Rabbit Haemorrhagic Disease

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Tanja Strive - One of the best experts on this subject based on the ideXlab platform.

  • differential serological diagnostics of different Rabbit Haemorrhagic Disease viruses co circulating in australia
    bioRxiv, 2019
    Co-Authors: John Kovaliski, Lorenzo Capucci, Tanja Strive, Melissa Piper, Nina Huang, Roslyn Mourant, Tarnya E Cox
    Abstract:

    Abstract The lagovirus Rabbit Haemorrhagic Disease Virus (RHDV) has been circulating in Australia since the mid-1990s when it was deliberately released to control overabundant Rabbit populations. In recent years, the viral diversity of different RHDVs circulating in Australia has increased. An additional strain of an antigenic RHDV variant was deliberately released to boost Rabbit control in 2017, and two exotic incursions of lagoviruses, including the novel calicivirus RHDV2, have also been reported in Australia. RHDV2 has since become the dominant strain in Australian wild Rabbits. To allow for ongoing epidemiological studies and impact assessments of these viruses on Rabbit populations, it is essential that serological tools are updated. Here we describe the adaptation of a competition enzyme linked immunosorbent assay (cELISA) for the specific detection of antibodies against the Australian RHDV2 virus, as well as modified isotype ELISAs to allow for the more sensitive detection of RHDV2 specific IgM and IgA antibodies. We also assessed the patterns of cross-reactivity of sera raised against all virulent caliciviruses known to be present in Australia in a series of available competition ELISAs and isotype ELISAs originally developed for the prototype RHDV. The new serological assays provide valuable tools to study presence, prevalence and impact of RHDV2 on Australian Rabbit populations; however the discrimination of different antigenic variants of RHDVs at the serological level remains challenging.

  • prior exposure to non pathogenic calicivirus rcv a1 reduces both infection rate and mortality from Rabbit Haemorrhagic Disease in a population of wild Rabbits in australia
    Transboundary and Emerging Diseases, 2018
    Co-Authors: Brian Cooke, Lorenzo Capucci, Greg Mutze, June Liu, Tanja Strive, Richard P Duncan, I Mcdonald
    Abstract:

    Mortality caused by Rabbit Haemorrhagic Disease virus (RHDV) in wild Rabbits is reduced in parts of Australia where the related, non-pathogenic calicivirus RCV-A1 is endemic. Laboratory experiments previously showed that prior infection with RCV-A1 enabled Rabbits to better withstand subsequent infection with highly virulent RHDV, and this was assumed to explain higher survival. Here, we analyse serological data from the field suggesting that reduced mortality rates among wild Rabbits may also result from Rabbits previously infected with RCV-A1 having a reduced likelihood of RHDV infection. We discuss the possible mechanisms underlying this finding and its implications. The methods we describe for analysing field data gave far greater insights into epidemiological processes and virus interactions than gained from reporting basic seroprevalence rates alone.

  • an in vivo system for directed experimental evolution of Rabbit Haemorrhagic Disease virus
    PLOS ONE, 2017
    Co-Authors: Lorenzo Capucci, Michael Frese, Robyn N Hall, Markus Matthaei, Tanja Strive, Simona Esposito, Peter J Kerr
    Abstract:

    The calicivirus Rabbit Haemorrhagic Disease virus (RHDV) is widely used in Australia as a biocontrol agent to manage wild European Rabbit (Oryctolagus cuniculus) populations. However, widespread herd immunity limits the effectiveness of the currently used strain, CAPM V-351. To overcome this, we developed an experimental platform for the selection and characterisation of novel RHDV strains. As RHDV does not replicate in cell culture, variant viruses were selected by serially passaging a highly virulent RHDV field isolate in immunologically naive laboratory Rabbits that were passively immunised 18-24 hours post-challenge with a neutralising monoclonal antibody. After seven passages, two amino acid substitutions in the P2 domain of the capsid protein became fixed within the virus population. Furthermore, a synonymous substitution within the coding sequence of the viral polymerase appeared and was also maintained in all subsequent passages. These findings demonstrate proof-of-concept that RHDV evolution can be experimentally manipulated to select for virus variants with altered phenotypes, in this case partial immune escape.

