Susceptibility of Hares and Rabbits to the European Brown Hare Syndrome Virus (EBHSV) and Rabbit Haemorrhagic Disease Virus (RHDV) under Experimental Conditions*

1996 ◽  
Vol 43 (1-10) ◽  
pp. 401-410 ◽  
Author(s):  
A. Lavazza ◽  
M. T. Scicluna ◽  
L. Capucci
Keyword(s):  
Disease Virus ◽  
Brown Hare ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Experimental Conditions ◽  
European Brown Hare ◽  
Rabbit Haemorrhagic Disease ◽  
European Brown Hare Syndrome ◽  
Haemorrhagic Disease

scholarly journals Full-genome sequencing of German rabbit haemorrhagic disease virus uncovers recombination between RHDV (GI.2) and EBHSV (GII.1)

2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Kevin P Szillat ◽  
Dirk Höper ◽  
Martin Beer ◽  
Patricia König
Keyword(s):  
Genetic Variability ◽  
Disease Virus ◽  
Full Genome ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Structural Genes ◽  
Full Genome Sequencing ◽  
European Brown Hare ◽  
Whole Genome Analysis ◽  
Rabbit Haemorrhagic Disease ◽  
Haemorrhagic Disease

Abstract Rabbit haemorrhagic disease virus (RHDV; genotypes GI.1 and GI.2) and European brown hare syndrome virus (EBHSV; genotype GII.1) are caliciviruses belonging to the genus Lagovirus. These viruses pose a serious threat to wild and domestic rabbit and hare populations around the world. In recent years, an expanding genetic diversity has been described within the genus, with recombination events occurring between the different genotypes. Here, we generated and analysed 56 full-genome sequences of RHDV and EBHSV from rabbit and hare livers, collected in Germany between the years 2013 and 2020. We could show that genotype Gl.2 (RHDV-2) almost entirely replaced Gl.1 (classical RHDV) in the German rabbit population. However, GI.1 is still present in Germany and has to be included into disease control and vaccination strategies. Three recombinant strains were identified from rabbit samples that contain the structural genes of genotype Gl.2 and the non-structural genes of genotype Gl.1b. Of special interest is the finding that sequences from two hare samples showed recombination events between structural genes of RHDV Gl.2 and non-structural genes of EBHSV GII.1, a recombination between different genogroups that has not been described before. These findings lead to the assumption that also a recombination of the non-structural genes of RHDV Gl.2 with the structural genes of EBHSV Gll.1 might be possible and therefore increase the potential genetic variability of lagoviruses immensely. Our findings underline the importance of whole genome analysis with next-generation sequencing technology as one of new tools now available for in-depth studies that allow in depth molecular epidemiology with continuous monitoring of the genetic variability of viruses that would otherwise likely stay undetected if only routine diagnostic assays are used.

scholarly journals The emergence of rabbit haemorrhagic disease virus: will a non-pathogenic strain protect the UK?

2001 ◽  
Vol 356 (1411) ◽  
pp. 1087-1095 ◽  
Author(s):  
P.J. White ◽  
R.A. Norman ◽  
R.C. Trout ◽  
E.A. Gould ◽  
P.J. Hudson
Keyword(s):  
Disease Virus ◽  
Pathogenic Strain ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Rabbit Haemorrhagic Disease ◽  
Seroprevalence Data ◽  
Age Structured ◽  
Reproductive Rates ◽  
The Uk ◽  
Haemorrhagic Disease ◽  
Age Structured Model

Rabbit haemorrhagic disease virus emerged in China in 1984, and has killed hundreds of millions of wild rabbits in Australia and Europe. In the UK there appears to be an endemic non–pathogenic strain, with high levels of seroprevalence being recorded, in the absence of associated mortality. Using a seasonal, age–structured model we examine the hypothesis that differences in rabbit population demography differentially affect the basic reproductive rates ( R 0 ) of the pathogenic and non–pathogenic strains, leading to each dominating in some populations and not others. The strain with the higher R 0 excluded the other, with the dynamics depending upon the ratio of the two R 0 values. When the non–pathogenic strain dominated, the pathogenic strain caused only transient mortality, although this could be significant when the two R 0 values were similar. When the pathogenic strain dominated, repeated epidemics led to host eradication. Seroprevalence data suggest that the non–pathogenic strain may be protecting some, but not all UK populations, with half being ‘at risk’ from invasion by the pathogenic strain and a fifth prone to significant transient mortality. We identify key questions for empirical research to test this prediction.

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