Journal articles on the topic 'RHDV'
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1
Fitzner, Andrzej, and Wiesław Niedbalski. "Diversity of RHD virus: epidemiological, diagnostic and immunological importance." Medycyna Weterynaryjna 73, no. 12 (2017): 811–18. http://dx.doi.org/10.21521/mw.5815.
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Rabbit haemorrhagic disease (RHD) was first recognized in China in 1984. In Europe, the disease appeared in 1986 in Italy, and in the following years RHD was observed in many other European countries, including Poland in 1988. The disease is caused by RHD virus (RHDV), classified as a representative of the Lagovirus genus within the Caliciviridae family. Lagoviruses include the non-pathogenic rabbit calicivirus (RCV) and the European brown hare syndrome virus (EBHSV). There are three basic variants (subtypes) of pathogenic RHD viruses: classic (RHDV) and antigenic subtypes RHDVa and RHDV2 (RHDVb), distinguished on the basis of epidemiological characteristics, infectious properties and antigenic and genetic modifications. Phylogenetic analysis of RHDV revealed the presence of five genogroups (G1-G5) with similar time of isolation, regardless of the place of occurrence. RHDVa strains are genetically more variable than RHDV, and all RHDVa strains belong to genogroup G6. RHDV2 was diagnosed for the first time in 2010 in domestic and wild rabbits in France, and later in the Iberian Peninsula, and it was called RHDVb. Like the previously identified variants of the RHD virus, RHDV2 spreads to other regions of the world, and in 2011-2016 it was diagnosed in many European countries, North America, Africa and Australia. Strains of RHD2 form a separate, uniform phylogenetic group and are more similar to the non-pathogenic rabbit calicivirus than to pathogenic RHDV and RHDVa. Infections with different variants of RHD viruses are a serious epidemiological, diagnostic and immunological problem. Advanced antigenic changes in RHD viruses limit the usefulness of standard RHD vaccines in controlling the disease....
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Reemers, Sylvia, Leon Peeters, Joyce van Schijndel, Beth Bruton, David Sutton, Leo van der Waart, and Saskia van de Zande. "Novel Trivalent Vectored Vaccine for Control of Myxomatosis and Disease Caused by Classical and a New Genotype of Rabbit Haemorrhagic Disease Virus." Vaccines 8, no. 3 (August 5, 2020): 441. http://dx.doi.org/10.3390/vaccines8030441.
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Myxoma virus (MV) and rabbit haemorrhagic disease virus (RHDV) are the major causes of lethal viral diseases in the European rabbit. In 2010, a new RHDV genotype (RHDV2) emerged in the field that had limited cross-protection with the classical RHDV (RHDV1). For optimal protection of rabbits and preventing spread of disease, a vaccine providing protection against all three key viruses would be ideal. Therefore, a novel trivalent myxoma vectored RHDV vaccine (Nobivac Myxo-RHD PLUS) was developed similar to the existing bivalent myxoma vectored RHDV vaccine Nobivac Myxo-RHD. The new vaccine contains the Myxo-RHDV1 strain already included in Nobivac Myxo-RHD and a similarly produced Myxo-RHDV2 strain. This paper describes several key safety and efficacy studies conducted for European licensing purposes. Nobivac Myxo-RHD PLUS showed to be safe for use in rabbits from five weeks of age onwards, including pregnant rabbits, and did not spread from vaccinated rabbits to in-contact controls. Furthermore, protection to RHDV1 and RHDV2 was demonstrated by challenge, while the serological response to MV was similar to that after vaccination with Nobivac Myxo-RHD. Therefore, routine vaccination with Nobivac Myxo-RHD PLUS can prevent the kept rabbit population from these major viral diseases.
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Abade dos Santos, Fábio A., Carolina Magro, Carina L. Carvalho, Pedro Ruivo, Margarida D. Duarte, and Maria C. Peleteiro. "A Potential Atypical Case of Rabbit Haemorrhagic Disease in a Dwarf Rabbit." Animals 11, no. 1 (December 28, 2020): 40. http://dx.doi.org/10.3390/ani11010040.
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Rabbit haemorrhagic disease (RHD) is a highly contagious infectious disease of European wild and domestic rabbits. Rabbit haemorrhagic disease virus (RHDV, GI.1) emerged in 1986 in Europe, rapidly spreading all over the world. Several genotypes of RHDV have been recognised over time, but in 2010, a new virus (RHDV2/RHDVb, GI.2) emerged and progressively replaced the previous RHDV strains, due to the lack of cross-immunity conferred between RHDV and RHDV2. RHDV2 has a high mutation rate, similarly to the other calivirus and recombines with strains of RHDV and non-pathogenic calicivirus (GI.4), ensuring the continuous emergence of new field strains. Although this poses a threat to the already endangered European rabbit species, the available vaccines against RHDV2 and the compliance of biosafety measures seem to be controlling the infection in the rabbit industry Pet rabbits, especially when kept indoor, are considered at lower risk of infections, although RHDV2 and myxoma virus (MYXV) constitute a permanent threat due to transmission via insects. Vaccination against these viruses is therefore recommended every 6 months (myxomatosis) or annually (rabbit haemorrhagic disease). The combined immunization for myxomatosis and RHDV through a commercially available bivalent vaccine with RHDV antigen has been extensively used (Nobivac® Myxo-RHD, MSD, Kenilworth, NJ, USA). This vaccine however does not confer proper protection against the RHDV2, thus the need for a rabbit clinical vaccination protocol update. Here we report a clinical case of hepatitis and alteration of coagulation in a pet rabbit that had been vaccinated with the commercially available bivalent vaccine against RHDV and tested positive to RHDV2 after death. The animal developed a prolonged and atypical disease, compatible with RHD. The virus was identified to be an RHDV2 recombinant strain, with the structural backbone of RHDV2 (GI.2) and the non-structural genes of non-pathogenic-A1 strains (RCV-A1, GI.4). Although confirmation of the etiological agent was only made after death, the clinical signs and analytic data were very suggestive of RHD.
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Capucci, Lorenzo, Patrizia Cavadini, and Antonio Lavazza. "Viral haemorrhagic disease: RHDV type 2 ten years later." World Rabbit Science 30, no. 1 (March 31, 2022): 1–11. http://dx.doi.org/10.4995/wrs.2022.16505.
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Until the early 1980s, it was totally unknown that lagomorphs were the hosts of several caliciviruses, which were included in the genus Lagovirus by the International Committee on Taxonomy of Viruses (ICTV) in 2000. In those years, two new diseases appeared, with very similar clinical and pathological profiles and associated high mortality rates: rabbit haemorrhagic disease (RHD) in rabbits and European Brown Hare Syndrome (EBHS) in European brown hares. It took a few years to ascertain that both diseases, actually acute and fatal forms of hepatitis, were caused by two genetically related caliciviruses, but they were finally classified by ICTV into two distinct viral species on the basis of their molecular characterisation and epidemiological data: RHDV in rabbit and EBHSV in brown hare. RHD has had a devastating effect on rabbit farms, causing great economic damage, especially in China, where RHD was first noticed around 1982, and in Europe. RHD has also severely affected wild rabbit populations, whose drastic decline has caused serious ecological imbalances in territories such as Spain, where rabbits are a central link in the wildlife food chain. Since the early 1990s, with the increased availability on the market of RHDV vaccines effective in protecting rabbits from RHD, the impact of the disease on rabbit farms has been significantly reduced. In the following years, also considering that RHDV is an endemic virus that cannot be eradicated, farmers learned how to manage the continuous use of RHDV vaccine in relation to the epidemiological situation, the type of breeding farm and the costs of vaccination prophylaxis. Although precarious, management of the RHD risk for rabbit farmers reached an acceptable equilibrium, which was, however, completely upset starting from 2010 by the emergence of another lagovirus also causing RHD. The genome of the newly emerged virus shows limited differences from that of RHDV, but the phenotypic traits of the two viruses are distinctive in at least three main respects: 1) The antigenic profile of the virus (the “face” of the virus recognised by the antibodies) is largely different from that of RHDV. 2) Newborn rabbits only a couple of weeks old die of RHD when infected with the new virus, while RHDV infections run asymptomatic until 7-8 wk of age. 3) The new virus, which started in Europe, has spread over the years to several continents, affecting wild and/or domestic rabbit populations. During this worldwide distribution, the new virus infected several lagomorph species and was shown to cause RHD in most of them. Considering these marked differences and the fact that the new virus is not a variant of RHDV, we proposed the name RHDV type 2 (RHDV2). All these main distinctive traits that differentiate RHDV from RHDV2 have the following consequences in practice: 1) The antigenic difference between RHDV and RHDV2 (their ‘faces’) is so great that we need “new” specific vaccines to control RHDV2 (i.e. RHDV2 is a new serotype). 2) In the event of an RHDV2 infection in suckling rabbits, the presence of maternal antibodies to RHDV2 in the blood is the only way to prevent RHD. In contrast, newborns are naturally resistant to RHD if infected with RHDV and therefore, in terms of protection, the presence of maternal antibodies is useless. 3) When RHD outbreaks occur in territories where rabbits live in sympatry with populations of other lagomorphs, viral contamination in the environment reaches sufficiently high levels to facilitate the transmission of RHDV2 to other lagomorphs, including those with a lower susceptibility to infection than the rabbit. Taken together, these phenotypic traits characteristic of RHDV2 are the reason for its rapid spread across the territory and the concomitant disappearance of RHDV. Probably the most striking example of the epidemiological consequences related to the peculiar features of RHDV2 is its rapid spread in the USA and Mexico, where it is now practically endemic. There, despite repeated isolated outbreaks of RHD caused by RHDV from 2000 onwards in small rabbit farms, RHDV has never been able to become endemic.
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Magouz, A. F., E. A. Elsayed, and A. Y. Metwally. "Detection and characterisation of rabbit haemorrhagic disease virus strains circulating in Egypt." BULGARIAN JOURNAL OF VETERINARY MEDICINE 22, no. 4 (2019): 409–18. http://dx.doi.org/10.15547/bjvm.2085.