  • expression and partial characterisation of Rabbit Haemorrhagic Disease virus non structural proteins
    Virology, 2015
    Co-Authors: Nadya Urakova, Michael Frese, Robyn N Hall, June Liu, Markus Matthaei, Tanja Strive
    Abstract:

    The intracellular replication and molecular virulence mechanisms of Rabbit Haemorrhagic Disease virus (RHDV) are poorly understood, mainly due to the lack of an effective cell culture system for this virus. To increase our understanding of RHDV molecular biology, the subcellular localisation of recombinant non-structural RHDV proteins was investigated in transiently transfected Rabbit kidney (RK-13) cells. We provide evidence for oligomerisation of p23, and an ability of the viral protease to cleave the p16:p23 junction in trans, outside the context of the nascent polyprotein chain. Notably, expression of the viral polymerase alone and in the context of the entire RHDV polyprotein resulted in a redistribution of the Golgi network. This suggests that, similar to other positive-strand RNA viruses, RHDV may recruit membranes of the secretory pathway during replication, and that the viral polymerase may play a critical role during this process.

  • increased virulence of Rabbit Haemorrhagic Disease virus associated with genetic resistance in wild australian Rabbits oryctolagus cuniculus
    Virology, 2014
    Co-Authors: Peter Elsworth, John Kovaliski, Brian Cooke, Tanja Strive, Edward C Holmes, Ronald Sinclair
    Abstract:

    The release of myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV) in Australia with the aim of controlling overabundant Rabbits has provided a unique opportunity to study the initial spread and establishment of emerging pathogens, as well as their co-evolution with their mammalian hosts. In contrast to MYXV, which attenuated shortly after its introduction, rapid attenuation of RHDV has not been observed. By studying the change in virulence of recent field isolates at a single field site we show, for the first time, that RHDV virulence has increased through time, likely because of selection to overcome developing genetic resistance in Australian wild Rabbits. High virulence also appears to be favoured as Rabbit carcasses, rather than Diseased animals, are the likely source of mechanical insect transmission. These findings not only help elucidate the co-evolutionary interaction between Rabbits and RHDV, but reveal some of the key factors shaping virulence evolution.

Lorenzo Capucci - One of the best experts on this subject based on the ideXlab platform.

  • differential serological diagnostics of different Rabbit Haemorrhagic Disease viruses co circulating in australia
    bioRxiv, 2019
    Co-Authors: John Kovaliski, Lorenzo Capucci, Tanja Strive, Melissa Piper, Nina Huang, Roslyn Mourant, Tarnya E Cox
    Abstract:

    Abstract The lagovirus Rabbit Haemorrhagic Disease Virus (RHDV) has been circulating in Australia since the mid-1990s when it was deliberately released to control overabundant Rabbit populations. In recent years, the viral diversity of different RHDVs circulating in Australia has increased. An additional strain of an antigenic RHDV variant was deliberately released to boost Rabbit control in 2017, and two exotic incursions of lagoviruses, including the novel calicivirus RHDV2, have also been reported in Australia. RHDV2 has since become the dominant strain in Australian wild Rabbits. To allow for ongoing epidemiological studies and impact assessments of these viruses on Rabbit populations, it is essential that serological tools are updated. Here we describe the adaptation of a competition enzyme linked immunosorbent assay (cELISA) for the specific detection of antibodies against the Australian RHDV2 virus, as well as modified isotype ELISAs to allow for the more sensitive detection of RHDV2 specific IgM and IgA antibodies. We also assessed the patterns of cross-reactivity of sera raised against all virulent caliciviruses known to be present in Australia in a series of available competition ELISAs and isotype ELISAs originally developed for the prototype RHDV. The new serological assays provide valuable tools to study presence, prevalence and impact of RHDV2 on Australian Rabbit populations; however the discrimination of different antigenic variants of RHDVs at the serological level remains challenging.

