Is increased juvenile infection the key to recovery of wild rabbit populations from the impact of rabbit haemorrhagic disease?

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.     

Distribution of cells bearing B-cell alloantigen(s) in North Indian rheumatic fever/rheumatic heart disease patients

Numerous investigators have developed monoclonal antibodies against B-cell alloantigen(s) of rheumatic fever. However, the developed monoclonals do not have the same significance in all the populations. We have developed a battery of monoclonals against B-cell alloantigens of North Indian rheumatic fever patients. In the present study, we have used these monoclonals to examine the frequency of rheumatic antigens in 30 patients with recurrence of rheumatic activity (RRA), 30 of rheumatic heart disease (RHD) patients and 50 controls using alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. These patients were examined at the time of registry and after three months follow up. RRA patients showed higher percentage of lymphocyte positive as compare to RHD and controls. Interestingly, On follow-up RRA patients showed significant decline in positive lymphocyte as compare to first visit whereas no such change was observed in RHD patients. There were 90–93% of RRA and RHD patients positive with these monoclonals. A significant age variation of rheumatic cells was also noticed in all groups of rheumatic patients. We conclude that monoclonals raised from the same ethnic population are highly specific and cost effective to use them to develop an easy field test system such as APAAP, to identify the individual at risk, to develop rheumatic fever. It is also suggested that the alloantigen marker may persist through out life and gets activated after recurrence of the disease.     

Adaptive changes in the genomes of wild rabbits after 16 years of viral epidemics

Since its introduction to control overabundant invasive European rabbits (Oryctolagus cuniculus), the highly virulent rabbit haemorrhagic disease virus (RHDV) has caused regular annual disease outbreaks in Australian rabbit populations. Although initially reducing rabbit abundance by 60%, continent‐wide, experimental evidence has since indicated increased genetic resistance in wild rabbits that have experienced RHDV‐driven selection. To identify genetic adaptations, which explain the increased resistance to this biocontrol virus, we investigated genome‐wide SNP (single nucleotide polymorphism) allele frequency changes in a South Australian rabbit population that was sampled in 1996 (pre‐RHD genomes) and after 16 years of RHDV outbreaks. We identified several SNPs with changed allele frequencies within or close to genes potentially important for increased RHD resistance. The identified genes are known to be involved in virus infections and immune reactions or had previously been identified as being differentially expressed in healthy versus acutely RHDV‐infected rabbits. Furthermore, we show in a simulation study that the allele/genotype frequency changes cannot be explained by drift alone and that several candidate genes had also been identified as being associated with surviving RHD in a different Australian rabbit population. Our unique data set allowed us to identify candidate genes for RHDV resistance that have evolved under natural conditions, and over a time span that would not have been feasible in an experimental setting. Moreover, it provides a rare example of host genetic adaptations to virus‐driven selection in response to a suddenly emerging infectious disease.     

Establishing a serological surveillance protocol for rabbit hemorrhagic disease by combining mathematical models and field data: implication for rabbit conservation

Rabbit hemorrhagic disease (RHD) became endemic in wild rabbit (Oryctolagus cuniculus) populations in the Iberian Peninsula after its first arrival in 1988. This had significant implications for both the economy and environmental conservation because rabbits are one of the main game species in the Iberian Peninsula and a keystone species in the Mediterranean ecosystems. As a consequence, it is planned to include RHD surveillance in the Spanish Wildlife Disease Surveillance Strategy. Nevertheless, there is no practical methodology included in this program to help conservationists and gamekeepers understand the impact of disease on wild rabbit populations. Results from sera collected during the hunting season from 11 rabbit populations of Central and South Spain, which differed in their population abundance and trends, allowed us to use mathematical models to interpret the serological results gathered and determine the best strategy for finalizing a plan of RHD surveillance. Put simply, we focused our field surveys within the hunting season (October-January), and those times when the rabbit populations are at their highest (June or July). Field results showed that both rabbit abundance and population trend are closely related to the prevalence of RHD antibodies when rabbit abundance was at its annual low point (usually October-November). Rabbit population trends were positive only if antibody prevalence was high (>40%), and always negative if prevalence was low. Moreover, rabbit populations where abundance was low always showed low antibody prevalence. Since our models predicted a low variability in the prevalence obtained during the hunting season, it is suggested that future serological surveys should be carried out within this period to avoid problems related to the low sample size in low density rabbit populations.     

