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The host innate immune response to viral infection often involves the activation of type I interferons. Not surprisingly, many viruses have evolved various mechanisms to disable the interferon pathway and evade the antiviral response involving innate immunity. Rabbit hemorrhagic disease (RHD) is caused by RHD virus (RHDV), but whether it can antagonize the production of host interferon to establish infection has not been investigated. In this study, we found that during RHDV infection, the expressions of interferon and the interferon-stimulated gene were not activated. We constructed eukaryotic expression plasmids of all RHDV proteins, and found that RHDV 3C protein inhibited poly(I:C)-induced interferon expressions. Using siRNA to interfere with the expressions of TLR3 and MDA5, we found that the MDA5 signal pathway was used by the 3C protein to inhibit poly(I:C)-induced interferon expression. This effect was mediated by cleaving the interferon promoter stimulated 1 (IPS-1) protein. Finally, our study showed that interferon was effective against RHDV infection. In summary, our findings showed that the RHDV 3C protein was a new interferon antagonist. These results increase our understanding of the escape mechanism from innate immunity mediated by the RHDV 3C protein. [ABSTRACT FROM AUTHOR]

Lagovirus europaeus/GI.1 causes a fatal viral condition in rabbits characterized by acute viral hepatitis and disseminated intravascular coagulation. Due to rapid viral and environmental changes variants (Lagovirus europaeus/GI.1a and GI.2) have appeared and few immunological studies were performed. The aim of the study was to determine innate and adaptive immunity parameters in rabbits infected with six Lagovirus europeus/GI.1a viruses. To achieve the goal several methods were used, i.e. cytometry, microscopy, biochemical and cytochemical tests, spectrophotometry. The results show that three immunotypes exists among the studied strains and they differ in innate (mainly) and adaptive immunity, partly depending on hemagglutination. The peak of changes is 24 h post infection in phagocytosis markers of polymorphonuclear cells and CD8+ T cells. Lagovirus europaeus/GI.1a strains differ from Lagovirus europaeus/GI.1 in terms of immunological response based on our previous work concerning the same parameters in immunological response against this disease. [ABSTRACT FROM AUTHOR]

Rabbit hemorrhagic disease is an acute fatal highly contagious viral infectious disease that causes high losses among rabbitries. The disease was first reported in China in 1984 and later on in Saudi Arabia in 1996. The aim of this study was to investigate the emergence and pathogenicity of new rabbit hemorrhagic disease virus (RHDV) strains in Saudi Arabia. The pathogenicity was confirmed by inoculation in susceptible rabbits. Three RHDV strains were detected by reverse transcriptase polymerase chain reaction (RT-PCR) using primers targeting VP60 capsid protein gene in infected rabbitries during 2012 and 2013. These strains clustered into two genetically distinct genogroups related to year of isolation (G2 and G3). All new Saudi Arabia viruses clustered with the European strains, while the old strains clustered with strains from China and America. Based on amino acids and nucleotide sequences, the Saudi Arabia strains (RHD/1/SA/2012, RHD/2/SA/2012, and RHD/3/SA /2013) had high identity with Mexico89, Ca11-ITA, and 00-13,FRA virus; on the other hand, there was a relatively high identity with Bahrain strain. The evolutionary relationship of Saudi RHDVs strains revealed significant nucleotides and amino acid substitutions in hypervariable region E, suggesting the emergence of new RHDVs circulating in Saudi Arabia rabbitries. These antigenic changes represented by the antigenic index might be a potential cause of vaccination failure and raises the need to review the vaccination strategies against RHD. [ABSTRACT FROM AUTHOR]

