Journal articles: 'Rabbit calicivirus'

1

Enosi Tuipulotu, Daniel, Tulio M. Fumian, Natalie E. Netzler, Jason M. Mackenzie, and Peter A. White. "The Adenosine Analogue NITD008 has Potent Antiviral Activity against Human and Animal Caliciviruses." Viruses 11, no. 6 (May 30, 2019): 496. http://dx.doi.org/10.3390/v11060496.

Full text

Abstract:

The widespread nature of calicivirus infections globally has a substantial impact on the health and well-being of humans and animals alike. Currently, the only vaccines approved against caliciviruses are for feline and rabbit-specific members of this group, and thus there is a growing effort towards the development of broad-spectrum antivirals for calicivirus infections. In this study, we evaluated the antiviral activity of the adenosine analogue NITD008 in vitro using three calicivirus model systems namely; feline calicivirus (FCV), murine norovirus (MNV), and the human norovirus replicon. We show that the nucleoside analogue (NA), NITD008, has limited toxicity and inhibits calicivirus replication in all three model systems with EC50 values of 0.94 μM, 0.91 µM, and 0.21 µM for MNV, FCV, and the Norwalk replicon, respectively. NITD008 has a similar level of potency to the most well-studied NA 2′-C-methylcytidine in vitro. Significantly, we also show that continual NITD008 treatment effectively cleared the Norwalk replicon from cells and treatment with 5 µM NITD008 was sufficient to completely prevent rebound. Given the potency displayed by NITD008 against several caliciviruses, we propose that this compound should be interrogated further to assess its effectiveness in vivo. In summary, we have added a potent NA to the current suite of antiviral compounds and provide a NA scaffold that could be further modified for therapeutic use against calicivirus infections.

APA, Harvard, Vancouver, ISO, and other styles

2

Chasey, David. "Rabbit haemorrhagic disease: the new scourge of Oryctolagus cuniculus." Laboratory Animals 31, no. 1 (January 1, 1997): 33–44. http://dx.doi.org/10.1258/002367797780600279.

Full text

Abstract:

A new, widespread and important disease of rabbits, rabbit haemorrhagic disease (RHD), is concisely reviewed and discussed. RHD is an acute, infectious condition of adult rabbits and morbidity and mortality, after a relatively short incubation period, can be very high. The disease appears typically as a necrotizing hepatitis with associated haemorrhaging, and death occurs as a result of generalized organ dysfunction. RHD is caused by a calicivirus, antigenically related to a similar virus found in brown hares but distinct from other known caliciviruses, and is spread to susceptible rabbits by a number of routes and vectors. The disease is easily identified and can be effectively controlled in commercial and domestic rabbit populations by slaughter and vaccination regimes. The occurrence of pre-existing cross-reacting antibody in a proportion of rabbits unchallenged by the disease implies the presence of non-pathogenic strains of the virus. This antibody protects against disease on subsequent exposure to RHD. Uniquely, pre-existing antibody does not occur in rabbits in Australia where, after accidental release, the virus is currently spreading rapidly.

APA, Harvard, Vancouver, ISO, and other styles

3

Sharp, Andy, Kerry Holmes, Melinda Norton, and Adam Marks. "Observations on the effects of rabbit calicivirus disease on low and medium density rabbit populations in western New South Wales." Rangeland Journal 23, no. 2 (2001): 194. http://dx.doi.org/10.1071/rj01006.

Full text

Abstract:

Between winter 1995 and winter 1998, seasonal spotlight counts for rabbits were conducted along three transects in western New South Wales. Rabbit Calicivirus (RCV) arrived at the study site in spring 1996 and had an immediate marked effect on rabbit densities. Prior to the advent of Rabbit Calicivirus Disease (RCD), rabbit abundance followed the expected annual pattern of positive growth during the winter to summer period and negligible or negative growth during the summer to winter period. With the arrival of RCV, rabbit abundance was observed to decline by 47% and 75% within low density populations and by 84% within a medium density population. In the subsequent 21 months, the low density populations returned to levels approximating those prior to the arrival of RCV. In contrast, rabbit abundance within the medium density population remained at consistently lowered levels. These data suggest that RCD will have a minimal effect on semi-arid zone rabbit populations below a density of 0.4/ha and that additional management actions will be required to further reduce rabbit abundances.

APA, Harvard, Vancouver, ISO, and other styles

4

Marques, R. M., A. P. Águas, A. Costa-e-Silva, and P. G. Ferreira. "Inflammatory response of young rabbits to calicivirus infection." Microscopy and Microanalysis 15, S3 (July 2009): 19–20. http://dx.doi.org/10.1017/s1431927609990559.