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Rabbit haemorrhagic disease (RHD) is a highly virulent viral disease of Oryctolagus cuniculus which threatens the rabbit population in Egypt and worldwide. The etiological agent is the rabbit haemorrhagic disease virus (RHDV), a member of the family Caliciviridae. The aim of this study was to identify the possible evolutionary changes of the currently circulating RHDV in Egypt. Twenty suspected cases were collected from outbreaks that occurred in non-vaccinated rabbit flocks during 2015 and 2016. Liver homogenate samples were investigated for detection and identification of circulating RHDV using haemagglutination (HA) and reverse transcriptase polymerase chain reaction. Further characterisation of selected five viral strains was performed by nucleotide sequencing of VP60 gene. All twenty tested samples were haemagglutinin positive and VP60 gene was amplified. Based on nucleotide sequence analysis, four isolates were identified as classical RHDV strains, while one isolate was assigned as RHDVa variant strain but with the same HA pattern. The new RHDVb variant was not identified.
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Saidi, Aissa, and Abdelouahed Aboutaib. "Confirmation of the Rabbit Hemorrhagic Disease Virus Type 2 (GI.2) Circulation in North Africa." Acta Veterinaria 72, no. 4 (December 1, 2022): 433–41. http://dx.doi.org/10.2478/acve-2022-0035.
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Abstract Rabbit hemorrhagic disease (RHD) is a highly contagious viral disease that causes fatal acute hepatitis in domestic and wild lagomorphs. It has taken on major economic importance in countries like Morocco. In addition to the classical virus (RHDV), a novel emerged genotype (RHDV2) is circulating, especially in the north shore of the Mediterranean basin since 2010. Many small animal farmers reported clinical cases from several rabbitries in Agadir (Morocco) despite systematic vaccination against the RHDV. The main objective was to characterize the current RHDV strains circulating in the studied area to help to choose an adequate vaccine. For that, we extracted viral RNA from rabbit livers, carried out the PCR analyses, and we sequenced the viral structural capsid protein (VP60) of the RHDV. The phylogenetic analysis results allowed us to state that the novel genotype (RHDV2) is circulating in the studied geographical area, and to characterize the isolated sequences. As a conclusion, we recommend updating RHD epidemiological relating data and reviewing the vaccine protocols by both targeting RHDV (GI.1) and RHDV2 (GI.2) in any future preventive program.
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ABD EL-GHANY, WAFAA A. "A Review on Rabbit Hemorrhagic Disease with a Special Reference to Egyptian Situation." Journal of the Hellenic Veterinary Medical Society 71, no. 3 (October 15, 2020): 2243. http://dx.doi.org/10.12681/jhvms.25065.
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Rabbit hemorrhagic disease (RHD) is considered as one of the most important viral diseases that affects and threatens rabbit’s flocks. This disease has affected rabbits since mid-1980. Two epidemics of RHD had been discovered; the first was in mid-1980 and known as classical RHD virus (RHDV), while the second was in 2011 and described as variant virus (RHDVb/RHDV2). Domestic and wild rabbits are susceptible to RHD. All ages can be affected, but adults are more susceptible to young kitten. RHD is presented in three forms; per-acute, acute and subacute or chronic form. Mortality rate is usually high especially in per-acute and acute stages and it is associated with disseminated intravascular coagulopathy and necrotic hepatitis. The main lesions have been observed in the liver, lungs and spleen. Diagnosis of RHD is based on the clinical picture and detection of RHDV or specific antibodies. The prevention and control strategies depend mainly on using of preventive inactivated vaccine together with adoptionof hygienic measures. However, there is no specific treatment of RHDV infection. So, this review article puts a spot light on RHD regarding the epidemiology, the clinical and laboratory diagnosis as well as the prevention and control strategies with a special reference to Egyptian situation.
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Rosell, Joan M., L. Fernando de la Fuente, Francisco Parra, Kevin P. Dalton, J. Ignacio Badiola Sáiz, Ana Pérez de Rozas, Juan J. Badiola Díez, et al. "Myxomatosis and Rabbit Haemorrhagic Disease: A 30-Year Study of the Occurrence on Commercial Farms in Spain." Animals 9, no. 10 (October 10, 2019): 780. http://dx.doi.org/10.3390/ani9100780.
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In this retrospective study, we describe the relative occurrence of clinical myxomatosis, and rabbit haemorrhagic disease (RHD), on 1714 commercial farms visited in Spain, between 1988 and 2018. We determined the annual prevalence based on 817 visits to 394 farms affected by myxomatosis. Myxomatosis was more prevalent from August to March, being lowest in June (3%) and highest in September (8.9%). With regard to RHD, we assessed 253 visits to 156 affected farms. We analyzed mean annual and monthly incidence. Two important RHD epidemics occurred; the first in 1988–1989 due to RHDV GI.1 (also known as RHDV), and the second from 2011 to 2013 due to RHDV GI.2 (RHDV2 or RHDVb). These epidemics occurred at times when effective vaccination had not been carried out. Relative monthly incidence in 2011–2018 was higher from April to August (p < 0.001). The results we obtained from 1404 necropsies on 102 farms did not clearly relate serosanguinous nasal discharge in rabbits with disease caused by GI.2 infection. We also assessed vaccination schedules used on 200 doe farms visited from the end of 2014 to 2018; 95.5% vaccinated against myxomatosis and 97.5% against RHD. Both diseases remain prevalent; however, effective vaccination has produced a steady decline in myxomatosis and RHDV GI.1 and GI.2 on-farm detection. The maintenance of high hygienic standards will be needed to continue and improve this control. However, further studies are required to investigate the causes of sustained virus presence and vaccine breaks.
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Fitzner, Andrzej. "Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak." Bulletin of the Veterinary Institute in Pulawy 58, no. 2 (June 1, 2014): 177–86. http://dx.doi.org/10.2478/bvip-2014-0027.
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Abstract 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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Hall, Robyn N., Tegan King, Tiffany W. O’Connor, Andrew J. Read, Sylvia Vrankovic, Melissa Piper, and Tanja Strive. "Passive Immunisation against RHDV2 Induces Protection against Disease but Not Infection." Vaccines 9, no. 10 (October 18, 2021): 1197. http://dx.doi.org/10.3390/vaccines9101197.
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Rabbit haemorrhagic disease virus 2 (RHDV2) is a lagovirus in the family Caliciviridae. The closely related Rabbit haemorrhagic disease virus (RHDV, termed RHDV1 throughout this manuscript for clarity) has been used extensively as a biocontrol agent in Australia since the mid-1990s to manage wild rabbit populations, a major economic and environmental pest species. Releasing RHDV1 into populations with a high proportion of rabbits less than 8–10 weeks of age leads to non-lethal infection in many of these young animals, with subsequent seroconversion and long-term immunity against reinfection. In contrast, RHDV2 causes lethal disease even in young rabbits, potentially offering substantial benefits for rabbit management programs over RHDV1. However, it is not clear how acquired resistance from maternal antibodies may influence immunity after RHDV2 infection. In this study, we assessed serological responses after RHDV2 challenge in young rabbits of three different ages (5-, 7-, or 9-weeks-old) that were passively immunised with either high- (titre of 2560 by RHDV IgG ELISA; 2.41 mg/mL total protein) or low- (titre of 160–640 by RHDV IgG ELISA; 1.41 mg/mL total protein) dose RHDV2 IgG to simulate maternal antibodies. All rabbits treated with a high dose and 75% of those treated with a low dose of RHDV2 IgG survived virus challenge. Surviving animals developed robust lagovirus-specific IgA, IgM, and IgG responses within 10 days post infection. These findings demonstrate that the protection against RHDV2 conferred by passive immunisation is not sterilising. Correspondingly, this suggests that the presence of maternal antibodies in wild rabbit populations may impede the effectiveness of RHDV2 as a biocontrol.
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Bao, Shijun, Kai An, Chunguo Liu, Xiaoyong Xing, Xiaoping Fu, Huiwen Xue, Fengqin Wen, Xijun He, and Jingfei Wang. "Rabbit Hemorrhagic Disease Virus Isolated from Diseased Alpine Musk Deer (Moschus sifanicus)." Viruses 12, no. 8 (August 17, 2020): 897. http://dx.doi.org/10.3390/v12080897.
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Rabbit hemorrhagic disease virus (RHDV) is the causative agent of rabbit hemorrhagic disease (RHD), and its infection results in mortality of 70–90% in farmed and wild rabbits. RHDV is thought to replicate strictly in rabbits. However, there are also reports showing that gene segments from the RHDV genome or antibodies against RHDV have been detected in other animals. Here, we report the detection and isolation of a RHDV from diseased Alpine musk deer (Moschussifanicus). The clinical manifestations in those deer were sudden death without clinical signs and hemorrhage in the internal organs. To identify the potential causative agents of the disease, we used sequence independent single primer amplification (SISPA) to detect gene segments from viruses in the tissue samples collected from the dead deer. From the obtained sequences, we identified some gene fragments showing very high nucleotide sequence similarity with RHDV genome. Furthermore, we identified caliciviral particles using an electron microscope in the samples. The new virus was designated as RHDV GS/YZ. We then designed primers based on the genome sequence of an RHDV strain CD/China to amplify and sequence the whole genome of the virus. The genome of the virus was determined to be 7437 nucleotides in length, sharing the highest genome sequence identity of 98.7% with a Chinese rabbit strain HB. The virus was assigned to the G2 genotype of RHDVs according to the phylogenetic analyses based on both the full-length genome and VP60 gene sequences. Animal experiments showed that GS/YZ infection in rabbits resulted in the macroscopic and microscopic lesions similar to that caused by the other RHDVs. This is the first report of RHDV isolated from Alpine musk deer, and our findings extended the epidemiology and host range of RHDV.
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Fitzner, A., and W. Niedbalski. "Serological Survey for RHD Antibodies in Rabbits from Two Types of Rabbit Breeding Farms." Polish Journal of Veterinary Sciences 19, no. 3 (September 1, 2016): 597–607. http://dx.doi.org/10.1515/pjvs-2016-0075.