  • prior exposure to non pathogenic calicivirus rcv a1 reduces both infection rate and mortality from Rabbit Haemorrhagic Disease in a population of wild Rabbits in australia
    Transboundary and Emerging Diseases, 2018
    Co-Authors: Brian Cooke, Lorenzo Capucci, Greg Mutze, June Liu, Tanja Strive, Richard P Duncan, I Mcdonald
    Abstract:

    Mortality caused by Rabbit Haemorrhagic Disease virus (RHDV) in wild Rabbits is reduced in parts of Australia where the related, non-pathogenic calicivirus RCV-A1 is endemic. Laboratory experiments previously showed that prior infection with RCV-A1 enabled Rabbits to better withstand subsequent infection with highly virulent RHDV, and this was assumed to explain higher survival. Here, we analyse serological data from the field suggesting that reduced mortality rates among wild Rabbits may also result from Rabbits previously infected with RCV-A1 having a reduced likelihood of RHDV infection. We discuss the possible mechanisms underlying this finding and its implications. The methods we describe for analysing field data gave far greater insights into epidemiological processes and virus interactions than gained from reporting basic seroprevalence rates alone.

  • arrival of Rabbit Haemorrhagic Disease virus 2 to northern europe emergence and outbreaks in wild and domestic Rabbits oryctolagus cuniculus in sweden
    Transboundary and Emerging Diseases, 2018
    Co-Authors: Lorenzo Capucci, Aleksija Neimanis, Harri Ahola, Siamak Zohari, Larsson U Pettersson, Caroline Brojer, Dolores Gavierwiden
    Abstract:

    Incursion of Rabbit Haemorrhagic Disease virus (RHDV) into Sweden was documented in 1990 and it is now considered endemic in wild Rabbit (Oryctolagus cuniculus) populations. Rabbit Haemorrhagic Disease virus 2 (RHDV2), a new, related lagovirus was first detected in France in 2010, and has spread rapidly throughout Europe and beyond. However, knowledge of RHDV2 in northern Europe is sporadic and incomplete, and in Sweden, routinely available diagnostic methods to detect Rabbit Haemorrhagic Disease (RHD) do not distinguish between types of virus causing Disease. Using RHDV2-specific RT-qPCR, sequencing of the VP60 gene and immunological virus typing of archived and prospective case material from the National Veterinary Institute's (SVA) wildlife Disease surveillance programme and diagnostic pathology service, we describe the emergence of RHDV2 in Sweden in both wild and domestic Rabbits. The earliest documented outbreak occurred on 22 May 2013, and from May 2013 to May 2016, 10 separate incidents of RHDV2 were documented from six different municipalities in the southern half of Sweden. Phylogenetic analysis of the VP60 gene shows clear clustering of Swedish isolates into three separate clusters within two different clades according to geographic location and time, suggesting viral evolution, multiple introduction events or both. Almost all cases of RHD examined by SVA from May 2013 to May 2016 were caused by RHDV2, suggesting that RHDV2 may be replacing RHDV as the predominant cause of RHD in Sweden.

  • increased pathogenicity in Rabbit Haemorrhagic Disease virus type 2 rhdv2
    Veterinary Record, 2017
    Co-Authors: Lorenzo Capucci, Patrizia Cavadini, Guerino Lombardi, M Schiavitto, Antonio Lavazza
    Abstract:

    Rabbit Haemorrhagic Disease (RHD) is an acute and lethal form of viral hepatitis in Rabbits ( Oryctolagus cuniculus ) with a mortality rate in adults ranging from 70 per cent to 100 per cent. RHD was first reported in China in 1984, in Europe in 1986, where it caused severe losses to Rabbit, and in Australia in 1996 (Abrantes and others 2012). RHD is caused by the lagovirus RHD virus (RHDV) in the family Caliciviridae. In the course of its evolution, RHDV split into six genotypes (Kerr and others 2009), all highly pathogenic and virulent. Genotype 6 is the antigenic subtype (RHDVa) that became prevalent in certain countries, including the USA (McIntosh and others 2007). In addition, other enteric non-pathogenic Rabbit caliciviruses (RCVs) related to RHDV have been identified in Europe and Australia (Capucci and others 1996, Strive and others 2009, Le Gall-Recule and others 2011a). In 2010, a new lagovirus was identified in France. This virus showed a capsid protein sequence identity of about 80 per cent with RHDV and was able to cause RHD in vaccinated and young Rabbits (15–25 days old) (Le Gall-Recule and others 2011a, b). In addition, it showed a distinct antigenic profile and induced an average mortality rate of 20–30 per cent in both experimental infections and natural cases; such a low mortality rate was never observed in the many experimental Rabbit infections carried out with other strains of RHDV. The remaining 70–80 per cent of the Rabbits survived the infection without showing typical signs of RHD (Le Gall-Recule and others 2011b). Unexpectedly, in autumn 2011, this new virus also caused fatal cases in cape hares ( Lepus capensis var meditteraneus) (Puggioni and others 2013). All these features strongly suggested that the virus was not derived from RHDV but …