Full text

Abstract:

AbstractCaliciviruses cause rabbit haemorrhagic disease (RHD) that kills more than 90% of the infected adult animals within 1 a 3 days of infection. The virus replicates in the liver and causes a fulminant hepatitis in adult rabbits leading to RHD. A mystery of the calicivirus infection is that young rabbits (less than 8-weeks old) are resistant to the infection, in spite of undergoing viral replication in the liver and of expressing transient hepatitis. Heterophils were the predominant inflammatory cells seen in hepatic tissue of infected adult rabbits, whereas mononuclear cells dominated the inflammatory infiltrates of the infected young rabbits (4-weeks-old). In order to define the role of inflammation in the pathogenesis of the calicivirus infection, we have studied the cellular inflammatory response in young rabbits experimentally infected by calicivirus. For this, we have used transmission electron microscopy (TEM) and flow cytometry to identify the inflammatory cells that infiltrate the hepatic tissue of young rabbits at 48 hours of calicivirus infection. In same infected rabbits, lymphoid organs (spleen and thymus) were used to quantify by flow cytometry the total number of leukocytes seen inside these organs.

APA, Harvard, Vancouver, ISO, and other styles

5

Landström, Catharina. "The Australian Rabbit Calicivirus Disease Program." Social Studies of Science 31, no. 6 (December 2001): 912–49. http://dx.doi.org/10.1177/030631201031006005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Bergin, Ingrid L., Annabel G. Wise, Steven R. Bolin, Thomas P. Mullaney, Matti Kiupel, and Roger K. Maes. "Not-So-Novel Michigan Rabbit Calicivirus." Emerging Infectious Diseases 16, no. 8 (August 2010): 1331–32. http://dx.doi.org/10.3201/1608.100711.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Jahnke, Marlene, Edward C. Holmes, Peter J. Kerr, John D. Wright, and Tanja Strive. "Evolution and Phylogeography of the Nonpathogenic Calicivirus RCV-A1 in Wild Rabbits in Australia." Journal of Virology 84, no. 23 (September 22, 2010): 12397–404. http://dx.doi.org/10.1128/jvi.00777-10.

Full text

Abstract:

ABSTRACT Despite its potential importance for the biological control of European rabbits, relatively little is known about the evolution and molecular epidemiology of rabbit calicivirus Australia 1 (RCV-A1). To address this issue we undertook an extensive evolutionary analysis of 36 RCV-A1 samples collected from wild rabbit populations in southeast Australia between 2007 and 2009. Based on phylogenetic analysis of the entire capsid sequence, six clades of RCV-A1 were defined, each exhibiting strong population subdivision. Strikingly, our estimates of the time to the most recent common ancestor of RCV-A1 coincide with the introduction of rabbits to Australia in the mid-19th century. Subsequent divergence events visible in the RCV-A1 phylogenies likely reflect key moments in the history of the European rabbit in Australia, most notably the bottlenecks in rabbit populations induced by the two viral biocontrol agents used on the Australian continent, myxoma virus and rabbit hemorrhagic disease virus (RHDV). RCV-A1 strains therefore exhibit strong phylogeographic separation and may constitute a useful tool to study recent host population dynamics and migration patterns, which in turn could be used to monitor rabbit control in Australia.

APA, Harvard, Vancouver, ISO, and other styles

8

Cooke, Brian, Keith Springer, Lorenzo Capucci, and Greg Mutze. "Rabbit haemorrhagic disease: Macquarie Island rabbit eradication adds to knowledge on both pest control and epidemiology." Wildlife Research 44, no. 2 (2017): 93. http://dx.doi.org/10.1071/wr16221.

Full text

Abstract:

Rabbit haemorrhagic disease virus (RHDV), introduced into in Australia and New Zealand as a biological-control agent for wild rabbits, is least efficacious in cool humid areas where a non-pathogenic calicivirus (RCV-A1) also circulates. Heavy rabbit mortality following release of RHDV on cold sub-Antarctic Macquarie Island, where RCV-A1 was apparently absent, not only complemented the planned rabbit eradication operations, especially by reducing secondary poisoning of sea-birds from aerial baiting, but also ruled out cool or humid climate as a major limiting factor of disease spread. In turn, this has advanced the idea that RCV-A1 antibodies inhibit RHDV spread as well as reducing disease severity and mortality.

APA, Harvard, Vancouver, ISO, and other styles

9

König, Matthias, Heinz-Jürgen Thiel, and Gregor Meyers. "Detection of Viral Proteins after Infection of Cultured Hepatocytes with Rabbit Hemorrhagic Disease Virus." Journal of Virology 72, no. 5 (May 1, 1998): 4492–97. http://dx.doi.org/10.1128/jvi.72.5.4492-4497.1998.