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Abstract Seroprevalence studies of RHDV antibodies in domestic rabbits were conducted between 2008-2014. A total of 12,169 sera from the provinces of central, southern and south-east Poland, including 7,570 samples collected from mixed-breed rabbits reared in smallholder farms and nearly 4,600 sera taken mainly from unvaccinated rabbits kept in industrial farms, were examined using ELISA tests. Additionally, cross-reactivity of selected tested and control archival sera using both classic RHDV and RHDVa antigens was determined by HI assay. The overall seroprevalence was 13.3%. In rabbits with unkown history of immunisation or RHD infection which came from small farms, RHDV antibodies were detected in 6.1% ranging between 1.0% to 17.2% of animals. In rabbits of the same group, but with a declared vaccination status, or confirmed exposure to an infectious virus, or coming from exposed females, the seroprevalence ranged from 83% to 100%. Among unvaccinated meat rabbits aged 71 to 90 days from industrial farms, low (1.85%, 4.17%, 11%), medium (34%, 54%) or high rates (98.7%) of seropositivity were detected. The seroconversion recorded in adult vaccinated females from industrial farms was 70% and 95%. Generally, the antibody levels examined by ELISAs and HI were comparable. However, a number of sera from the rabbits from small farms, as well as archival sera, showed clear differences. Several-fold differences in antibody titers, evidenced mainly in the postoutbreak sera, indictaed the contact of animals with RHDVa antigen. The overall results of the survey revealed a great proportion of seronegative rabbits potentially highly susceptible to RHD infection. In combination with the emergence of a novel pathogenic RHD virus type (RHDV2), it poses a severe risk of a next wave of fatal disease cases spreading in the native population of domestic rabbits, especially in farms with a traditional system of husbandry.
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Leuthold, Mila M., Kevin P. Dalton, and Grant S. Hansman. "Structural Analysis of a Rabbit Hemorrhagic Disease Virus Binding to Histo-Blood Group Antigens." Journal of Virology 89, no. 4 (December 10, 2014): 2378–87. http://dx.doi.org/10.1128/jvi.02832-14.
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ABSTRACTRabbit hemorrhagic disease virus (RHDV) is a member of theCaliciviridaefamily (Lagovirusgenus). 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,Norovirusgenus), 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.
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Erfan, Ahmed M., and Azhar G. Shalaby. "Genotyping of rabbit hemorrhagic disease virus detected in diseased rabbits in Egyptian Provinces by VP60 sequencing." June-2020 13, no. 6 (2020): 1098–107. http://dx.doi.org/10.14202/vetworld.2020.1098-1107.
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Background and Aim: Rabbit hemorrhagic disease (RHD) is an economically important disorder of rabbits, where infection results in severe losses to the meat and fur industries. Our goal was to characterize the RHD virus (RHDV) strains currently circulating in different regions of Egypt. Materials and Methods: Fifty rabbits suspected of harboring RHDV from 15 Egyptian governorates were evaluated. Diseased rabbits were identified by clinical signs and postmortem lesions. RHDV was confirmed through hemagglutination assay (HA) and polymerase chain reaction (PCR). Partial sequencing of the VP60 gene was performed for genotyping. Results: From 50 rabbits, we identified 16 cases of RHDV (32%) by HA and PCR, including seven males and nine females. We identified two distinct genotypes through sequencing of an amplified fragment of the virus VP 60 gene. One group is composed of those circulating primarily in upper Egypt, which is closely related to the classical G3-G5 virus strains, and the second group, circulating predominantly in lower Egypt, was more closely related to the RHDV2 variant. The overall nucleotide sequence identity ranged from 78.4% to 100%, and identity with the vaccine strains ranged from 78.8% to 91.1%. Conclusion: Our results constitute important documentation of RHDV strains currently circulating in Egypt. The findings suggest that there may be a limit to the effectiveness of currently applied vaccine strains as this formulation may not cover all circulating strains. A wider investigation that includes both domestic and wild rabbits will be needed to identify appropriate control measures for this disease.
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Zheng, Tao, Anna M. Napier, John P. Parkes, Joseph S. O'Keefe, and Paul H. Atkinson. "Detection of RNA of rabbit haemorrhagic disease virus from New Zealand wild rabbits." Wildlife Research 29, no. 6 (2002): 683. http://dx.doi.org/10.1071/wr01071.
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Rabbit numbers have returned to high levels in some areas of New Zealand following the initial spread of rabbit haemorrhagic disease virus (RHDV). We undertook to determine whether possible infection with an RHDV-related virus was interfering with the initiation of new outbreaks of rabbit haemorrhagic disease (RHD). RHDV RNA was detected by polymerase chain reaction with reverse transcription (RT-PCR) using RHDV-specific primers from tissue samples of wild rabbits that had been shot in the field. RHDV RNA was detected in 11 of 19 rabbits from an area of Otago where the rabbit population had greatly expanded and in 2 of 8 rabbits from the West Coast where outbreaks of RHD had not been previously reported. Among the 13 rabbits positive for RHDV RNA, 10 had detectable antibodies against RHDV. The nucleotide sequences of the isolates — a segment of the RHDV capsid gene — shared about 99% identity with that of the Czech strain V351 and that of a 1997 New Zealand wild isolate, but shared only about 84% identity with that of a European benign rabbit calicivirus. These results provide evidence for persistent infection of RHDV in rabbits.
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Wang, Li, Tian Xia, Tiantian Guo, Yi Ru, Yanping Jiang, Wen Cui, Han Zhou, et al. "Recombinant Lactobacillus casei Expressing Capsid Protein VP60 can Serve as Vaccine Against Rabbit Hemorrhagic Disease Virus in Rabbits." Vaccines 7, no. 4 (November 2, 2019): 172. http://dx.doi.org/10.3390/vaccines7040172.
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Rabbit hemorrhagic disease virus (RHDV) is the causative agent of rabbit hemorrhagic disease (RHD). RHD, characterized by hemorrhaging, liver necrosis, and high morbidity and mortality in rabbits and hares, causes severe economic losses in the rabbit industry worldwide. Due to the lack of an efficient in-vitro propagation system for RHDV, the current vaccine is produced via chemical inactivation of crude RHDV preparation derived from the livers of infected rabbits. Inactivated vaccines are effective for controlling RHD, but the potential problems of biosafety and animal welfare have negative effects on the application of inactivated vaccines. In this study, an oral Lactobacillus casei (L. casei) vaccine was used as an antigen delivery system to express RHDV capsid protein VP60(VP1)-eGFP fusion protein. The expression of the recombinant protein was confirmed via western blotting and immunofluorescence (IFA). Our results indicate that oral administration of this probiotic vaccine can stimulate secretory immunoglobulin A (SIgA)-based mucosal and IgG-based humoral immune responses in rabbits. The immunized rabbits were completely protected against challenge with RHDV. Our findings indicate that the L. casei expression system is a new strategy for the development of a safe and efficient vaccine against RHDV.
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Bruce, John S., Laurie E. Twigg, and Garry S. Gray. "The epidemiology of rabbit haemorrhagic disease, and its impact on rabbit populations, in south-western Australia." Wildlife Research 31, no. 1 (2004): 31. http://dx.doi.org/10.1071/wr02069.
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The impact of rabbit haemorrhagic disease (RHD) on free-ranging rabbit populations, their immunological response, and the abundance of insect vectors, were monitored in detail in the southern agricultural region of Western Australia. Further, a broad-scale rabbit monitoring program was also established at nine locations across a rainfall gradient in the southern half of Western Australia to monitor the natural arrival, or controlled release, of rabbit haemorrhagic disease virus (RHDV). Changes in rabbit populations and the immune status of RHDV antibodies were monitored in these areas to enable further understanding of the epidemiology of RHD, and its impact on rabbit numbers.RHDV had the greatest impact on rabbit populations in the arid and semi-arid areas (<360 mm per annum), where rabbit numbers were reduced to, and maintained at, 10% of pre-RHD levels. Conversely, the effects of RHD on rabbit numbers in higher-rainfall areas (360–700 mm per annum) were highly variable and patchy, and in some instances RHD had little apparent impact. In higher-rainfall areas where RHD was effective, rabbit numbers were reduced by 50–78%. RHDV was first confirmed in the southern agricultural region of Western Australia in early September 1996, ~1 year after its escape from Wardang Island, South Australia. At the detailed monitoring site (485 mm rainfall per annum), rabbit numbers declined by 65% within 2 weeks of RHDV being detected. However, ~70% of the remaining rabbits had antibodies against RHDV, indicating that they had survived the disease. There was also a demographic shift towards young rabbits (<1 year old) at this time. Further, even though there was no clinical evidence of RHD recurring in this population during the 3-year study, the presence of IgM antibodies in some rabbits well after the initial epizootic suggests that low-level transient outbreaks of RHDV had occurred at this site. Although the impact of these low-level outbreaks on population dynamics were uncertain, rabbit numbers at this site had recovered to pre-RHD levels within two breeding seasons.The abundance of insect vectors on the detailed monitoring site was similar between years with and without RHD outbreaks. Thus, the failure of RHDV to develop clinical disease on this site after the initial epizootic was unlikely to have been caused by the lack of suitable transmission vectors. The apparent lack of disease recurrence at the detailed monitoring site may have been caused by the presence of a non-pathogenic form of RHDV, which seemed to impart at least some cross-immunity to RHDV in these rabbits. The presence of RHDV also caused a shift in the timing of natural epizootics of myxomatosis at this site.
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Mutze, G., P. Bird, S. Jennings, D. Peacock, N. de Preu, J. Kovaliski, B. Cooke, and L. Capucci. "Recovery of South Australian rabbit populations from the impact of rabbit haemorrhagic disease." Wildlife Research 41, no. 7 (2014): 552. http://dx.doi.org/10.1071/wr14107.
Full textAbstract:
Context Recovery of Australian rabbit populations from the impact of rabbit haemorrhagic disease virus (RHDV) contrasts with more prolonged suppression of wild rabbits in Europe, and has been widely discussed in the scientific community, but not yet documented in formal scientific literature. The underlying causes of recovery remain unclear, but resistance to RHDV infection has been reported in laboratory studies of wild-caught rabbits. Aims We document numerical changes in two South Australian wild rabbit populations that were initially suppressed by RHDV, and examine serological data to evaluate several alternative hypotheses for the cause of recovery. Methods Rabbit numbers were assessed from spotlight transect counts and dung mass transects between 1991 and 2011, and age and RHDV antibody sero-prevalence were estimated from rabbits shot in late summer. Key results Rabbit numbers were heavily suppressed by RHDV between 1995 and 2002, then increased 5- to 10-fold between 2003 and 2010. During the period of increase, annual RHDV infection rates remained stable or increased slightly, average age of rabbits remained stable and annual rainfall was below average. Conclusions Rabbit populations recovered but neither avoidance of RHDV infection, gradual accumulation of long-lived RHD-immune rabbits, nor high pasture productivity were contributing factors. This leaves increased annual survival from RHDV infection as the most likely cause of recovery. Implications Previously documented evidence of resistance to RHDV infection may be of little consequence to post-RHD recovery in rabbit numbers, unless the factors that influence the probability of infection also shape the course of infection and affect survival of infected rabbits.