  • an in vivo system for directed experimental evolution of Rabbit Haemorrhagic Disease virus
    PLOS ONE, 2017
    Co-Authors: Lorenzo Capucci, Michael Frese, Robyn N Hall, Markus Matthaei, Tanja Strive, Simona Esposito, Peter J Kerr
    Abstract:

    The calicivirus Rabbit Haemorrhagic Disease virus (RHDV) is widely used in Australia as a biocontrol agent to manage wild European Rabbit (Oryctolagus cuniculus) populations. However, widespread herd immunity limits the effectiveness of the currently used strain, CAPM V-351. To overcome this, we developed an experimental platform for the selection and characterisation of novel RHDV strains. As RHDV does not replicate in cell culture, variant viruses were selected by serially passaging a highly virulent RHDV field isolate in immunologically naive laboratory Rabbits that were passively immunised 18-24 hours post-challenge with a neutralising monoclonal antibody. After seven passages, two amino acid substitutions in the P2 domain of the capsid protein became fixed within the virus population. Furthermore, a synonymous substitution within the coding sequence of the viral polymerase appeared and was also maintained in all subsequent passages. These findings demonstrate proof-of-concept that RHDV evolution can be experimentally manipulated to select for virus variants with altered phenotypes, in this case partial immune escape.

Brian Cooke - One of the best experts on this subject based on the ideXlab platform.

  • prior exposure to non pathogenic calicivirus rcv a1 reduces both infection rate and mortality from Rabbit Haemorrhagic Disease in a population of wild Rabbits in australia
    Transboundary and Emerging Diseases, 2018
    Co-Authors: Brian Cooke, Lorenzo Capucci, Greg Mutze, June Liu, Tanja Strive, Richard P Duncan, I Mcdonald
    Abstract:

    Mortality caused by Rabbit Haemorrhagic Disease virus (RHDV) in wild Rabbits is reduced in parts of Australia where the related, non-pathogenic calicivirus RCV-A1 is endemic. Laboratory experiments previously showed that prior infection with RCV-A1 enabled Rabbits to better withstand subsequent infection with highly virulent RHDV, and this was assumed to explain higher survival. Here, we analyse serological data from the field suggesting that reduced mortality rates among wild Rabbits may also result from Rabbits previously infected with RCV-A1 having a reduced likelihood of RHDV infection. We discuss the possible mechanisms underlying this finding and its implications. The methods we describe for analysing field data gave far greater insights into epidemiological processes and virus interactions than gained from reporting basic seroprevalence rates alone.

  • Recovery of South Australian Rabbit populations from the impact of Rabbit Haemorrhagic Disease
    Wildlife Research, 2015
    Co-Authors: Greg Mutze, John Kovaliski, Peter Bird, Scott Jennings, David Peacock, N. De Preu, Brian Cooke, Lorenzo Capucci
    Abstract:

    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.

  • Rabbit Haemorrhagic Disease virus persistence and adaptation in australia
    Evolutionary Applications, 2014
    Co-Authors: Nina Schwensow, John Kovaliski, David Peacock, Brian Cooke, Ron Sinclair, Joerns Fickel, Simone Sommer
    Abstract:

    In Australia, the Rabbit Haemorrhagic Disease virus (RHDV) has been used since 1996 to reduce numbers of introduced European Rabbits (Oryctolagus cuniculus) which have a devastating impact on the native Australian environment. RHDV causes regular, short Disease outbreaks, but little is known about how the virus persists and survives between epidemics. We examined the initial spread of RHDV to show that even upon its initial spread, the virus circulated continuously on a regional scale rather than persisting at a local population level and that Australian Rabbit populations are highly interconnected by virus-carrying flying vectors. Sequencing data obtained from a single Rabbit population showed that the viruses that caused an epidemic each year seldom bore close genetic resemblance to those present in previous years. Together, these data suggest that RHDV survives in the Australian environment through its ability to spread amongst Rabbit subpopulations. This is consistent with modelling results that indicated that in a large interconnected Rabbit meta-population, RHDV should maintain high virulence, cause short, strong Disease outbreaks but show low persistence in any given subpopulation. This new epidemiological framework is important for understanding virus–host co-evolution and future Disease management options of pest species to secure Australia's remaining natural biodiversity.