Full text

Abstract:

ABSTRACT The calicivirus rabbit hemorrhagic disease virus (RHDV), which replicates predominantly in the livers of infected rabbits, cannot be propagated in tissue culture. To enable the performance of in vitro studies, rabbit hepatocytes were isolated by liver perfusion and gradient centrifugation. After inoculation with purified RHDV, more than 50% of the cells proved to be infected. Protein analyses led to the detection of 13 RHDV-specific polypeptides within the infected cells. These proteins were assigned to defined regions of the viral genome, resulting in a refined model of RHDV genome organization.

APA, Harvard, Vancouver, ISO, and other styles

10

Beale, Bob. "Attack of the killer rabbits: how the rabbit calicivirus story escaped." Australian Zoologist 32, no. 2 (February 2003): 316–23. http://dx.doi.org/10.7882/az.2003.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Mahar, Jackie E., Leila Nicholson, John-Sebastian Eden, Sebastián Duchêne, Peter J. Kerr, Janine Duckworth, Vernon K. Ward, Edward C. Holmes, and Tanja Strive. "Benign Rabbit Caliciviruses Exhibit Evolutionary Dynamics Similar to Those of Their Virulent Relatives." Journal of Virology 90, no. 20 (August 10, 2016): 9317–29. http://dx.doi.org/10.1128/jvi.01212-16.

Full text

Abstract:

ABSTRACTTwo closely related caliciviruses cocirculate in Australia: rabbit hemorrhagic disease virus (RHDV) and rabbit calicivirus Australia 1 (RCV-A1). RCV-A1 causes benign enteric infections in the European rabbit (Oryctolagus cuniculus) in Australia and New Zealand, while its close relative RHDV causes a highly pathogenic infection of the liver in the same host. The comparison of these viruses provides important information on the nature and trajectory of virulence evolution, particularly as highly virulent strains of RHDV may have evolved from nonpathogenic ancestors such as RCV-A1. To determine the evolution of RCV-A1 we sequenced the full-length genomes of 44 RCV-A1 samples isolated from healthy rabbits and compared key evolutionary parameters to those of its virulent relative, RHDV. Despite their marked differences in pathogenicity and tissue tropism, RCV-A1 and RHDV have evolved in a very similar manner. Both viruses have evolved at broadly similar rates, suggesting that their dynamics are largely shaped by high background mutation rates, and both exhibit occasional recombination and an evolutionary environment dominated by purifying selection. In addition, our comparative analysis revealed that there have been multiple changes in both virulence and tissue tropism in the evolutionary history of these and related viruses. Finally, these new genomic data suggest that either RCV-A1 was introduced into Australia after the introduction of myxoma virus as a biocontrol agent in 1950 or there was drastic reduction of the rabbit population, and hence of RCV-A1 genetic diversity, perhaps coincident with the emergence of myxoma virus.IMPORTANCEThe comparison of closely related viruses that differ profoundly in propensity to cause disease in their hosts offers a powerful opportunity to reveal the causes of changes in virulence and to study how such changes alter the evolutionary dynamics of these pathogens. Here we describe such a novel comparison involving two closely related RNA viruses that cocirculate in Australia, the highly virulent rabbit hemorrhagic disease virus (RHDV) and the nonpathogenic rabbit calicivirus Australia 1 (RCV-A1). Both viruses infect the European rabbit, but they differ in virulence, tissue tropism, and mechanisms of transmission. Surprisingly, and despite these fundamental differences, RCV-A1 and RHDV have evolved at very similar (high) rates and with strong purifying selection. Furthermore, candidate key mutations were identified that may play a role in virulence and/or tissue tropism and therefore warrant further investigation.

APA, Harvard, Vancouver, ISO, and other styles

12

Sharp, A., L. Gibson, M. Norton, B. Ryan, A. Marks, and L. Semeraro. "The breeding season diet of wedge-tailed eagles (Aquila audax) in western New South Wales and the influence of Rabbit Calicivirus Disease." Wildlife Research 29, no. 2 (2002): 175. http://dx.doi.org/10.1071/wr00077.

Full text

Abstract:

A total of 2071 individual prey items were identified from 34 active and 55 inactive wedge-tailed eagle nests following the 1995, 1996 and 1997 breeding seasons. Overall, the eagle's diet was comparable to that reported in other studies within semi-arid regions, with rabbits, reptiles and macropods accounting for 47.8, 22.6 and 13.7% of prey items, respectively. In spring 1996 rabbit calicivirus moved into the study area, resulting in a 44-78% reduction in rabbit abundance (Sharp et al. 2001). An index was developed to enable the time since death for individual prey items to be approximated and a historical perspective of the eagle's diet to be constructed. Rabbits constituted 56-69% of dietary items collected during the pre-rabbit calicivirus disease (RCD) samples, but declined to 31% and 16% in the two post-RCD samples. A reciprocal trend was observed for the proportion of reptiles in the diet, which increased from 8-21% of pre-RCD dietary items to 49-54% after the advent of RCD. Similarly, the proportion of avian prey items was observed to increase in the post-RCD samples. These data suggested that prey switching may have occurred following the RCD epizootic. However, a lack of data on the relative abundances of reptiles and birds prevented an understanding of the eagle's functional responses to be developed and definitive conclusions to be drawn. Nevertheless, the eagles were observed to modify their diet to the change in rabbit densities by consuming larger quantities of native prey species.