Mortality patterns over 3 years in a sparse population of wild rabbits (Oryctolagus cuniculus) in New Zealand, with an emphasis on rabbit haemorrhagic disease (RHD)

A sparse rabbit population in New Zealand was monitored over 3 years to assess the temporal dynamics of rabbit mortality, in particular to understand the mortality patterns due to rabbit haemorrhagic disease (RHD). A total of 107 deaths were recorded, of which 93 could be classified by cause. The predominant cause of mortality was predation (47% of deaths), followed by RHD (20%). Deaths due to RHD were clustered in time (within 3 weeks), predation occurred most actively from late autumn to spring, while other causes of death did not show pronounced seasonal peaks. No differences in cause-specific death risk were observed between sexes. Predation was the main cause of death in younger animals, while RHD mortality occurred mainly in older rabbits. This study has shown that the impact of RHD can vary considerably between years, indicating that a variety of risk factors are required to initiate a RHD epidemic with a high mortality rate among rabbits.     

High adaptive variability and virus-driven selection on major histocompatibility complex (MHC) genes in invasive wild rabbits in Australia

The rabbit haemorrhagic disease virus (RHDV) was imported into Australia in 1995 as a biocontrol agent to manage one of the most successful and devastating invasive species, the European rabbit (Oryctolagus cuniculus cuniculus). During the first disease outbreaks, RHDV caused mortality rates of up to 97% and reduced Australian rabbit numbers to very low levels. However, recently increased genetic resistance to RHDV and strong population growth has been reported. Major histocompatibility complex (MHC) class I immune genes are important for immune responses against viruses, and a high MHC variability is thought to be crucial in adaptive processes under pathogen-driven selection. We asked whether strong population bottlenecks and presumed genetic drift would have led to low MHC variability in wild Australian rabbits, and if the retained MHC variability was enough to explain the increased resistance against RHD. Despite the past bottlenecks we found a relatively high number of MHC class I sequences distributed over 2–4 loci. We identified positive selection on putative antigen-binding sites of the MHC. We detected evidence for RHDV-driven selection as one MHC supertype was negatively associated with RHD survival, fitting expectations of frequency-dependent selection. Gene duplication and pathogen-driven selection are possible (and likely) mechanisms that maintained the adaptive potential of MHC genes in Australian rabbits. Our findings not only contribute to a better understanding of the evolution of invasive species, they are also important in the light of planned future rabbit biocontrol in Australia.     

Do Exotic Vertebrates Structure the Biota of Australia? An Experimental Test in New South Wales

From 1993 to 2001, we conducted a series of experiments in a mixed grassland–woodland system in central New South Wales (NSW) to quantify the interactions between red foxes and their prey and competitors. Foxes were removed from two areas around the perimeter of Lake Burrendong, and data were collected from these areas and a nearby untreated area before, during, and after the period of fox control. The arrival of rabbit hemorrhagic disease (RHD) in 1996 provided an opportunity to examine the interactive effects of controlling foxes and rabbits. In this landscape, typical of central NSW, (a) the fox population was not affected by a large reduction in the abundance of rabbits, or vice versa; (b) the cat population declined in areas where foxes were removed after the large RHD-induced reduction in rabbit numbers, but there was no consistent response to the removal of foxes; (c) the abundance of some macropod species increased in response only to the combined removal of rabbits and foxes; (d) there were no consistent changes in the abundances of bird species in response to the removal of either foxes or rabbits, but there were clear habitat differences in bird species richness; and (e) there was likely to be an increase in woody plant species after the large reduction in rabbit populations by RHD. We conclude that (a) long-term field experiments (more than 3 years) are required to quantify the indirect consequences of controlling foxes and rabbits, and (b) single manipulations, such as fox control or rabbit control, are not necessarily sufficient for the conservation of remnant woodland communities in southeastern Australia.     

Identification and characterization of the virus causing rabbit hemorrhagic disease.