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Du, Hongxu, Shuaibing Zhang, Miao He, Ke Ming, Jinli Wang, Wenjuan Yuan, Mingyu Qiao, et al. "Evaluation of the Therapeutic Effect of a Flavonoid Prescription against Rabbit Hemorrhagic Disease In Vivo." BioMed Research International 2019 (April 4, 2019): 1–10. http://dx.doi.org/10.1155/2019/5201790.
Full textAbstract:
Rabbit hemorrhagic disease (RHD) is an acute, high fatal contagious disease induced by rabbit hemorrhagic disease virus (RHDV) with acute severe hepatic injury and causes huge economic loss worldwide. In order to develop an effective and reliable drug to treat this disease in clinic, a prescription formulated with baicalin, linarin, icariin, and notoginsenoside R1 (BLIN) according to the theory of syndrome differentiation and treatment in traditional Chinese veterinary medicine was applied to investigate its curative effects against RHD in vivo. The preliminary study results showed that BLIN prescription exerted good curative effect on RHD therapy. To further validate the curative effect and to investigate the possible related curative mechanisms of this drug, the survival rates, the plasma biochemical indexes of hepatic function, the plasma evaluation indexes of oxidative injury, and the RHDV gene expression levels were detected and then the correlation among these indexes was also analyzed. These results showed that BLIN prescription could significantly increase the survival rate, reduce the hepatic injury severity, alleviate the oxidative injury, and decrease the RHDV gene expression level in rabbits infected with RHDV. All these results indicate that BLIN prescription possesses outstanding curative effect against RHD, and the curative mechanism may be related to its antioxidant and anti-RHDV activities. Therefore, this prescription can be expected to be exploited into a new candidate for RHD therapy in clinic.
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Abrantes, Joana, and Ana M. Lopes. "A Review on the Methods Used for the Detection and Diagnosis of Rabbit Hemorrhagic Disease Virus (RHDV)." Microorganisms 9, no. 5 (April 30, 2021): 972. http://dx.doi.org/10.3390/microorganisms9050972.
Full textAbstract:
Since the early 1980s, the European rabbit (Oryctolagus cuniculus) has been threatened by the rabbit hemorrhagic disease (RHD). The disease is caused by a lagovirus of the family Caliciviridae, the rabbit hemorrhagic disease virus (RHDV). The need for detection, identification and further characterization of RHDV led to the development of several diagnostic tests. Owing to the lack of an appropriate cell culture system for in vitro propagation of the virus, much of the methods involved in these tests contributed to our current knowledge on RHD and RHDV and to the development of vaccines to contain the disease. Here, we provide a comprehensive review of the RHDV diagnostic tests used since the first RHD outbreak and that include molecular, histological and serological techniques, ranging from simpler tests initially used, such as the hemagglutination test, to the more recent and sophisticated high-throughput sequencing, along with an overview of their potential and their limitations.
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Robinson, A. J., P. D. Kirkland, R. I. Forrester, L. Capucci, B. D. Cooke, and A. W. Philbey. "Serological evidence for the presence of a calicivirus in Australian wild rabbits, Oryctolagus cuniculus, before the introduction of rabbit haemorrhagic disease virus (RHDV): its potential influence on the specificity of a competitive ELISA for RHDV." Wildlife Research 29, no. 6 (2002): 655. http://dx.doi.org/10.1071/wr00096.
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The objective of the study was to determine for Australian wild rabbits the specificity of a competitive enzyme-linked immunosorbent assay (cELISA) developed in Italy for detecting antibodies to RHDV. Analysis of 657 sera collected before the arrival of RHDV (pre-RHD) indicated that between 17 and 38% appeared to give false positive results depending on the cut-off criteria used. The finding of pre-RHD sera reacting positively in the cELISA prompted the testing of sera in a cELISA using as antigen smooth forms of RHDV (cELISA-sf) and a solid-phase ELISA (spELISA), both of which detect reactivity to an epitope shared by the lagomorph caliciviruses. Testing of a subset of the pre-RHD sera in the cELISA-sf and the spELISA revealed that 86 and 91%, respectively, were positive. Similar results were obtained for a set of sera collected pre-RHD in the Australian Capital Territory (ACT). Sera collected from wild-stock rabbits born and raised in isolation in an animal house in the ACT were all negative in the cELISA, 6% were positive in the cELISA-sf and 13% in the spELISA. It was concluded that a calicivirus related to RHDV and European brown hare syndrome virus (EBHSV) was present in the rabbit population before the arrival of RHDV, and may still be present. The potential consequences of these findings for epidemiological studies on RHD in Australia are discussed.
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Müller, Claudia, Rafał Hrynkiewicz, Dominika Bębnowska, Jaime Maldonado, Massimiliano Baratelli, Bernd Köllner, and Paulina Niedźwiedzka-Rystwej. "Immunity against Lagovirus europaeus and the Impact of the Immunological Studies on Vaccination." Vaccines 9, no. 3 (March 13, 2021): 255. http://dx.doi.org/10.3390/vaccines9030255.
Full textAbstract:
In the early 1980s, a highly contagious viral hemorrhagic fever in rabbits (Oryctolagus cuniculus) emerged, causing a very high rate of mortality in these animals. Since the initial occurrence of the rabbit hemorrhagic disease virus (RHDV), several hundred million rabbits have died after infection. The emergence of genetically-different virus variants (RHDV GI.1 and GI.2) indicated the very high variability of RHDV. Moreover, with these variants, the host range broadened to hare species (Lepus). The circulation of RHDV genotypes displays different virulences and a limited induction of cross-protective immunity. Interestingly, juvenile rabbits (<9 weeks of age) with an immature immune system display a general resistance to RHDV GI.1, and a limited resistance to RHDV GI.2 strains, whereas less than 3% of adult rabbits survive an infection by either RHDV GI.1. or GI.2. Several not-yet fully understood phenomena characterize the RHD. A very low infection dose followed by an extremely rapid viral replication could be simplified to the induction of a disseminated intravascular coagulopathy (DIC), a severe loss of lymphocytes—especially T-cells—and death within 36 to 72 h post infection. On the other hand, in animals surviving the infection or after vaccination, very high titers of RHDV-neutralizing antibodies were induced. Several studies have been conducted in order to deepen the knowledge about the virus’ genetics, epidemiology, RHDV-induced pathology, and the anti-RHDV immune responses of rabbits in order to understand the phenomenon of the juvenile resistance to this virus. Moreover, several approaches have been used to produce efficient vaccines in order to prevent an infection with RHDV. In this review, we discuss the current knowledge about anti-RHDV resistance and immunity, RHDV vaccination, and the further need to establish rationally-based RHDV vaccines.
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Bruce, John S., and Laurie E. Twigg. "Rabbit Haemorrhagic Disease Virus: serological evidence of a non-virulent RHDV-like virus in south-western Australia." Wildlife Research 31, no. 6 (2004): 605. http://dx.doi.org/10.1071/wr04009.
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Although several different cELISAs have been used to assess the exposure of European rabbits to rabbit haemorrhagic disease (RHD), the interpretation of the results of such assays is not always straight-forward. Here we report on such difficulties, and on the likely presence of a non-virulent rabbit haemorrhagic disease virus–like virus (nvRHDV-LV) in south-western Australia. Analysis of sera collected from European rabbits at Kojaneerup (near Albany) in Western Australia provided the first serological evidence of the likely presence of a nvRHDV-LV in wild rabbit populations outside the east coast of Australia and New Zealand, before the deliberate introduction of RHDV as biological control agent in both countries. Six out of 30 rabbits (20%) sampled 1–2 months before the known arrival of RHDV at Kojaneerup were seropositive to RHD on the basis of their IgG isoELISAs. However, none of these positive samples were positive for the RHDV antibody cELISA (1 : 10), indicating likely exposure to nvRHDV-LV. Subsequent serological analysis of 986 rabbits sampled between September 1996 and August 1999 at Kojaneerup indicated that nvRHDV-LV persisted in these rabbits following the natural arrival of RHDV in September 1996. At least 10–34% of rabbits appeared to have been exposed to nvRHDV-LV during the 3-year study. The presence of nvRHDV-LV seemed to offer only limited protection to rabbits from RHDV during the initial epizootic; however, persistence of nvRHDV-LV may have mitigated further RHDV activity after this epizootic. Fewer than 1% of rabbits (9 of 986) showed evidence of RHDV-challenge during the 30 months following the initial RHDV epizootic. Furthermore, except for the epizootic in September 1996, no clinical signs of the disease were apparent in the population until RHDV was deliberately reintroduced in April 1999. Mortality of rabbits exposed to RHDV at this time appeared to be correlated with their IgG isoELISA titre.
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Cooke, B. D., S. McPhee, A. J. Robinson, and L. Capucci. "Rabbit haemorrhagic disease: does a pre-existing RHDV-like virus reduce the effectiveness of RHD as a biological control in Australia?" Wildlife Research 29, no. 6 (2002): 673. http://dx.doi.org/10.1071/wr00092.
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Serological data from wild rabbits support the hypothesis that a second RHDV-like virus was already present in Australia before rabbit haemorrhagic disease virus (RHDV) was introduced as a biological control agent. This putative virus apparently persists in most wild rabbit populations in the presence of RHDV, and antibodies raised against it appear to protect some rabbits from fatal rabbit haemorrhagic disease (RHD). High titres of these antibodies are most commonly found in rabbits from high rainfall areas; this may explain why the initial mortality from RHD declined as the disease spread from dry areas into wetter regions and why it remains less effective as a biological control in wetter regions today. The implications for further advances in rabbit control are discussed, including the need to isolate this putative RHDV-like virus and develop specific ELISA tests to facilitate its detection in the field.
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Cooke, B. D., and F. Fenner. "Rabbit haemorrhagic disease and the biological control of wild rabbits, Oryctolagus cuniculus, in Australia and New Zealand." Wildlife Research 29, no. 6 (2002): 689. http://dx.doi.org/10.1071/wr02010.
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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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Miao, Qiuhong, Ruibing Qi, Luut Veldkamp, Jooske Ijzer, Marja L. Kik, Jie Zhu, Aoxing Tang, et al. "Immunogenicity in Rabbits of Virus-Like Particles from a Contemporary Rabbit Haemorrhagic Disease Virus Type 2 (GI.2/RHDV2/b) Isolated in The Netherlands." Viruses 11, no. 6 (June 14, 2019): 553. http://dx.doi.org/10.3390/v11060553.