APA, Harvard, Vancouver, ISO, and other styles

13

Seal, Bruce S., James A. House, Cecelia A. Whetstone, and John D. Neill. "Analysis of the Serologic Relationship among San Miguel Sea Lion Virus and Vesicular Exanthema of Swine Virus Isolates. Application of the Western Blot Assay for Detection of Antibodies in Swine Sera to these Virus Types." Journal of Veterinary Diagnostic Investigation 7, no. 2 (April 1995): 190–95. http://dx.doi.org/10.1177/104063879500700204.

Full text

Abstract:

Caliciviruses are positive-sense single-stranded RNA viruses with a single capsid protein. The serotypes of the marine mammal calicivirus, San Miguel sea lion virus (SMSV), are antigenically related to vesicular exanthema of swine virus (VESV) and are potentially hazardous to swine. Western blot assays using purified SMSV serotypes 1 and 4 were used to further examine the serologic relationship among SMSV and VESV isolates. With the exception of SMSV 8 and SMSV 12, rabbit polyclonal antisera generated against all the available SMSV and VESV isolates reacted positively, as assessed by western blot, with purified capsid protein from SMSV 1 and SMSV 4. Consequently, the SMSV 8 and SMSV 12 virus isolates may not be members of the SMSV/VESV calicivirus group. Using antisera from pigs experimentally inoculated with SMSV and VESV as positive controls, a western blot assay for these virus types was utilized to check for the presence of antibodies to caliciviruses in swine sera. Sera from colostrum-deprived gnotobiotic pigs were used as a negative control in all experiments. Examination of sera from domestic and feral swine collected in Iowa, California, and Florida was completed using this technique. The presence of antibodies to these virus types was not detected in any of the porcine sera tested.

APA, Harvard, Vancouver, ISO, and other styles

14

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

15

Studdert, Michael J. "Rabbit haemorrhagic disease virus: a calicivirus with differences." Australian Veterinary Journal 71, no. 8 (August 1994): 264–66. http://dx.doi.org/10.1111/j.1751-0813.1994.tb03428.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Tung, T., D. Phalen, and J.-ALML Toribio. "Adverse reactions in a population of Sydney pet rabbits vaccinated against rabbit calicivirus." Australian Veterinary Journal 93, no. 11 (October 26, 2015): 405–11. http://dx.doi.org/10.1111/avj.12373.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Barlow, N. D., and J. M. Kean. "Simple models for the impact of rabbit calicivirus disease (RCD) on Australasian rabbits." Ecological Modelling 109, no. 3 (June 1998): 225–41. http://dx.doi.org/10.1016/s0304-3800(98)00009-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

19

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 text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

20

Meyers, Gregor. "Characterization of the Sequence Element Directing Translation Reinitiation in RNA of the Calicivirus Rabbit Hemorrhagic Disease Virus." Journal of Virology 81, no. 18 (June 27, 2007): 9623–32. http://dx.doi.org/10.1128/jvi.00771-07.

Full text

Abstract:

ABSTRACT The calicivirus minor capsid protein VP2 is expressed via reinitiation of protein synthesis after termination of translation of the preceding VP1 gene. A sequence element of about 80 nucleotides denoted “termination upstream ribosomal binding site” (TURBS) (25) is crucial for reinitiation. Deletion mapping in the TURBS of a rabbit calicivirus identified two short sequence motifs that were crucial for VP2 expression. Motif 1 is conserved among caliciviruses and is complementary to a sequence in the 18S rRNA. Single-residue exchanges in this motif severely impaired reinitiation when they affected the putative rRNA binding, whereas an exchange preserving complementarity had only a minor effect. Single exchanges in motif 2 were rather well tolerated, but the introduction of double exchanges almost blocked VP2 expression. In contrast, the deletion analyses showed that the RNA between the two motifs is of minor importance. The distance between motif 2 and the start site was found to be important, since deletions of increasing length in this sequence or upstream positioning of the start codon reduced VP2 expression stepwise to low levels, whereas multiple-nucleotide exchanges in this region were tolerated. The low flexibility of the arrangement of TURBS motif 2 and the start codon stand in marked contrast to the requirements with regard to the location of the stop codon of the preceding VP1 gene, which could be moved far downstream with continuous reduction, but without loss, of VP2 translation. The sequence mapping resulted in a refined model of the reinitiation mechanism leading to VP2 expression.

APA, Harvard, Vancouver, ISO, and other styles

21

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.

Full text

Abstract:

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....

