, Revealed a Unique Endemic Strain with More Than 17 Years of Independent Evolution
    Viruses, 2014
    Co-Authors: Pedro J. Esteves, Ana M. Lopes, Maria José Magalhães, Ana Pinheiro, David Gonçalves, Joana Abrantes
    Abstract:

    Rabbit Hemorrhagic Disease is caused by a calicivirus, Rabbit Hemorrhagic Disease virus (RHDV), which is responsible for high mortality in domestic and wild European Rabbits (Oryctolagus cuniculus). RHDV strains were sequenced from wild European Rabbits (Oryctolagus cuniculus algirus) collected in the Azorean island of Pico, Portugal. Phylogenetic analyses showed that the Pico RHDV strains diverge from all of the others described so far, but cluster with the genogroups 1–5 (G1–G5). The genetic distance between the Pico RHDV sequences and each G1, G2 and G3–G5 genogroup (~0.08) is compatible with an RHDV introduction at least 17 years ago. Our results show that in Pico, RHDV is the outcome of an independent evolution from the original RHDV strain that appeared in its European Rabbit population. These are the first sequences of RHDV obtained in the subspecies O. c. algirus, outside of its original region, the Iberian Peninsula. Furthermore, we discuss the risk of Rabbit translocations from the Azores to the Iberian Peninsula, where the Rabbit wild populations are suffering high mortalities.