Liver tissue from animals that died of rabbit hemorrhagic disease (RHD) was used to identify the causative agent. After extraction of liver homogenates and sucrose density gradient ultracentrifugation, distinct bands were obtained. The respective gradient fractions reacted positively in an enzyme-linked immunosorbent assay as well as in hemagglutination assays and were infective for rabbits. These fractions contained virions which had a diameter of 40 nm and resembled morphologically those of the family Caliciviridae. By immunoblotting, a major structural protein with a molecular weight of 60,000 was identified. Highly pure RNA of about 8 kilobases was isolated from virions. Labeled cDNA synthesized from virion RNA detected two RNAs of 8 and 2 kilobases in Northern (RNA) blots of liver RNA from animals infected with RHD virus. Finally, isolated virion RNA injected into the liver of rabbits produced a disease with clinical symptoms and pathological findings typical of RHD. We conclude that a calicivirus represents the causative agent of RHD.     

Resistance to RHD virus in wild Australian rabbits: Comparison of susceptible and resistant individuals using a genomewide approach

Deciphering the genes involved in disease resistance is essential if we are to understand host–pathogen coevolutionary processes. The rabbit haemorrhagic disease virus (RHDV) was imported into Australia in 1995 as a biocontrol agent to manage one of the most successful and devastating invasive species, the European rabbit (Oryctolagus cuniculus). During the first outbreaks of the disease, RHDV caused mortality rates of up to 97%. Recently, however, increased genetic resistance to RHDV has been reported. Here, we have aimed to identify genomic differences between rabbits that survived a natural infection with RHDV and those that died in the field using a genomewide next‐generation sequencing (NGS) approach. We detected 72 SNPs corresponding to 133 genes associated with survival of a RHD infection. Most of the identified genes have known functions in virus infections and replication, immune responses or apoptosis, or have previously been found to be regulated during RHD. Some of the genes identified in experimental studies, however, did not seem to play a role under natural selection regimes, highlighting the importance of field studies to complement the genomic background of wildlife diseases. Our study provides a set of candidate markers as a tool for the future scanning of wild rabbits for their resistance to RHDV. This is important both for wild rabbit populations in southern Europe where RHD is regarded as a serious problem decimating the prey of endangered predator species and for assessing the success of currently planned RHDV variant biocontrol releases in Australia.     

Large-scale spatio-temporal shifts in the diet of a predator mediated by an emerging infectious disease of its main prey

Aim To explore the influence of an emerging infectious disease (EID) affecting a prey species on the spatial patterns and temporal shifts in the diet of a predator over a large geographical scale. We reviewed studies on the diet of Bonelli’s eagles (Hieraaetus fasciatus) in order to determine the repercussions of the reduction in the density of its main prey, the rabbit (Oryctolagus cuniculus), caused by outbreaks of rabbit haemorrhagic disease (RHD) since 1988. Location Western continental Europe. Methods We compiled published and unpublished information on the diet of breeding Bonelli’s eagles from Portugal, Spain and France for a 39‐year study period (1968–2006). Nonparametric tests were used in order to analyse temporal shifts in diet composition and trophic diversity (H′) between the periods of ‘high’ (before outbreak of RHD) and ‘low’ rabbit density (after outbreak of RHD). A combination of hierarchical agglomerative clustering and non‐metric multidimensional scaling (NMDS) analyses were used to test for the existence of geographical patterns in the diet of Bonelli’s eagles in each period. Results The diet of the Bonelli’s eagle consisted of rabbit (28.5%), pigeons (24.0%), partridges (15.3%), ‘other birds’ (11.6%), ‘other mammals’ (7.1%), corvids (7.0%), and herptiles (6.4%). However, RHD had large consequences for its feeding ecology: the consumption of rabbits decreased by one‐third after the outbreak of RHD. Conversely, trophic diversity (H′) increased after outbreak of RHD. At the same time, the analyses showed clear geographical patterns in the diet of the Bonelli’s eagle before, but not after, RHD outbreak. Main conclusions Geographical patterns in the diet of the Bonelli’s eagle in western Europe seem to be driven mainly by spatio‐temporal variation in the abundance of rabbits and, to a lesser extent, by the local (territorial) environmental features conditioning the presence and density of alternative prey species. We show that an EID can disrupt predator–prey relationships at large spatial and temporal scales through a severe decline in the population of the main prey species. Hence we argue that strict guidelines should be drawn up to prevent human‐aided dissemination of ‘pathogen pollution’, which can threaten wildlife not only at the population and species level but also at the community and ecosystem scale.     