APA, Harvard, Vancouver, ISO, and other styles

22

Molsher, Robyn, Alan Newsome, and Chris Dickman. "Feeding ecology and population dynamics of the feral cat (Felis catus) in relation to the availability of prey in central-eastern New South Wales." Wildlife Research 26, no. 5 (1999): 593. http://dx.doi.org/10.1071/wr98058.

Full text

Abstract:

The diet of feral cats (Felis catus) was studied at Lake Burrendong, central-eastern New South Wales, from July 1994 to June 1997. Mammals were the major prey in 499 scats that were analysed. Rabbits (Oryctolagus cuniculus) were the staple prey, while carrion was an important secondary food. Invertebrates, other mammalian prey, vegetation, birds and reptiles were generally minor components of the diet. Few significant seasonal differences in diet were found; however, invertebrates contributed less and possums more to the diet in winter and summer respectively. A significant dietary response was found to changes in rabbit abundance, but not for the other prey types. Cats continued to prey heavily on rabbits even after a 90% decline in rabbit abundance occurred, which coincided with the advent of Rabbit Calicivirus Disease (RCD). House mice (Mus domesticus) increased in importance in the diet ten months post-RCD. Although the abundance of cats was correlated with the abundance of some prey species, other factors may have influenced the observed patterns; these are discussed.

APA, Harvard, Vancouver, ISO, and other styles

23

Liu, June, Peter J. Kerr, John D. Wright, and Tanja Strive. "Serological assays to discriminate rabbit haemorrhagic disease virus from Australian non-pathogenic rabbit calicivirus." Veterinary Microbiology 157, no. 3-4 (June 2012): 345–54. http://dx.doi.org/10.1016/j.vetmic.2012.01.018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Parkes, J. P., G. L. Norbury, R. P. Heyward, and G. Sullivan. "Epidemiology of rabbit haemorrhagic disease (RHD) in the South Island, New Zealand, 1997 - 2001." Wildlife Research 29, no. 6 (2002): 543. http://dx.doi.org/10.1071/wr00108.

Full text

Abstract:

Rabbit haemorrhagic disease (RHD) was illegally released in New Zealand in August 1997 and subsequently spread by farmers and naturally over all areas inhabited by rabbits. The disease has persisted, causing either annual or biennial epidemics that appear to start each spring by infecting susceptible adult rabbits and running through to the autumn infecting young rabbits of the year. Rabbit densities have been suppressed by more than 90% in many areas where numbers were initially high and epidemics returned annually, and by about 50% in areas with low initial densities and biennial epidemics, leaving between 35% and 20%, respectively, of the survivors immunised. In some areas the disease has not reduced rabbit densities and has left more than 80% (at worst) of the survivors across all age cohorts with antibodies to RHD. A possible cause of this apparent longitudinal transmission is that seropositive adult rabbits (which may retain virus) may be infectious and pass virus on to their offspring at just the right dose and age to impart immunity. A pen trial, in which we orally dosed 9-week-old rabbits born to seropositive mothers, showed that they survived and did not seroconvert, but were fully susceptible when re-dosed at about 17 weeks. We have evidence that the possible pre-existing calicivirus does not impart immunity to RHD in at least one part of New Zealand.

APA, Harvard, Vancouver, ISO, and other styles

25

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

26

McIntosh, Michael T., Shawn C. Behan, Fawzi M. Mohamed, Zhiqiang Lu, Karen E. Moran, Thomas G. Burrage, John G. Neilan, et al. "A pandemic strain of calicivirus threatens rabbit industries in the Americas." Virology Journal 4, no. 1 (2007): 96. http://dx.doi.org/10.1186/1743-422x-4-96.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Abd-Eldaim, Mohamed, Leon Potgieter, and Melissa Kennedy. "Genetic Analysis of Feline Caliciviruses Associated with a Hemorrhagic-Like Disease." Journal of Veterinary Diagnostic Investigation 17, no. 5 (September 2005): 420–29. http://dx.doi.org/10.1177/104063870501700503.

Full text

Abstract:

Feline calicivirus (FCV) is 1 of the most common causes of upper respiratory tract disease in cats. Other disease syndromes associated with FCV infection have been reported. Recently, calicivirus infection associated with a hemorrhagic-like disease leading to significant mortality in cats has been reported. The clinical signs are similar to those observed with the calicivirus of rabbit hemorrhagic disease. This study characterized 2 FCV isolates associated with hemorrhagic-like disease. Nucleotide sequencing of the complete genome has been done for these 2 isolates as well as for 4 additional isolates representing other disease syndromes. Previously reported sequence data for the entire genome of classical FCV (6 isolates) and a portion of the capsid gene for hemorrhagic-like FCV (3 isolates), isolated in different regions of United States were used in the genetic analysis. Sequence data were used to determine relationships among the isolates and any correlation with phenotype. Nucleotide sequence comparisons of the entire genome and individual open reading frames revealed high homology among all isolates. Data suggest that the virulence may have genetic determinants on the basis of phylogenetic clustering of the isolates associated with hemorrhagic-like disease.