Full textAbstract:
Rabbit haemorrhagic disease virus (RHDV) type 2 (GI.2/RHDV2/b) is an emerging pathogen in wild rabbits and in domestic rabbits vaccinated against RHDV (GI.1). Here we report the genome sequence of a contemporary RHDV2 isolate from the Netherlands and investigate the immunogenicity of virus-like particles (VLPs) produced in insect cells. RHDV2 RNA was isolated from the liver of a naturally infected wild rabbit and the complete viral genome sequence was assembled from sequenced RT-PCR products. Phylogenetic analysis based on the VP60 capsid gene demonstrated that the RHDV2 NL2016 isolate clustered with other contemporary RHDV2 strains. The VP60 gene was cloned in a baculovirus expression vector to produce VLPs in Sf9 insect cells. Density-gradient purified RHDV2 VLPs were visualized by transmission electron microscopy as spherical particles of around 30 nm in diameter with a morphology resembling authentic RHDV. Immunization of rabbits with RHDV2 VLPs resulted in high production of serum antibodies against VP60, and the production of cytokines (IFN-γ and IL-4) was significantly elevated in the immunized rabbits compared to the control group. The results demonstrate that the recombinant RHDV2 VLPs are highly immunogenic and may find applications in serological detection assays and might be further developed as a vaccine candidate to protect domestic rabbits against RHDV2 infection.
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Baratelli, Massimiliano, Joan Molist-Badiola, Alba Puigredon-Fontanet, Mariam Pascual, Oriol Boix, Francesc Xavier Mora-Igual, Michelle Woodward, Antonio Lavazza, and Lorenzo Capucci. "Characterization of the Maternally Derived Antibody Immunity against Rhdv-2 after Administration in Breeding Does of an Inactivated Vaccine." Vaccines 8, no. 3 (August 28, 2020): 484. http://dx.doi.org/10.3390/vaccines8030484.
Full textAbstract:
Inactivated strain-specific vaccines have been successfully used to control rabbit haemorrhagic disease (RHD) caused by RHDV-2 in the rabbit industry. It is unknown whether and how vaccination of breeding does contributed to protect the population of young susceptible rabbit kits. The present study investigates whether the immunity against RHDV-2 produced by vaccination of breeding does is transmitted to their progeny and its dynamic once inherited by kits. For this purpose, New Zealand female rabbits of 8–9 weeks of age were allocated into 2 groups of 40 subjects each and bred during 6 reproductive cycles. The first experimental group was vaccinated with a commercially available inactivated vaccine against RHDV-2 whereas the second group was inoculated with PBS. Moreover, the present study was also meant to identify the mechanisms of transmission of that maternal immunity. For this reason, rabbit kits of vaccinated and non-vaccinated breeding does were cross-fostered before milk uptake. The RHDV-2 antibody response was monitored in the blood serum of breeding does and of their kits by competition ELISA (cELISA) and solid-phase ELISA (spELISA). Since it has been clearly demonstrated that cELISA positive rabbits are protected from RHD, we avoided the resorting of the challenge of the kits with RHDV-2. Results showed that RHDV-2 antibodies were inherited by kits up to one year from vaccination of breeding does. Once inherited, the maternally derived antibody response against RHDV-2 lasted at least until 28 days of life. Finally, the study also elucidated that the major contribution to the maternal derived immunity against RHDV-2 in kits was provided during gestation and probably transmitted through transplacental mechanisms although lactation provided a little contribution to it. The present study contributed to elucidate the characteristics of the maternal antibody immunity produced by vaccination and its mechanisms of transmission.
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Story, G., D. Berman, R. Palmer, and J. Scanlan. "The impact of rabbit haemorrhagic disease on wild rabbit (Oryctolagus cuniculus) populations in Queensland." Wildlife Research 31, no. 2 (2004): 183. http://dx.doi.org/10.1071/wr00099.
Full textAbstract:
Rabbit haemorrhagic disease virus (RHDV) escaped from quarantine facilities on Wardang Island in September 1995 and spread through South Australia to Queensland by December 1995. To determine the impact of this biological control agent on wild rabbit populations in Queensland, shot sample and spotlight count data were collected at six sites. RHDV spread across Queensland from the south-west to the east at a rate of at least 91 km month–1 between October 1995 and October 1996. The initial impact on rabbit density appeared highly variable, with an increase of 81% (255 ± 79 (s.e.) to 385 ± 73 rabbits km–2) at one site and a decrease of 83% (129 ± 27 to 22 ± 18 rabbits km–2) at another during the first outbreak. However, after 30 months of RHDV activity, counts were at least 90% below counts conducted before RHDV arrived. Using a population model to account for environmental conditions, the mean suppression of rabbit density caused by rabbit haemorrhagic disease (RHD) was estimated to be 74% (ranging from 43% to 94% between sites). No outbreaks were observed when the density of susceptible rabbits was lower than 12 km–2. Where rabbit density remains low for long periods RHDV may not persist. This is perhaps most likely to occur in the isolated populations towards the northern edge of the range of rabbits in Australia. RHDV may have to be reintroduced into these populations. Further south in areas more suitable for rabbits, RHDV is more likely to persist, resulting in a high density of immune rabbits. In such areas conventional control techniques may be more important to enhance the influence of RHD.
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Story, G., J. Scanlan, R. Palmer, and D. Berman. "Corrigendum to: The impact of rabbit haemorrhagic disease on wild rabbit (Oryctolagus cuniculus) populations in Queensland." Wildlife Research 31, no. 6 (2004): 651. http://dx.doi.org/10.1071/wr00099_co.
Full textAbstract:
Rabbit haemorrhagic disease virus (RHDV) escaped from quarantine facilities on Wardang Island in September 1995 and spread through South Australia to Queensland by December 1995. To determine the impact of this biological control agent on wild rabbit populations in Queensland, shot sample and spotlight count data were collected at six sites. RHDV spread across Queensland from the south-west to the east at a rate of at least 91 km month–1 between October 1995 and October 1996. The initial impact on rabbit density appeared highly variable, with an increase of 81% (255 ± 79 (s.e.) to 385 ± 73 rabbits km–2) at one site and a decrease of 83% (129 ± 27 to 22 ± 18 rabbits km–2) at another during the first outbreak. However, after 30 months of RHDV activity, counts were at least 90% below counts conducted before RHDV arrived. Using a population model to account for environmental conditions, the mean suppression of rabbit density caused by rabbit haemorrhagic disease (RHD) was estimated to be 74% (ranging from 43% to 94% between sites). No outbreaks were observed when the density of susceptible rabbits was lower than 12 km–2. Where rabbit density remains low for long periods RHDV may not persist. This is perhaps most likely to occur in the isolated populations towards the northern edge of the range of rabbits in Australia. RHDV may have to be reintroduced into these populations. Further south in areas more suitable for rabbits, RHDV is more likely to persist, resulting in a high density of immune rabbits. In such areas conventional control techniques may be more important to enhance the influence of RHD.
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Henning, J., P. R. Davies, and J. Meers. "Seropositivity to rabbit haemorrhagic disease virus in non-target mammals during periods of viral activity in a population of wild rabbits in New Zealand." Wildlife Research 33, no. 4 (2006): 305. http://dx.doi.org/10.1071/wr03061.
Full textAbstract:
As part of a longitudinal study of the epidemiology of rabbit haemorrhagic disease virus (RHDV) in New Zealand, serum samples were obtained from trapped feral animals that may have consumed European rabbit (Oryctolagus cuniculus) carcasses (non-target species). During a 21-month period when RHDV infection was monitored in a defined wild rabbit population, 16 feral house cats (Felis catus), 11 stoats (Mustela erminea), four ferrets (Mustela furo) and 126 hedgehogs (Erinaceus europaeus) were incidentally captured in the rabbit traps. The proportions of samples that were seropositive to RHDV were 38% for cats, 18% for stoats, 25% for ferrets and 4% for hedgehogs. Seropositive non-target species were trapped in April 2000, in the absence of an overt epidemic of rabbit haemorrhagic disease (RHD) in the rabbit population, but evidence of recent infection in rabbits was shown. Seropositive non-target species were found up to 2.5 months before and 1 month after this RHDV activity in wild rabbits was detected. Seropositive predators were also trapped on the site between 1 and 4.5 months after a dramatic RHD epidemic in February 2001. This study has shown that high antibody titres can be found in non-target species when there is no overt evidence of RHDV infection in the rabbit population, although a temporal relationship could not be assessed statistically owning to the small sample sizes. Predators and scavengers might be able to contribute to localised spread of RHDV through their movements.
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Fresco-Taboada, Alba, Mercedes Montón, Istar Tapia, Elena Soria, Juan Bárcena, Cécile Guillou-Cloarec, Ghislaine Le Gall-Reculé, Esther Blanco, and Paloma Rueda. "Development and Evaluation of a Duplex Lateral Flow Assay for the Detection and Differentiation between Rabbit Haemorrhagic Disease Virus Lagovirus europaeus/GI.1 and /GI.2." Biology 11, no. 3 (March 5, 2022): 401. http://dx.doi.org/10.3390/biology11030401.
Full textAbstract:
Rabbit Haemorrhagic Disease Virus 2 (RHDV2, recently named Lagovirus europaeus/GI.2) was first reported in France in 2010 and has spread globally since then, replacing most of the circulating former RHDV (genotype GI.1) in many countries. The detection and differentiation of both genotypes is of crucial importance for the surveillance of the disease. In this article, a duplex lateral flow assay (LFA) for antigen detection is described and evaluated, providing the first description of a quick and easy-to-use test that allows for the simultaneous detection and differentiation of RHDV genotypes GI.1 and GI.2. A panel of GI.1- or GI.2-infected and non-infected rabbit liver samples and liver exudates (136 samples) was analysed, obtaining a total sensitivity of 94.4% and specificity of 100%. These data confirm that the developed duplex LFA can be used as a reliable diagnostic test for RHD surveillance, especially in farms and the field.
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Mutze, Greg, Ron Sinclair, David Peacock, John Kovaliski, and Lorenzo Capucci. "Does a benign calicivirus reduce the effectiveness of rabbit haemorrhagic disease virus (RHDV) in Australia? Experimental evidence from field releases of RHDV on bait." Wildlife Research 37, no. 4 (2010): 311. http://dx.doi.org/10.1071/wr09162.