  • increased virulence of Rabbit Haemorrhagic Disease virus associated with genetic resistance in wild australian Rabbits oryctolagus cuniculus
    Virology, 2014
    Co-Authors: Peter Elsworth, John Kovaliski, Brian Cooke, Tanja Strive, Edward C Holmes, Ronald Sinclair
    Abstract:

    The release of myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV) in Australia with the aim of controlling overabundant Rabbits has provided a unique opportunity to study the initial spread and establishment of emerging pathogens, as well as their co-evolution with their mammalian hosts. In contrast to MYXV, which attenuated shortly after its introduction, rapid attenuation of RHDV has not been observed. By studying the change in virulence of recent field isolates at a single field site we show, for the first time, that RHDV virulence has increased through time, likely because of selection to overcome developing genetic resistance in Australian wild Rabbits. High virulence also appears to be favoured as Rabbit carcasses, rather than Diseased animals, are the likely source of mechanical insect transmission. These findings not only help elucidate the co-evolutionary interaction between Rabbits and RHDV, but reveal some of the key factors shaping virulence evolution.

  • Australia's War Against Rabbits: The Story of Rabbit Haemorrhagic Disease
    2014
    Co-Authors: Brian Cooke
    Abstract:

    The management of wild Rabbits is a vexing problem worldwide. In countries such as Australia and New Zealand, wild Rabbits are regarded as serious pests to agriculture and the environment, while in many European countries they are considered an important hunting resource, and are a cornerstone species in Mediterranean ecosystems, modifying habitats and supporting important predator populations such as the Iberian lynx. The introduction of two viral Diseases, myxomatosis and Rabbit Haemorrhagic Disease, as biological control agents in Australia has been met favourably, yet their spread in southern Europe threatens natural Rabbit populations. Despite this, scientists with very different goals still work together with a common interest in understanding Rabbit biology and epidemiology. Australia's War Against Rabbits uses Rabbit Haemorrhagic Disease as an important case study in understanding how animal populations adapt to Diseases, caused in this case by an RNA virus. Looking at Rabbit Haemorrhagic Disease (RHD) in an ecological framework enables insights into both virus and Rabbit biology that are relevant for understanding other emerging Diseases of importance to humans. This book provides up-to-date information on recent advances in areas ranging from virus structure and Disease mechanics through to the sociological implications of using biological control agents and the benefits to the economy and biodiversity. It is a compelling read for wildlife Disease researchers, wildlife managers, Rabbit biologists, people working in the public health and education sectors, and landholders and farmers with experience or interest in RHD.

John Kovaliski - One of the best experts on this subject based on the ideXlab platform.

  • differential serological diagnostics of different Rabbit Haemorrhagic Disease viruses co circulating in australia
    bioRxiv, 2019
    Co-Authors: John Kovaliski, Lorenzo Capucci, Tanja Strive, Melissa Piper, Nina Huang, Roslyn Mourant, Tarnya E Cox
    Abstract:

    Abstract The lagovirus Rabbit Haemorrhagic Disease Virus (RHDV) has been circulating in Australia since the mid-1990s when it was deliberately released to control overabundant Rabbit populations. In recent years, the viral diversity of different RHDVs circulating in Australia has increased. An additional strain of an antigenic RHDV variant was deliberately released to boost Rabbit control in 2017, and two exotic incursions of lagoviruses, including the novel calicivirus RHDV2, have also been reported in Australia. RHDV2 has since become the dominant strain in Australian wild Rabbits. To allow for ongoing epidemiological studies and impact assessments of these viruses on Rabbit populations, it is essential that serological tools are updated. Here we describe the adaptation of a competition enzyme linked immunosorbent assay (cELISA) for the specific detection of antibodies against the Australian RHDV2 virus, as well as modified isotype ELISAs to allow for the more sensitive detection of RHDV2 specific IgM and IgA antibodies. We also assessed the patterns of cross-reactivity of sera raised against all virulent caliciviruses known to be present in Australia in a series of available competition ELISAs and isotype ELISAs originally developed for the prototype RHDV. The new serological assays provide valuable tools to study presence, prevalence and impact of RHDV2 on Australian Rabbit populations; however the discrimination of different antigenic variants of RHDVs at the serological level remains challenging.