APA, Harvard, Vancouver, ISO, and other styles

28

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

29

González-Reyes, Salomé, Alberto García-Manso, Gloria del Barrio, Kevin P. Dalton, Lorenzo González-Molleda, José Arrojo-Fernández, Inés Nicieza, and Francisco Parra. "Role of annexin A2 in cellular entry of rabbit vesivirus." Journal of General Virology 90, no. 11 (November 1, 2009): 2724–30. http://dx.doi.org/10.1099/vir.0.013276-0.

Full text

Abstract:

The mechanisms of calicivirus attachment and internalization are not well understood, mainly due to the lack of a reliable cell-culture system for most of its members. In this study, rabbit vesivirus (RaV) virions were shown to bind annexin A2 (ANXA2) in a membrane protein fraction from HEK293T cells, using a virus overlay protein-binding assay and matrix-assisted laser desorption/ionization time-of-flight analysis. A monoclonal anti-ANXA2 antibody and small interfering RNA-mediated knockdown of ANXA2 expression in HEK293T cells reduced virus infection significantly, further supporting the role of ANXA2 in RaV attachment and/or internalization.

APA, Harvard, Vancouver, ISO, and other styles

30

ELSWORTH, P. G., J. KOVALISKI, and B. D. COOKE. "Rabbit haemorrhagic disease: are Australian rabbits (Oryctolagus cuniculus) evolving resistance to infection with Czech CAPM 351 RHDV?" Epidemiology and Infection 140, no. 11 (January 16, 2012): 1972–81. http://dx.doi.org/10.1017/s0950268811002743.

Full text

Abstract:

SUMMARYRabbit haemorrhagic disease is a major tool for the management of introduced, wild rabbits in Australia. However, new evidence suggests that rabbits may be developing resistance to the disease. Rabbits sourced from wild populations in central and southeastern Australia, and domestic rabbits for comparison, were experimentally challenged with a low 60 ID50oral dose of commercially available Czech CAPM 351 virus – the original strain released in Australia. Levels of resistance to infection were generally higher than for unselected domestic rabbits and also differed (0–73% infection rates) between wild populations. Resistance was lower in populations from cooler, wetter regions and also low in arid regions with the highest resistance seen within zones of moderate rainfall. These findings suggest the external influences of non-pathogenic calicivirus in cooler, wetter areas and poor recruitment in arid populations may influence the development rate of resistance in Australia.

APA, Harvard, Vancouver, ISO, and other styles

31

Capucci, L., P. Fusi, A. Lavazza, M. L. Pacciarini, and C. Rossi. "Detection and preliminary characterization of a new rabbit calicivirus related to rabbit hemorrhagic disease virus but nonpathogenic." Journal of virology 70, no. 12 (1996): 8614–23. http://dx.doi.org/10.1128/jvi.70.12.8614-8623.1996.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Meyers, Gregor, Christoph Wirblich, and Heinz-Jürgen Thiel. "Rabbit hemorrhagic disease virus—molecular cloning and nucleotide sequencing of a calicivirus genome." Virology 184, no. 2 (October 1991): 664–76. http://dx.doi.org/10.1016/0042-6822(91)90436-f.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Hoehn, Marion, Peter J. Kerr, and Tanja Strive. "In situ hybridisation assay for localisation of rabbit calicivirus Australia-1 (RCV-A1) in European rabbit (Oryctolagus cuniculus) tissues." Journal of Virological Methods 188, no. 1-2 (March 2013): 148–52. http://dx.doi.org/10.1016/j.jviromet.2012.11.043.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Lemaitre, Evelyne, Françoise Zwingelstein, Stéphane Marchandeau, and Ghislaine Le Gall-Reculé. "First complete genome sequence of a European non-pathogenic rabbit calicivirus (lagovirus GI.3)." Archives of Virology 163, no. 10 (July 5, 2018): 2921–24. http://dx.doi.org/10.1007/s00705-018-3901-z.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Ferreira, P. G., A. Costa-E-Silva, M. J. R. Oliveira, E. Monteiro, and A. P. Águas. "Leukocyte–hepatocyte interaction in calicivirus infection: differences between rabbits that are resistant or susceptible to rabbit haemorrhagic disease (RHD)." Veterinary Immunology and Immunopathology 103, no. 3-4 (February 2005): 217–21. http://dx.doi.org/10.1016/j.vetimm.2004.09.028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Gromadzka, Beata, Bogusław Szewczyk, Grazyna Konopa, Andrzej Fitzner, and Andrzej Kesy. "Recombinant VP60 in the form of virion-like particles as a potential vaccine against rabbit hemorrhagic disease virus." Acta Biochimica Polonica 53, no. 2 (May 30, 2006): 371–76. http://dx.doi.org/10.18388/abp.2006_3351.