Full textAbstract:
Context. European rabbits are serious environmental and agricultural pests throughout their range in Australia. Rabbit haemorrhagic disease virus (RHDV) greatly reduced rabbit numbers in arid central Australia but had less impact in cooler, higher-rainfall areas. RHDV-like benign caliciviruses (bCVs) have been implicated in limiting the impact of RHDV in the higher-rainfall regions of Australia and also in Europe. Aims. Experimental releases of RHDV on bait were tested as a means of initiating disease outbreaks. Serological evidence of antibodies to bCVs was examined to determine whether they reduce mortality rates and/or spread of the released RHDV, and how that might influence the effectiveness of future RHDV releases for rabbit management. Methods. Four experimental releases were conducted in high-rainfall and coastal regions of southern Australia. Virus activity was implied from recapture rates and serological changes in marked rabbits, and genetic sequencing of virus recovered from dead rabbits. Changes in rabbit abundance were estimated from spotlight transect counts. Key results. Release of RHDV on bait produced disease outbreaks that challenged almost all animals within the general release area and spread up to 4 km beyond the release sites. Recapture rates were high in marked rabbits that possessed antibodies from previous exposure to RHDV and extremely low amongst rabbits that lacked any detectable antibodies. Rabbits carrying antibodies classified as being due to previous infection with bCVs had recapture rates that were dependent on circulating antibody titre and were ~55% of recapture rates in rabbits with clear antibodies to RHDV. Conclusions. This is the first quantified evidence that antibodies produced against bCVs provide significant protection against RHD outbreaks in field populations of rabbits. Implications. bCVs can greatly reduce the impact of RHDV on wild-rabbit populations in Australia and presumably elsewhere. RHDV can be effectively released on bait although further releases are likely to be of minor or inconsistent benefit for controlling rabbit numbers where bCVs are common.
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O’Connor, Tiffany W., Andrew J. Read, Robyn N. Hall, Tanja Strive, and Peter D. Kirkland. "Immunological Cross-Protection between Different Rabbit Hemorrhagic Disease Viruses—Implications for Rabbit Biocontrol and Vaccine Development." Vaccines 10, no. 5 (April 22, 2022): 666. http://dx.doi.org/10.3390/vaccines10050666.
Full textAbstract:
The use of rabbit hemorrhagic disease virus (RHDV) as a biocontrol agent to control feral rabbit populations in Australia, in combination with circulating endemic strains, provides a unique environment to observe the interactions between different lagoviruses competing for the same host. Following the arrival of RHDV2 (GI.2) in Australia, it became necessary to investigate the potential for immunological cross-protection between different variants, and the implications of this for biocontrol programs and vaccine development. Laboratory rabbits of various immune status—(1) rabbits with no detectable immunity against RHDV; (2) rabbits with experimentally acquired immunity after laboratory challenge; (3) rabbits immunised with a GI.2-specific or a multivalent RHDV inactivated virus prototype vaccine; or (4) rabbits with naturally acquired immunity—were challenged with one of three different RHDV variants (GI.1c, GI.1a or GI.2). The degree of cross-protection observed in immune rabbits was associated with the variant used for challenge, infectious dose of the virus and age, or time since acquisition of the immunity, at challenge. The immune status of feral rabbit populations should be determined prior to intentional RHDV release because of the high survival proportions in rabbits with pre-existing immunity. In addition, to protect domestic rabbits in Australia, a multivalent RHDV vaccine should be considered because of the limited cross-protection observed in rabbits given monovalent vaccines.
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Kerr, Peter J., Andrew Kitchen, and Edward C. Holmes. "Origin and Phylodynamics of Rabbit Hemorrhagic Disease Virus." Journal of Virology 83, no. 23 (September 16, 2009): 12129–38. http://dx.doi.org/10.1128/jvi.01523-09.
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ABSTRACT 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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Bruce, John S., and Laurie E. Twigg. "The reintroduction, and subsequent impact, of rabbit haemorrhagic disease virus in a population of wild rabbits in south-western Australia." Wildlife Research 32, no. 2 (2005): 139. http://dx.doi.org/10.1071/wr04025.
Full textAbstract:
The natural arrival of rabbit haemorrhagic disease virus (RHDV) in south-western Australia in September 1996 resulted in a reduction in rabbit numbers of ~65% (~90% morbidity, with ~72% mortality of infected rabbits). As no signs of the disease (clinical or serological) were seen over the next two years, and as rabbit numbers over the last 12-month monitoring period at the site were similar to those observed before the natural 1996 RHDV epizootic (i.e. pre-RHD), RHDV was deliberately reintroduced into this rabbit population in April 1999 (autumn). Seven RHDV-inoculated rabbits were released prior to the main breeding season when <3% of sampled rabbits (n = 118) were seropositive for RHDV antibodies. Following the deliberate release, the overall decline in rabbit numbers (68%) was comparable to that seen during the natural 1996 epizootic. However, on the basis of the observed changes in rabbit numbers, and in their serology, the impact of the deliberate RHDV release appeared to be more variable across the six trapping areas than was seen during the natural 1996 spring epizootic. The reductions in rabbit numbers on these areas 6–8 weeks after RHDV-release ranged from 55% to 90%. The serology of the surviving rabbits on the trapping areas was also variable over this period, with the proportion of seropositive rabbits ranging from 5% to 90%. Overall, only 15% of the surviving rabbit population showed evidence of recent challenge by RHDV, giving a morbidity rate of 73% 8 weeks after the release. However, over 90% of infected rabbits died. This provides further evidence that some rabbits remained un-challenged by RHDV for up to 8 weeks after its release. The variable impact of the April 1999 release may have been partially caused by the observed differences in abundance of insect vectors, and/or an apparent increase in the incidence of non-virulent RHDV in the months preceding the release.
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Niedźwiedzka-Rystwej, P., B. Tokarz-Deptuła, and W. Deptuła. "White and red blood cell picture in rabbits experimentally infected with strains of the rabbit haemorrhagic disease (RHD) virus without or with variable haemagglutination capacity." Polish Journal of Veterinary Sciences 19, no. 4 (December 1, 2016): 865–76. http://dx.doi.org/10.1515/pjvs-2016-0108.
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Abstract The aim of the study was to establish if haemagglutination of rabbit haemorrhagic disease virus (RHDV) affects haematological picture of peripheral blood in rabbits and the pathogenicity of the virus. The study analyzed white and red blood cell picture in rabbits experimentally infected with two non-haemagglutinating (HA-) RHDV strains (Frankfurt and Asturias) and one strain with variable haemagglutination capacity (HA+/−) (Hagenow). Studies with HA− and HA +/− are rare and relate only to 4 HA− strains (2 RHDV: BLA and Rainham; 2 RHDVa: Pv97 and 9905) and 1 HA+/− RHDV strain: ŻD, where less changes in haematological indices and less pathogenicity were observed. We found that changes caused by HA− Frankfurt strain were related to the number of neutrophils and thrombocytes, while in HA− strain Asturias, in thrombocytes and leukocytes. Changes evoked by HA+/− Hagenow strain pertained to the number of eosinophils, thrombocytes, leukocytes, monocytes, and concentration of hemoglobin. Mortality caused by the Frankfurt strain was 100% between 36 and 48 h post infection (p.i.), while that caused by Asturias strain was 100% between 24 and 36 h p.i., and that observed in case of Hagenow strain was 90% between 36 and 48 h p.i. The changes in haematological picture caused by the HA− and HA+/− RHDV strains were less intensive than those found in case of the HA+ RHDV strains, which cannot be confirmed for pathogenicity, and is not in line with the existing hypothesis suggesting higher pathogenicity in HA+ viruses.
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Bárcena, Juan, Mónica Morales, Belén Vázquez, José A. Boga, Francisco Parra, Javier Lucientes, Albert Pagès-Manté, José M. Sánchez-Vizcaíno, Rafael Blasco, and Juan M. Torres. "Horizontal Transmissible Protection against Myxomatosis and Rabbit Hemorrhagic Disease by Using a Recombinant Myxoma Virus." Journal of Virology 74, no. 3 (February 1, 2000): 1114–23. http://dx.doi.org/10.1128/jvi.74.3.1114-1123.2000.
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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.
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Pacioni, Carlo, Robyn N. Hall, Tanja Strive, David S. L. Ramsey, Mandev S. Gill, and Timothy G. Vaughan. "Comparative Epidemiology of Rabbit Haemorrhagic Disease Virus Strains from Viral Sequence Data." Viruses 15, no. 1 (December 21, 2022): 21. http://dx.doi.org/10.3390/v15010021.
Full textAbstract:
Since their introduction in 1859, European rabbits (Oryctolagus cuniculus) have had a devastating impact on agricultural production and biodiversity in Australia, with competition and land degradation by rabbits being one of the key threats to agricultural and biodiversity values in Australia. Biocontrol agents, with the most important being the rabbit haemorrhagic disease virus 1 (RHDV1), constitute the most important landscape-scale control strategies for rabbits in Australia. Monitoring field strain dynamics is complex and labour-intensive. Here, using phylodynamic models to analyse the available RHDV molecular data, we aimed to: investigate the epidemiology of various strains, use molecular data to date the emergence of new variants and evaluate whether different strains are outcompeting one another. We determined that the two main pathogenic lagoviruses variants in Australia (RHDV1 and RHDV2) have had similar dynamics since their release, although over different timeframes (substantially shorter for RHDV2). We also found a strong geographic difference in their activities and evidence of overall competition between the two viruses.
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Hermans, K., I. Moeremans, M. Verlinden, and A. Garmyn. "België ontsnapt niet aan het “rabbit hemorrhagic disease virus-2” (RHDV2) bij konijnen." Vlaams Diergeneeskundig Tijdschrift 85, no. 5 (October 28, 2016): 309–14. http://dx.doi.org/10.21825/vdt.v85i5.16323.