  • Recovery of South Australian Rabbit populations from the impact of Rabbit Haemorrhagic Disease
    Wildlife Research, 2015
    Co-Authors: Greg Mutze, John Kovaliski, Peter Bird, Scott Jennings, David Peacock, N. De Preu, Brian Cooke, Lorenzo Capucci
    Abstract:

    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.

  • Rabbit Haemorrhagic Disease virus persistence and adaptation in australia
    Evolutionary Applications, 2014
    Co-Authors: Nina Schwensow, John Kovaliski, David Peacock, Brian Cooke, Ron Sinclair, Joerns Fickel, Simone Sommer
    Abstract:

    In Australia, the Rabbit Haemorrhagic Disease virus (RHDV) has been used since 1996 to reduce numbers of introduced European Rabbits (Oryctolagus cuniculus) which have a devastating impact on the native Australian environment. RHDV causes regular, short Disease outbreaks, but little is known about how the virus persists and survives between epidemics. We examined the initial spread of RHDV to show that even upon its initial spread, the virus circulated continuously on a regional scale rather than persisting at a local population level and that Australian Rabbit populations are highly interconnected by virus-carrying flying vectors. Sequencing data obtained from a single Rabbit population showed that the viruses that caused an epidemic each year seldom bore close genetic resemblance to those present in previous years. Together, these data suggest that RHDV survives in the Australian environment through its ability to spread amongst Rabbit subpopulations. This is consistent with modelling results that indicated that in a large interconnected Rabbit meta-population, RHDV should maintain high virulence, cause short, strong Disease outbreaks but show low persistence in any given subpopulation. This new epidemiological framework is important for understanding virus–host co-evolution and future Disease management options of pest species to secure Australia's remaining natural biodiversity.

  • increased virulence of Rabbit Haemorrhagic Disease virus associated with genetic resistance in wild australian Rabbits oryctolagus cuniculus
    Virology, 2014
    Co-Authors: Peter Elsworth, John Kovaliski, Brian Cooke, Tanja Strive, Edward C Holmes, Ronald Sinclair
    Abstract:

    The release of myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV) in Australia with the aim of controlling overabundant Rabbits has provided a unique opportunity to study the initial spread and establishment of emerging pathogens, as well as their co-evolution with their mammalian hosts. In contrast to MYXV, which attenuated shortly after its introduction, rapid attenuation of RHDV has not been observed. By studying the change in virulence of recent field isolates at a single field site we show, for the first time, that RHDV virulence has increased through time, likely because of selection to overcome developing genetic resistance in Australian wild Rabbits. High virulence also appears to be favoured as Rabbit carcasses, rather than Diseased animals, are the likely source of mechanical insect transmission. These findings not only help elucidate the co-evolutionary interaction between Rabbits and RHDV, but reveal some of the key factors shaping virulence evolution.

  • is increased juvenile infection the key to recovery of wild Rabbit populations from the impact of Rabbit Haemorrhagic Disease
    European Journal of Wildlife Research, 2014
    Co-Authors: Greg Mutze, Lorenzo Capucci, David Peacock, Ron Sinclair, John Kovaliski
    Abstract:

    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.

Carlos Rouco - One of the best experts on this subject based on the ideXlab platform.

  • worldwide rapid spread of the novel Rabbit Haemorrhagic Disease virus gi 2 rhdv2 b
    Transboundary and Emerging Diseases, 2019
    Co-Authors: Carlos Rouco, Joana Abrantes, Juan Antonio Aguayoadan, Simone Santoro, Miguel Delibesmateos
    Abstract:

    We describe the extremely rapid worldwide spread of the Lagovirus europaeus/GI.2/RHDV2/b (henceforth GI.2), the causative infectious agent of the so‐called ‘novel’ Rabbit Haemorrhagic Disease of the European Rabbit (Oryctolagus cuniculus). We tracked down all novel confirmed detections of GI.2 between May 2010 and November 2018 by carrying out a two‐step in‐depth review. We suggest that such spread would not have been possible without anthropogenic involvement. Our results also point out the importance of reviewing and adapting the protocols of virus detection and management in order to control, mitigate and contain properly, not only GI.2, but also new viruses that may emerge in the future.