Spawning migration of American eel Anguilla rostrata from pristine (1843-1872) to contemporary (1963-1990) periods in the St Lawrence Estuary, Canada

A key for three putative species apparently found in three geographic areas, i.e. Coregonus clupeoides (in Scotland), Coregonus stigmaticus (in England), and Coregonus pennantii (in Wales) given in a recent review was tested quantitatively using 544 individuals from nine populations. The classification success of the key was very low (27%). It was concluded that there is currently no robust evidence for the recognition of the three putative species. Furthermore, the use of phenotypic characters alone to distinguish putative species in postglacial fish species such as those of the genus Coregonus that show homoplasy in many of these traits is questioned. In the absence of further evidence, it was concluded that a single highly variable species best describes the pattern of phenotypic variation in these U.K. populations. On this basis it is argued that taxonomic subdivision of U.K. European coregonids is inappropriate and that Coregonus lavaretus should prevail as the species name applicable to all populations.     

First case of rabbit haemorrhagic disease in Canada: contaminated flying insect, vs. long-term infection hypothesis

Following the announcement of the first case of rabbit haemorrhagic disease (RHD) in a pet rabbit, housed indoors in Canada for more than 1 year, I submitted an evidence‐based explanation to ProMed explaining how RHD might have caused the death of ‘one’ of the three pet rabbits. I suggested with supporting evidence, that it may have been persistently infected with rabbit haemorrhagic disease virus (RHDV) which may have reactivated to cause the fatal disease. However, in this issue, Peacock et al. have proposed an alternative ‘hypothesis’ for the appearance of RHD in the pet rabbit. They hypothesise that a non‐identified insect or fomite might have become contaminated by a Chinese strain of RHDV somewhere in the US. This insect/fomite then flew or was windborne, from the US to Canada where it entered the house containing three pet rabbits and infected one of them. RHD is non‐endemic and is rarely reported in the US, where it has only been observed in domestic European rabbits, held in rabbitries. My proposal was based on the details provided by ProMed, the veterinary report from Canada, where RHDV has never previously been identified and the epidemiological, ecological and evolutionary history of RHDV which includes serological and phylogenetic evidence that ancestral RHDV lineages circulated before 1984. The flying insect hypothesis of Peacock et al. is based on circumstantial evidence and, I believe, has a lower probability of being correct than my evidence‐based long‐term infection proposal.     

Predictors of clutch predation of a globally significant avifauna in New Zealand's braided river ecosystems

Predation by introduced mammals is decimating New Zealand's indigenous fauna. Understanding factors that influence this process allows resources for predator control to be applied with maximum effect. This study examines how predation of a secondary prey species (a relatively common but declining native plover, the banded dotterel Charadrius bicinctus ) varied with reductions in abundance of a major prey source (rabbits), kill-trapping of predators, nest density and habitat complexity. Banded dotterels mostly nest in open braided riverbeds alongside a number of endemic threatened species. We measured the fate of 753 dotterel clutches exposed to predation by cats, ferrets and hedgehogs. We found key times and places of high predation risk. Immediately after widespread reduction in rabbit populations by rabbit haemorrhagic disease (RHD), clutch predation rates were almost as high (mean, 50%) as those recorded during past rabbit poisoning programmes (mean, 57%). Both rates were significantly higher than the mean predation rate of 22% without rabbit control, suggesting a shift in predator diet immediately after rabbit population declines. Unlike after rabbit poisoning, clutch predation rate remained high in the years after RHD. Other patterns observed included higher clutch predation rate where nest density was lower, suggesting that predation can potentially cause local extinction. Clutch predation was also higher along riverbed margins where vegetation was dense. There was equivocal evidence for an effect of predator kill-trapping on clutch predation rate. Management strategies that could potentially reduce clutch predation risks include focusing predator mitigation measures during periods of rabbit decline, maintaining them for more than one breeding season if the rabbit declines are widespread (e.g. RHD epidemics), and applying greater effort at sites with relatively low nest density and along riverbed margins where predator use is more frequent.     