Full textAbstract:
Sinds 2016 is in België een duidelijke spreiding aan de gang van een nieuwe variant van het “rabbit hemorrhagic disease virus” (RHDV), aangeduid als RHDV2. Acute sterfte van konijnen is bij beide varianten van het virus het vaakst geziene verschijnsel. Vaccinatie tegen beide virusvarianten is mogelijk. Het vaccin dat momenteel in België geregistreerd is tegen RHD, beschermt niet tegen de variantstam. Via het cascadesysteem kan de dierenarts op eigen verantwoordelijkheid een vaccin invoeren dat in een andere EU-lidstaat daarvoor geregistreerd is. De actuele epidemiologische situatie verantwoordt dat konijnen preventief gevaccineerd worden tegen RHD. Ook myxomatose maakt echter nog steeds zeer veel slachtoffers, zowel onder wilde als onder tamme konijnen. Omwille van de actualiteit van het RHDV2 krijgt myxomatose momenteel te weinig aandacht. Er is een belangrijke taak weggelegd voor de dierenarts om konijneneigenaars correct te informeren over de belangrijke virale ziekten bij konijnen en de mogelijkheden tot preventie.
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Blatkiewicz, Małgorzata, and Beata Hukowska-Szematowicz. "Vimentin as a Cap of Invisibility: Proposed Role of Vimentin in Rabbit Hemorrhagic Disease Virus (RHDV) Infection." Viruses 13, no. 7 (July 20, 2021): 1416. http://dx.doi.org/10.3390/v13071416.
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Vimentin is an intermediate filament, a cytoskeleton protein expressed mainly in cells of mesenchymal origin. Increasing evidence indicates that vimentin could play a key role in viral infections. Therefore, changes in tissue and extracellular vimentin expression and associated signal trails may determine/protect the fate of cells and the progression of disease caused by viral infection. Rabbit hemorrhagic disease virus (RHDV), genotype GI.1, is an etiological agent that causes a severe and highly lethal disease—RHD (rabbit hemorrhagic disease). This article evaluates the gene and protein expression of vimentin in the tissues (liver, lungs, spleen, and kidneys) and serum of rabbits experimentally infected with two RHDV variants (GI.1a). The VIM mRNA expression levels in the tissues were determined using reverse transcription quantitative real-time PCR (RT-qPCR). In addition, the amount of vimentin protein in the serum was analyzed by an ELISA test. We observed significantly elevated expression levels of VIM mRNA and protein in the liver and kidney tissues of infected rather than healthy rabbits. In addition, VIM mRNA expression was increased in the lung tissues; meanwhile, we observed only protein-enhanced vimentin in the spleen. The obtained results are significant and promising, as they indicate the role of vimentin in RHDV infection and the course of RHD. The role of vimentin in RHDV infection could potentially rely on the one hand, on creating a cap of invisibility against the intracellular viral spread, or, on the other hand, after the damage of cells, vimentin could act as a signal of tissue damage.
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Kunikova, E. D., N. V. Moroz, M. A. Dolgova, L. V. Malakhova, and I. A. Komarov. "Optimization of RHDV type 1 and 2 inactivation modes." Veterinary Science Today 1, no. 1 (March 29, 2021): 22–28. http://dx.doi.org/10.29326/2304-196x-2021-1-36-22-28.
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The purpose of these studies was to optimize RHDV type 1 and 2 (RHDV1 and RHDV2) inactivation modes to use the obtained antigens in inactivated vaccines and diagnosticums. The inactivating effect of aminoethylethylenimine and β-propiolactone was studied in different concentrations in correlation with the exposure time and temperature. The correlation between the inactivating effect of the compound used and the accepted test conditions (concentration, temperature, and exposure time) was studied on a group of rabbits, each of which was injected intramuscularly with 1 cm3 of the inactivated material sample. At the end of the maximum exposure interval, a control sample of the viral material, kept under the same conditions without any inactivant added was similarly tested. Lethality was considered to evaluate the damaging action in the test and control groups: L = m/n, where m is the number of dead animals; n is the total number of rabbits in the group for testing of the inactivated material sample. The postmortem diagnosis was confirmed by testing the rabbit liver tissue homogenate for relative antigens using ELISA. It was found that aminoethylethylenimine and β-propiolactone did not have the same effect on the studied variants of the virus. In order to preserve at maximum the antigenic structures of the virus, the following inactivation modes were considered to be optimal: for RHDV1-aminoethylethylenimine at a concentration of 0.3% at 37 °C, exposure time – 72 hours, or β-propiolactone at a concentration of 0.1–0.3% at 25–37 °С, exposure time – 24–48 hours; for RHDV2 – aminoethylethylenimine at a concentration of 1% at 37 °C, exposure time – 72 hours, or β-propiolactone at a concentration 0.3% at 25 °С, exposure time – 24 hours.
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McPhee, S. R., K. L. Butler, J. Kovaliski, G. Mutze, L. Capucci, and B. D. Cooke. "Antibody status and survival of Australian wild rabbits challenged with rabbit haemorrhagic disease virus." Wildlife Research 36, no. 5 (2009): 447. http://dx.doi.org/10.1071/wr08137.
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In Australia, the epidemiology of rabbit haemorrhagic disease virus (RHDV) is complicated by non-pathogenic forms of calicivirus (bCV) co-circulating with RHDV and providing variable protection from RHDV. Currently no bCV virus-specific antibody tests exist; however, a series of four ELISAs used to detect antibodies to RHDV provided an indirect means to detect antibodies to bCV, enabling antibody categories of seronegative, maternal RHDV, RHDV or bCV to be determined. Rabbits (188) from four locations were challenged with RHDV and logistic regression models determined that, for rabbits <15 months old, survival was dependent on antibody titres alone and the relationship did not vary with age, capture site, gender, liveweight or reproductive status. All rabbits survived challenge after reaching 15 months of age, irrespective of their antibody titres. Where bCV antibodies were prevalent in young rabbits, the bCV category did not adequately summarise all information about rabbit survival that can be obtained from antibody titres. Within antibody categories, 95% of rabbits with RHDV, 33% with bCV, 40% with maternal RHDV and 22% with seronegative antibodies survived. The high survival rate of adults implies that natural outbreaks or controlled releases of RHDV will have little impact on adult breeding rabbits. Therefore, where RHDV and bCV are endemic, conventional rabbit-control programs targeting the immune breeding populations should provide the most predictable outcome for long-term maintenance of low rabbit populations.
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Henzell, Robert P., Ross B. Cunningham, and Helen M. Neave. "Factors affecting the survival of Australian wild rabbits exposed to rabbit haemorrhagic disease." Wildlife Research 29, no. 6 (2002): 523. http://dx.doi.org/10.1071/wr00083.
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Rabbit haemorrhagic disease virus (RHDV) is foreign to Australia, and first entered populations of Australian wild rabbits (Oryctolagus cuniculus L.) in Australia in late 1995. Rabbits are serious environmental and agricultural pests in Australia, and RHDV, a major new pathogen, was introduced as a biological control agent to reduce their numbers. Our study evaluated some of the factors affecting survival of wild rabbits exposed to rabbit haemorrhagic disease (RHD) at 78 sites across Australia.Our data on rabbit numbers consist of the number of rabbits per spotlight kilometre present shortly before and shortly after an RHD outbreak at each site. They are a direct measure of survival rather than mortality. By reducing the interval between the pre- and post-RHD counts to the minimum possible, we sought to minimise the influence on the analysis of other causes of change in rabbit numbers. We calculated proportional survival as the ratio (number of rabbits present after RHD)/(number present before RHD), and used regression analysis to relate it to environmental and other variables. Proportional survival was lower at higher densities of rabbits; was lower if RHDV arrived naturally at the site rather than if it was deliberately released; was lower in areas with hot, dry climates than in areas with cold, wet climates; was lower in southern, inland areas than in warm, coastal areas; and, if the outbreak occurred during summer, was lower in areas of winter rainfall than in areas of summer rainfall. Rainfall seasonality was not correlated with survival at other times of the year. Only in the last effect was there a significant interaction with the time of the year that the outbreak occurred.Our statistical model describes correlations among the data, but does not in itself establish cause and effect. We interpret the properties of our statistical model to draw the following conclusions. First, the effectiveness of RHD is reduced in cold, wet areas and warm, coastal areas, because of the prevalence in these areas of one or more pre-existing caliciviruses in rabbits that impart year-round resistance to RHD. Second, we conclude that the poor summertime performance of RHD in areas that are wet in summer could result from poor survival of RHDV exposed to the combination of high temperature and high relative humidity, although it is also possible that during summer the effectiveness of vectors declines.
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Liu, Guangqing, Zheng Ni, Tao Yun, Bin Yu, Liu Chen, Wei Zhao, Jionggang Hua, and Jianping Chen. "A DNA-launched reverse genetics system for rabbit hemorrhagic disease virus reveals that the VP2 protein is not essential for virus infectivity." Journal of General Virology 89, no. 12 (December 1, 2008): 3080–85. http://dx.doi.org/10.1099/vir.0.2008/003525-0.
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Rabbit hemorrhagic disease virus (RHDV), a member of the family Caliciviridae comprising positive-stranded RNA viruses, is a highly virulent pathogen of rabbits. Until recently, studies into the molecular mechanisms of RHDV replication and pathogenesis have been hindered by the lack of an in vitro culture system and reverse genetics. This study describes the generation of a DNA-based reverse genetics system for RHDV and the subsequent investigation of the biological role of the RHDV VP2 protein. The full-length RHDV genome was assembled as a single cDNA clone and placed under the control of the eukaryotic human cytomegalovirus promoter. Transfection of cells with the DNA clone resulted in a clear cytopathic effect and the generation of infectious progeny virions. The reconstituted virus was stable and grew to titres similar to that of the parental virus. Although previous reports have suggested that the minor structural protein (VP2) of other caliciviruses is essential for the production of infectious virions, using the DNA-launch-based RHDV reverse genetics system described here it was demonstrated that VP2 is not essential for RHDV infectivity. Transfection of cells with a cDNA clone of RHDV lacking VP2 resulted in the generation of infectious virions. These studies indicate that the presence of VP2 could reduce the replication of RHDV, suggesting that it may play a regulatory role in the life cycle of RHDV.
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Hukowska-Szematowicz, Beata, Agata Maciejak-Jastrzębska, Małgorzata Blatkiewicz, Karolina Maciak, Monika Góra, Joanna Janiszewska, and Beata Burzyńska. "Changes in MicroRNA Expression during Rabbit Hemorrhagic Disease Virus (RHDV) Infection." Viruses 12, no. 9 (August 31, 2020): 965. http://dx.doi.org/10.3390/v12090965.