  • Oxidative stress in wild European Rabbits naturally infected with myxoma virus and Rabbit Haemorrhagic Disease virus
    European Journal of Wildlife Research, 2018
    Co-Authors: Isabel Pacios-palma, Sacramento Moreno, Colin Selman, Carlos Rouco
    Abstract:

    The European Rabbit ( Oryctolagus cuniculus ) is one of the most important vertebrate species in the Mediterranean Basin ecosystem. Over the last 60 years, the arrival of two viral Diseases, myxomatosis and Rabbit Haemorrhagic Disease, have led to dramatic declines in wild Rabbit populations across the Iberian Peninsula. These Diseases are currently endemic. Periodic outbreaks occur and have significant impacts on wild populations. Both infection types have diverse physiological effects on their hosts that are rooted in aerobic metabolic processes. To fight off these viruses, Rabbits activate their immune systems. However, the production of immune defences generates reactive oxygen species that may consequently damage host tissues. Hypothesising that immune responses increase oxidative stress, we examined whether wild Rabbits naturally infected with myxoma virus (MV) and Rabbit Haemorrhagic Disease virus (RHDV) had high oxidative stress. Using blood samples, we measured anti-MV and anti-RHDV antibody concentrations and different oxidative stress markers (i.e., glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase, and malondialdehyde). Our results show that Rabbits that were seropositive for both MV and RHDV had high concentrations of malondialdehyde. Age and body condition were also positively related to dual seropositivity. No significant relationships were observed between serostatus and the concentrations of the other oxidative stress markers. Although we expected infection with MV and RHDV to be correlated with oxidative stress, the influence of external sources of oxidative stress (e.g., climatic conditions) likely made it more difficult to detect such relationships in wild Rabbits.

  • a case of low success of blind vaccination campaigns against myxomatosis and Rabbit Haemorrhagic Disease on survival of adult european wild Rabbits
    Preventive Veterinary Medicine, 2016
    Co-Authors: Sacramento Moreno, Carlos Rouco, Simone Santoro
    Abstract:

    Vaccination campaigns against myxomatosis and Rabbit Haemorrhagic Disease (RHD) are commonly used in translocation programs conducted for the purpose of recovering wild European Rabbit populations in Iberian Mediterranean ecosystems. In most cases Rabbits are vaccinated 'blind' (i.e. without assessing their prior immunological status) for economic and logistic reasons. However, there is conflicting evidence on the effectiveness of such an approach. We tested whether blind vaccination against myxomatosis and Rabbit Haemorrhagic Disease improved Rabbit survival in a Rabbit translocation program where wild Rabbits were kept in semi-natural conditions in three enclosures. We conducted nine capture sessions over two years (2008-2010) and used the information collected to compare the survival of vaccinated (n=511) versus unvaccinated (n=161) adult wild Rabbits using capture-mark-recapture analysis. Average monthly survival was no different for vaccinated versus unvaccinated individuals, both in the period between release and first capture (short-term) and after the first capture onward (long-term). Rabbit survival was lower in the short term than in the long term regardless of whether Rabbits were vaccinated or not. Lower survival in the short-term could be due to the stress induced by the translocation process itself (e.g. handling stress). However, we did not find any overall effect of vaccination on survival which could be explained by two non-exclusive reasons. First, interference of the vaccine with the natural antibodies in the donor population. Due to donor populations have high density of Rabbits with, likely, high prevalence of antibodies as a result of previous natural exposure to these Diseases. Second, the lack of severe outbreaks during the study period. Based on our findings we argue that blind vaccination of adult Rabbits in translocation programs may be often mostly ineffective and unnecessarily costly. In particular, since outbreaks are hard to predict and vaccination of Rabbits with natural antibodies is ineffective, it is crucial to assess the immunological status of the donor population before translocating adult Rabbits.