Evolutionary genetics of the human Rh blood group system

The evolutionary history of variation in the human Rh blood group system, determined by variants in the RHD and RHCE genes, has long been an unresolved puzzle in human genetics. Prior to medical treatments and interventions developed in the last century, the D-positive (RhD positive) children of D-negative (RhD negative) women were at risk for hemolytic disease of the newborn, if the mother produced anti-D antibodies following sensitization to the blood of a previous D-positive child. Given the deleterious fitness consequences of this disease, the appreciable frequencies in European populations of the responsible RHD gene deletion variant (for example, 0.43 in our study) seem surprising. In this study, we used new molecular and genomic data generated from four HapMap population samples to test the idea that positive selection for an as-of-yet unknown fitness benefit of the RHD deletion may have offset the otherwise negative fitness effects of hemolytic disease of the newborn. We found no evidence that positive natural selection affected the frequency of the RHD deletion. Thus, the initial rise to intermediate frequency of the RHD deletion in European populations may simply be explained by genetic drift/founder effect, or by an older or more complex sweep that we are insufficiently powered to detect. However, our simulations recapitulate previous findings that selection on the RHD deletion is frequency dependent and weak or absent near 0.5. Therefore, once such a frequency was achieved, it could have been maintained by a relatively small amount of genetic drift. We unexpectedly observed evidence for positive selection on the C allele of RHCE in non-African populations (on chromosomes with intact copies of the RHD gene) in the form of an unusually high F( ST ) value and the high frequency of a single haplotype carrying the C allele. RhCE function is not well understood, but the C/c antigenic variant is clinically relevant and can result in hemolytic disease of the newborn, albeit much less commonly and severely than that related to the D-negative blood type. Therefore, the potential fitness benefits of the RHCE C allele are currently unknown but merit further exploration.     

cis基因交换形成RHD-CE(2-9)-D等位基因

以往通过基因组DNA分析,分别在高加索人和中国人中观察到少数Rh阴性个体存在RHD基因第1和第10外显子,但是该等位基因形成的具体分子机制尚有争论。本文分别针对RHD基因mRNA的5′-和3′-非编码区设计一对特异性引物,通过逆转录PCR（RT-PCR）和cDNA测序,分析2例RHD基因阳性（拥有第1和第10外显子）、D抗原表型阴性个体的全长mRNA/cDNA序列,同时以1例正常Rh阳性个体（CcDDee）作对照。结果正常Rh阳性个体拥有正常RHD基因mRNA,2名携带RHD基因的Rh阴性个体则均检出存在与正常RHD基因或RHCE基因转录产物相同长度、以及相同外显子构成的mRNA,但该转录子的第1和第10外显子及3′-非编码区序列与RHD基因一致,而第2～9外显子全部序列与RHCE(e)基因mRNA相同,表明2名个体均存在RHD-CE(2~9)-D融合RHD等位基因,即其RHD基因的第2～9外显子被同源RHCE(e)基因替换,导致不能编码正常RhD蛋白,形成个体D抗原阴性表型。     

Genetic variation in Bromus tectorum (Poaceae): differentiation in the eastern United States

Bromus tectorum, a devastating plant invader in western North America, had entered Pennsylvania by 1790. Although rare, or extirpated, in the east until the 1850s, it was collected with increasing frequency after 1859 from Vermont to Virginia. Using enzyme electrophoresis, we analyzed 38 populations of this grass in the eastern U.S. to determine their genetic variation and structure as well as assess their relatedness to populations in the west. Genetic variation among eastern U.S. populations is low: mean number of alleles per locus (A), percent polymorphic loci per population (%P), and expected heterozygosity (H(exp)) are 1.01, 1.05%, and 0.002, respectively. No heterozygotes were detected. The eastern populations are genetically similar: mean genetic identity for all populations was 0.990 with values among population pairs ranged from 0.913 to 1.000. Thirteen populations in eastern and western North America shared Pgm-1a and Pgm-2a, while eight populations shared Mdh-2b and Mdh-3b. Other alleles detected in western North America (Got-4c, Got-4d, and Pgi-2b) were not, however, found in eastern U.S. populations. The invasion of North America by B. tectorum occurred through multiple introductions on both coasts; results from historical and genetic evidence suggest that eastern populations stem from a minimum of two introductions. The 19th century westward spread of B. tectorum from the East appears to be plausible.     

Australia (Hepatitis-Associated) Antigen in Patients Attending a Venereal Disease Clinic

A total of 1,650 patients attending the venereal disease department at St. Mary''s Hospital, London, have been tested for Australia antigen. Twenty-three positive results were obtained, or 1·39%, which is more than 10 times the rate noted by others in blood donor populations in the U.K. and U.S.A. The positive rates among female patients and European male heterosexual patients were 0·36% and 0·19% respectively. High rates were obtained for homosexual patients (3·8%) and non-European heterosexual patients (3·1%). The reasons for the higher rates found in these groups merit further study.     

Damage caused by low-density exotic herbivore populations: the impact of introduced European rabbits on marsupial herbivores and Allocasuarina and Bursaria seedling survival in Australian coastal shrubland

The impact of over-abundant exotic herbivores is well recognised, but their impact at low population densities is poorly understood. This study examined interactions between European rabbits and native herbivores, and their impact on seedling recruitment in coastal South Australia, 2 years after rabbit haemorrhagic disease (RHD) had reduced rabbit density to 4.48 rabbits ha⁻¹. Rabbit density was further reduced to 0.44 rabbits ha⁻¹ in replicated experimental treatments. Rabbit control reduced total grazing pressure by 39% despite compensatory grazing increases of >100% for both western grey kangaroos and common wombats. Rabbit control slowed the rate of grazing and mortality for planted drooping sheoak and sweet bursaria seedlings, but few survived for 12 months: 0 and 3% of sheoak, in untreated areas and rabbit control treatments, respectively, and 3 and 11% of bursaria, respectively. Planted sheoaks survived well if protected by rabbit-proof netting (60%). Within treatments, seedling grazing and survival rates were negatively correlated with rabbit density but kangaroo and wombat density had no measurable effect. We conclude that RHD may briefly have reduced rabbit densities enough to allow recruitment of bursaria but that sheoak require much lower rabbit densities than those provided by existing biological control agents. If left unaddressed, rabbit grazing could ultimately lead to the loss of sheoaks throughout most of their current range, irrespective of other attempts to conserve them. More generally, these data show how species-specific damage caused by low-density exotic herbivore populations may occur in the presence of more abundant but less-damaging native herbivores.     

Tyzzer's disease in free-living cottontail rabbits (Sylvilagus floridanus) in Maryland

Complement-fixing (CF) antibody to Bacillus piliformis antigen was found in 9 of 14 (64%) serum samples obtained from cottontail rabbits (Sylvilagus floridanus) killed in the wild. CF antibody was not present in the serum of 8 cottontail rabbits trapped as juveniles in the same geographic areas and held in captivity for 4 years. Sero-negative cottontail rabbits died acutely with lesions typical of Tyzzer's disease following the intragastric administration of 10(3.8) ELD50 of B. piliformis spores. The possible influence of Tyzzer's disease upon the cyclic population pattern of cottontail rabbits in the wild is discussed. A hypothesis is presented that B. piliformis spores passed in the feces of diseased wild animals could contaminate pastures, hay and grain, and thereby serve as sources of infection to other animals.     

Non-specific immunity in rabbits infected with 10 strains of the rabbit haemorrhagic disease virus with different biological properties

To determine the parameters of non-specific immunity in rabbits infected with 10 biologically different strains of the rabbit haemorrhagic disease (RHD) virus (BS89, Hagenow, Rainham, Frankfurt, Asturias, Vt97, Triptis, Hartmannsdorf, Pv97, 9905 RHDVa) the following indices were assessed: polimorphonuclear cell (PMN) adherence capacity, absorption index, percentage of absorbing cells, spontaneous, stimulated as well as spectrophotometric test for reduction of the nitroblue tetrazolium (NBT), metabolic activity coefficient of neutrophilic granulocytes, stimulation index, myeloperoxidase activity, lysozyme concentration and activity index. The symptoms and the percentage of mortality in animals infected were recorded. On the basis of the estimated parameters, the present study confirmed the existence of immunotypes among the strains of the RHD virus. However, the results did not indicate a connection between biological property of the RHD virus (haemagglutination capacity and generation of antigenic variants) and the immunological profile of the strains.