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Current knowledge on the role of microRNAs (miRNAs) in rabbit hemorrhagic disease virus (RHDV) infection and the pathogenesis of rabbit hemorrhagic disease (RHD) is still limited. RHDV replicates in the liver, causing hepatic necrosis and liver failure. MiRNAs are a class of short RNA molecules, and their expression profiles vary over the course of diseases, both in the tissue environment and in the bloodstream. This paper evaluates the expression of miRNAs in the liver tissue (ocu-miR-122-5p, ocu-miR-155-5p, and ocu-miR-16b-5p) and serum (ocu-miR-122-5p) of rabbits experimentally infected with RHDV. The expression levels of ocu-miR-122-5p, ocu-miR-155-5p, and ocu-miR-16b-5p in liver tissue were determined using reverse transcription quantitative real-time PCR (RT-qPCR), and the expression level of circulating ocu-miR-122-5p was established using droplet digital PCR (ddPCR). The expression levels of ocu-miR-155-5p and ocu-miR-16b-5p were significantly higher in the infected rabbits compared to the healthy rabbits (a fold-change of 5.8 and 2.5, respectively). The expression of ocu-miR-122-5p was not significantly different in the liver tissue from the infected rabbits compared to the healthy rabbits (p = 0.990), while the absolute expression level of the circulating ocu-miR-122-5p was significantly higher in the infected rabbits than in the healthy rabbits (p < 0.0001). Furthermore, a functional analysis showed that ocu-miR-155-5p, ocu-miR-16b-5p, and ocu-miR-122-5p can regulate the expression of genes involved in processes correlated with acute liver failure (ALF) in rabbits. Search tool for the retrieval of interacting genes/proteins (STRING) analysis showed that the potential target genes of the three selected miRNAs may interact with each other in different pathways. The results indicate the roles of these miRNAs in RHDV infection and over the course of RHD and may reflect hepatic inflammation and impairment/dysfunction in RHD.
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Parkes, John P., Brent Glentworth, and Graham Sullivan. "Changes in immunity to rabbit haemorrhagic disease virus, and in abundance and rates of increase of wild rabbits in Mackenzie Basin, New Zealand." Wildlife Research 35, no. 8 (2008): 775. http://dx.doi.org/10.1071/wr08008.
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The evolutionary race between diseases and their hosts may lead to attenuation of the disease agent, increasing resistance in the host, or both. This is an undesirable outcome when the disease is being used as a biocontrol agent but a desired outcome when the host is valued by people. Introduced wild rabbits Oryctolagus cuniculus are a pest to agriculture and biodiversity values in New Zealand’s grasslands, particularly on the drier eastern sides of both islands. The costs to manage them using conventional control could not be sustained by landowners who since the 1980s have proposed the introduction of the viral biocontrol agents myxomatosis and then rabbit haemorrhagic disease virus (RHDV). Myxomatosis failed to establish but RHDV did establish and spread following its illegal introduction in 1997. However, since 1997, rabbit haemorrhagic disease (RHD) has become less effective for biocontrol of rabbits in New Zealand. Three lines of evidence from our four study sites in the Mackenzie Basin support this claim. First, the proportion of rabbits of all ages with antibodies to RHDV has increased in samples of rabbits shot each year since 1997. Taken alone this may simply reflect an accumulation in cross-sectional samples of seropositive older rabbits that have been exposed to infection but survived successive epizootics. Second, the proportion of young rabbits, sampled at an age when they have been exposed to a single epizootic event, that have antibodies to RHDV has also increased since 1997. This is strong evidence that something has changed in the rabbit–virus interaction. The cause of this effect remains unknown but is reflected in the third line of evidence, that the abundance of rabbits as indexed by standardised spotlight counts has increased since 1997. The rate of increase has, however, been much slower than that seen in the same populations as they recovered from conventional control before the arrival of RHD. Thus, we conclude that RHD is still an effective biocontrol but its efficacy is waning.
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Dalton, Kevin P., Carmen Alvarado, Edel Reytor, Maria del Carmen Nuñez, Ana Podadera, Diego Martínez-Alonso, Jose Manuel Martin Alonso, et al. "Chimeric VLPs Bearing VP60 from Two Serotypes of Rabbit Haemorrhagic Disease Virus Are Protective against Both Viruses." Vaccines 9, no. 9 (September 9, 2021): 1005. http://dx.doi.org/10.3390/vaccines9091005.
Full textAbstract:
The VP60 capsid protein from rabbit haemorrhagic disease virus (RHDV), the causative agent of one of the most economically important disease in rabbits worldwide, forms virus-like particles (VLPs) when expressed using heterologous protein expression systems such as recombinant baculovirus, yeasts, plants or mammalian cell cultures. To prevent RHDV dissemination, it would be beneficial to develop a bivalent vaccine including both RHDV GI.1- and RHDV GI.2-derived VLPs to achieve robust immunisation against both serotypes. In the present work, we developed a strategy of production of a dual-serving RHDV vaccine co-expressing the VP60 proteins from the two RHDV predominant serotypes using CrisBio technology, which uses Tricholusia ni insect pupae as natural bioreactors, which are programmed by recombinant baculovirus vectors. Co-infecting the insect pupae with two baculovirus vectors expressing the RHDV GI.1- and RHDV GI.2-derived VP60 proteins, we obtained chimeric VLPs incorporating both proteins as determined by using serotype-specific monoclonal antibodies. The resulting VLPs showed the typical size and shape of this calicivirus as determined by electron microscopy. Rabbits immunised with the chimeric VLPs were fully protected against a lethal challenge infection with the two RHDV serotypes. This study demonstrates that it is possible to generate a dual cost-effective vaccine against this virus using a single production and purification process, greatly simplifying vaccine manufacturing.
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Ben Chehida, Faten, Ana M. Lopes, João V. Côrte-Real, Soufien Sghaier, Rim Aouini, Lilia Messadi, and Joana Abrantes. "Multiple Introductions of Rabbit Hemorrhagic Disease Virus Lagovirus europaeus/GI.2 in Africa." Biology 10, no. 9 (September 8, 2021): 883. http://dx.doi.org/10.3390/biology10090883.
Full textAbstract:
Rabbit hemorrhagic disease (RHD) causes high mortality and morbidity in European rabbits (Oryctolagus cuniculus). In Africa, the presence of the causative agent, the rabbit hemorrhagic disease virus (RHDV), was first confirmed in 1992 (genotype Lagovirus europaeus/GI.1). In 2015, the new genotype Lagovirus europaeus/GI.2 (RHDV2/b) was detected in Tunisia. Currently, GI.2 strains are present in several North and Sub-Saharan African countries. Considerable economic losses have been observed in industrial and traditional African rabbitries due to RHDV. Like other RNA viruses, this virus presents high recombination rates, with the emergence of GI.2 being associated with a recombinant strain. Recombination events have been detected with both pathogenic (GI.1b and GII.1) and benign (GI.3 and GI.4) strains. We obtained complete genome sequences of Tunisian GI.2 strains collected between 2018 and 2020 and carried out phylogenetic analyses. The results revealed that Tunisian strains are GI.3P-GI.2 strains that were most likely introduced from Europe. In addition, the results support the occurrence of multiple introductions of GI.2 into Africa, stressing the need for characterizing complete genome sequences of the circulating lagoviruses to uncover their origin. Continued monitoring and control of rabbit trade will grant a better containment of the disease and reduce the disease-associated economic losses.
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Niedźwiedzka-Rystwej, P., B. Tokarz-Deptuła, and W. Deptuła. "Apoptosis of granulocytes and lymphocytes in peripheral blood in rabbits infected with haemagglutinating and non-haemagglutinating antigenic variants of the RHD (rabbit haemorrhagic disease) virus." Polish Journal of Veterinary Sciences 16, no. 2 (June 1, 2013): 223–29. http://dx.doi.org/10.2478/pjvs-2013-0032.
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Abstract This paper attempts to study the dynamics of apoptosis of granulocytes and lymphocytes in peripheral blood in rabbits infected with haemagglutinating (Vt97, Triptis, Hartmannsdorf) and non-haemagglutinating (Pv97, 9905 RHDVa) antigenic variants of the RHD virus. The pathogenicity of those antigenic variants was also assessed by recording the mortality of the infected animals. The animals were infected with antigenic variants and blood was sampled at hour 0,4,8,12,24,36 p.i. and the percentage of apoptotic granulocytes and lymphocytes was measured with the use of flow cytometry. The results of the study showed that apoptosis is included during RHDV infection, as the number of apoptotic granulocytes and lymphocytes increases throughout the experiment; depending on the antigenic variant, apoptosis joins in at 4-8-12 h p.i. and lasts until 24-36 h p.i. Furthermore, the mortality of rabbits infected with the examined strains of RHD virus varied from 30% to 100%. This study performed for the first time in this manner, indicates the importance of apoptosis during infection with the RHD virus.
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Strive, Tanja, and Tarnya E. Cox. "Lethal biological control of rabbits – the most powerful tools for landscape-scale mitigation of rabbit impacts in Australia." Australian Zoologist 40, no. 1 (January 1, 2019): 118–28. http://dx.doi.org/10.7882/az.2019.016.
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ABSTRACT The viral biocontrol agents Myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV1), released in 1950 and 1996 respectively, are the only control tools to have resulted in significant and lasting landscape-scale suppression of rabbit populations in Australia. Multiple conservation benefits and significant economic savings have resulted from the long-term and widespread reductions in rabbit numbers and impacts. In an effort to ‘boost’ rabbit biocontrol, an additional variant of RHDV1 ('K5') was recently released nationwide to counteract the decreasing effectiveness of both RHDV1 and MYXV that results from the evolutionary ‘arms race’ between viruses and their hosts. Two years prior to the K5 release, an exotic RHDV strain (RHDV2) appeared in Australia. The commercially available vaccine used to protect pet and farmed rabbits against the officially released K5 was ineffective against the exotic RHDV2, resulting in numerous deaths of domestic rabbits. This created substantial confusion about which strain was released as a biocontrol tool, as well as renewed concerns amongst pet rabbit owners and rabbit farmers about the use of viruses as lethal rabbit control tools in general. Ongoing effective control of wild rabbits in Australia is absolutely essential to protect the substantial conservation gains made by the long-term suppression of rabbit numbers over the past decades, and there is currently no alternative population control tool to achieve this at the required landscape scale. Vaccine formulations need updating to protect non-target farmed and pet rabbits from circulating field variants, including RHDV2, and to increase public acceptance for the ongoing use of viral biocontrol for feral rabbit populations.