Full text

Abstract:

Rabbit hemorrhagic disease virus (RHDV) which causes a highly contagious disease of wild and domestic rabbits belongs to the family Caliciviridae. It is a small, positive single-stranded RNA virus with a genome of 7.5 kb and has a diameter of approximately 40 nm. In negatively stained electron micrographs the virus shows typical calicivirus morphology with regularly arranged cup-shaped structures on the surface. It is a major pathogen of rabbits in many countries. Vp60 - a coat protein of molecular mass around 60 kDa is the major antigen of RHDV. It is present as 90 dimeric units per virion particle. We have expressed VP60 gene in the baculovirus system with the aim to use it as a potential vaccine against RHDV and a diagnostic reagent in immunological tests. cDNA of the vp60 gene of strain SGM, was cloned into a baculovirus transfer vector as full-length gene, as well as truncated gene lacking 600 5'-terminal nucleotides. The sequence of SGM VP60 differed markedly from that of the reference strain. Full-length recombinant VP60 protein from the SGM strain self-assembled to form virus-like particles (VLPs). These particles observed by electron microscopy were morphologically similar to native virions and were able to agglutinate human group 0 erythrocytes. After immunization the recombinant particles induced RHDV-specific antibodies in rabbits and guinea pigs. Rabbits immunized with the VLPs were fully protected against challenge with a virulent RHDV.

APA, Harvard, Vancouver, ISO, and other styles

37

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 text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

38

Hall, Robyn N., Tegan King, Tiffany O’Connor, Andrew J. Read, Jane Arrow, Katherine Trought, Janine Duckworth, Melissa Piper, and Tanja Strive. "Age and Infectious Dose Significantly Affect Disease Progression after RHDV2 Infection in Naïve Domestic Rabbits." Viruses 13, no. 6 (June 21, 2021): 1184. http://dx.doi.org/10.3390/v13061184.

Full text

Abstract:

Rabbit haemorrhagic disease virus 2 (RHDV2 or GI.2, referring to any virus with lagovirus GI.2 structural genes) is a recently emerged calicivirus that causes generalised hepatic necrosis and disseminated intravascular coagulation leading to death in susceptible lagomorphs (rabbits and hares). Previous studies investigating the virulence of RHDV2 have reported conflicting results, with case fatality rates ranging from 0% to 100% even within a single study. Lagoviruses are of particular importance in Australia and New Zealand where they are used as biocontrol agents to manage wild rabbit populations, which threaten over 300 native species and result in economic impacts in excess of $200 million AUD annually to Australian agricultural industries. It is critically important that any pest control method is both highly effective (i.e., virulent, in the context of viral biocontrols) and has minimal animal welfare impacts. To determine whether RHDV2 might be a suitable candidate biocontrol agent, we investigated the virulence and disease progression of a naturally occurring Australian recombinant RHDV2 in both 5-week-old and 11-week-old New Zealand White laboratory rabbits after either high or low dose oral infection. Objective measures of disease progression were recorded through continuous body temperature monitoring collars, continuous activity monitors, and twice daily observations. We observed a 100% case fatality rate in both infected kittens and adult rabbits after either high dose or low dose infection. Clinical signs of disease, such as pyrexia, weight loss, and reduced activity, were evident in the late stages of infection. Clinical disease, i.e., welfare impacts, were limited to the period after the onset of pyrexia, lasting on average 12 h and increasing in severity as disease progressed. These findings confirm the high virulence of this RHDV2 variant in naïve rabbits. While age and infectious dose significantly affected disease progression, the case fatality rate was consistently 100% under all conditions tested.

APA, Harvard, Vancouver, ISO, and other styles

39

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

40

Liu, June, Peter J. Kerr, and Tanja Strive. "A sensitive and specific blocking ELISA for the detection of rabbit calicivirus RCV-A1 antibodies." Virology Journal 9, no. 1 (2012): 182. http://dx.doi.org/10.1186/1743-422x-9-182.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Boniotti, B., C. Wirblich, M. Sibilia, G. Meyers, H. J. Thiel, and C. Rossi. "Identification and characterization of a 3C-like protease from rabbit hemorrhagic disease virus, a calicivirus." Journal of Virology 68, no. 10 (1994): 6487–95. http://dx.doi.org/10.1128/jvi.68.10.6487-6495.1994.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Vázquez, Ana López, José M. Martín Alonso, and Francisco Parra. "Mutation Analysis of the GDD Sequence Motif of a Calicivirus RNA-Dependent RNA Polymerase." Journal of Virology 74, no. 8 (April 15, 2000): 3888–91. http://dx.doi.org/10.1128/jvi.74.8.3888-3891.2000.