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

The arrival of a new variant of rabbit haemorrhagic disease virus, known as RHDV2, has recently taken place in the native range of the European rabbit ( Oryctolagus cuniculus ), a keystone species which has undergone a sharp decline over the last sixty years as a consequence of certain harmful factors. Several works have noted the presence of this new variant in wild rabbit populations, and have in some cases recorded high mortality rates. However, little is known about the response to the arrival of this new virus variant at the population level. The goal of this work is therefore to show recent trends in 26 wild rabbit populations between 2010 (before the outbreak of the disease) and 2014 (after its onset) in two different ecosystems (woodland and agricultural areas), in order to test how their abundances changed over this period, which coincided with the spread of the RHDV2. Overall, our results showed that rabbit abundance was much lower in 2014 than in 2010, and that only 11.5% of the populations monitored proved to have a positive trend, that is, a higher abundance in 2014 than 2010. A positive correlation between rabbit abundance in 2010 and rabbit population trends was obtained, thus suggesting that the impact of the new variant on rabbit abundance is less evident in high density populations. Our results suggest that smaller rabbit populations are those most vulnerable to the outbreak of RHDV 2 and are therefore likely to decline sharply or even become extinct. [ABSTRACT FROM AUTHOR]

The frequency and timing of rabbit haemorrhagic disease (RHD) epizootics and their impact on different age groups of rabbits were studied for 15 years in a recovering rabbit population in South Australia. We recorded the number and body size of rabbits dying during RHD epizootics, collected tissue for genetic analysis of rabbit haemorrhagic disease virus variants and compared the number of carcasses found to the number of susceptible rabbits present at the beginning of each epizootic. All RHD epizootics occurred between late winter and spring, but, progressively, epizootics started earlier and became more frequent and prolonged, fewer susceptible adult rabbits were present during epizootics, and the age of rabbits dying of RHD declined. Increased infection and virus shedding in juvenile rabbits offers the most plausible explanation for those epidemiological changes; the disease is now increasingly transmitted through populations of kittens, starting before young-of-the-year reach adult size and persisting late in the breeding season, so that most rabbits are challenged in their year of birth. These changes have increased juvenile mortality due to RHD but reduced total mortality across all age groups, because age-specific mortality rates are lower in young rabbits than in older rabbits. We hypothesise that this may be the proximate cause of recovery in rabbit populations across Australia and possibly elsewhere. [ABSTRACT FROM AUTHOR]

Based on the infectious full-length cDNA clone of rabbit hemorrhagic disease virus (RHDV), the in vitro transcripts are introduced into RK13 cells. 12 h later, CPE could be observed clearly, and virual antigen could also be detected by IFA. The titre of the recovered virus is 104.6/mL. Immune electron microscopic observation of the virus particles revealed that the particles were rotund with a diameter of about 30 nm. Besides, virus titre quantification obtained by qRT-PCR showed a correlation between time from infection and virus titre. All these results showed that we have recovered RHDV from RK13 cells by reverse genetics technology successfully, and this would be very useful in studies of the antigenicity, virulence, pathogenesis, maturation and new type vaccines of RHDV. [ABSTRACT FROM AUTHOR]

The gene encoding the p60 capsid protein from a Spanish isolate of the rabbit hemorrhagic disease virus (RHDV) has been cloned and sequenced. Both cDNA and the derived protein sequences have been compared with those from several contemporary European RHDV isolates. Genetic heterogeneity among cocirculating viruses is nearly constant along the p60-encoding gene, around 0.034 substitutions per nucleotide, and it does not allow prediction of the preferential regions for long-term fixation of mutations. However, sequence comparisons with the more distant, but phylogenetically closely related calicivirus, the European brown hare syndrome virus (EBHSV), reveal a great extent of genetic variability within both a segment of p60 gene (nucleotides 900-1300) and the encoded polypeptide, suggesting the existence of strong selective pressures acting over this region of the capsid protein. [ABSTRACT FROM AUTHOR]

Rabbit hemorrhagic disease virus (RHDV) is a member of the caliciviridae family. The nucleotidic sequence of a full-length cDNA of one RHDV isolate (RHDV-SD) is reported. The genome is 7437 bases long and includes two ORFs, ORF1 (7034 b) and ORF2 (353 b), coding for the polyprotein and the Vp12, respectively. The coding sequence for the second structural protein (the capsid protein, Vp60) is located at the 3′ end of ORF1. Comparison of RHDV-SD with the German RHDV isolate revealed 470 nucleotide substitutions (96% homology). The deduced amino acid sequences of the two isolates are closely related (98% identity), and no hypervariable region could be identified either in the structural or nonstructural proteins. [ABSTRACT FROM AUTHOR]