Full text

Abstract:

ABSTRACT The RNA-dependent RNA polymerase from rabbit hemorrhagic disease virus, a calicivirus, is known to have a conserved GDD amino acid motif and several additional regions of sequence homology with all types of polymerases. To test whether both aspartic acid residues are in fact involved in the catalytic activity and metal ion coordination of the enzyme, several defined mutations have been made in order to replace them by glutamate, asparagine, or glycine. All six mutant enzymes were produced in Escherichia coli, and their in vitro poly(U) polymerase activity was characterized. The results demonstrated that the first aspartate residue was absolutely required for enzyme function and that some flexibility existed with respect to the second, which could be replaced by glutamate.

APA, Harvard, Vancouver, ISO, and other styles

43

Fulton, Graham. "Additions to prey taken by Wedge-tailed Eagles Aquila audax after release of Rabbit Oryctolagus cuniculus haemorrhagic disease (Rabbit Calicivirus) in 1996." Australian Field Ornithology 36 (2019): 11–12. http://dx.doi.org/10.20938/afo36011012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Pech, R. P., and G. M. Hood. "Foxes, rabbits, alternative prey and rabbit calicivirus disease: consequences of a new biological control agent for an outbreaking species in Australia." Journal of Applied Ecology 35, no. 3 (June 1998): 434–53. http://dx.doi.org/10.1046/j.1365-2664.1998.00318.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Liu, June, Damien A. Fordham, Brian D. Cooke, Tarnya Cox, Greg Mutze, and Tanja Strive. "Distribution and Prevalence of the Australian Non-Pathogenic Rabbit Calicivirus Is Correlated with Rainfall and Temperature." PLoS ONE 9, no. 12 (December 8, 2014): e113976. http://dx.doi.org/10.1371/journal.pone.0113976.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Wirblich, C., H. J. Thiel, and G. Meyers. "Genetic map of the calicivirus rabbit hemorrhagic disease virus as deduced from in vitro translation studies." Journal of virology 70, no. 11 (1996): 7974–83. http://dx.doi.org/10.1128/jvi.70.11.7974-7983.1996.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

48

Urakova, Nadya, Natalie Netzler, Andrew Kelly, Michael Frese, Peter White, and Tanja Strive. "Purification and Biochemical Characterisation of Rabbit Calicivirus RNA-Dependent RNA Polymerases and Identification of Non-Nucleoside Inhibitors." Viruses 8, no. 4 (April 14, 2016): 100. http://dx.doi.org/10.3390/v8040100.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Wennesz, René, Christine Luttermann, Felix Kreher, and Gregor Meyers. "Structure–function relationship in the ‘termination upstream ribosomal binding site’ of the calicivirus rabbit hemorrhagic disease virus." Nucleic Acids Research 47, no. 4 (January 22, 2019): 1920–34. http://dx.doi.org/10.1093/nar/gkz021.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Bok, Karin, Victor G. Prikhodko, Kim Y. Green, and Stanislav V. Sosnovtsev. "Apoptosis in Murine Norovirus-Infected RAW264.7 Cells Is Associated with Downregulation of Survivin." Journal of Virology 83, no. 8 (February 11, 2009): 3647–56. http://dx.doi.org/10.1128/jvi.02028-08.

Full text

Abstract:

ABSTRACT Noroviruses (NVs) are recognized as a major cause of nonbacterial gastroenteritis in humans. Studies of the human NVs continue to be hampered by the inability to propagate them in any cell culture system. Until recently, most data concerning NV replication were derived from studies of feline calicivirus and rabbit hemorrhagic disease virus, which are cultivable members of the family Caliciviridae. From such studies, it was proposed that caliciviruses induce apoptosis to facilitate the dissemination of viral progeny in the host. The discovery that MNV type 1 (MNV-1) grows in RAW264.7 cells provided the first cell culture system for use in studying the role of apoptosis in NV infection. We first showed that MNV-1 replication triggered apoptosis in infected RAW264.7 cells and then demonstrated that cell death was associated with activation of caspase-9 and caspase-3 through the mitochondrial pathway. This process was dependent on virus replication, since inactivated virus failed to induce signs of apoptosis. In order to better understand the apoptotic process induced by MNV-1 infection of RAW264.7 cells, we investigated the expression profiles of MNV-1-infected versus mock-infected cells. Survivin, a member of the inhibitor of apoptosis protein family, was found to be significantly downregulated in an inverse relationship with the virus genome replication. This study showed that, unlike other viruses that upregulate survivin, MNV-1 is the first virus found to downregulate the levels of survivin. We observed that MNV-1 replication in RAW264.7 cells activated caspases, resulting in apoptosis through the mitochondrial pathway, possibly as a result of downregulation of survivin.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Rabbit calicivirus'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles