Bluetongue Virus Infection Of Ruminants Research Articles

A SUBCLINICAL BLUETONGUE VIRUS INFECTION IN RUMINANTS WITH THREE UNIQUE AMINO ACID VARIATIONS ON VP7 CORE PROTEIN OF TAIWAN ISOLATES

Bluetongue is an arthropod-borne disease in domestic and wild ruminants caused by bluetongue virus (BTV), and it leads to great economic loss worldwide. Previous studies showed that BTV in ruminants in Taiwan was often subclinical infection. The aim of this study was to determine the current status (years 2016–2017) of BTV infection in ruminants in Taiwan, to compare it to the results of a large-scale study conducted in the year 2003, and to investigate whether new viral strains exist. Competitive ELISA tests of serum samples for anti-BTV-VP7 group-specific antibody revealed seropositive rates of 26.7% in cattle by head, similar to 32.7% in the year 2003, suggestive of a BTV-vector-host (cattle) dynamic balance. In goats, the seropositive rate was 18.6%, slightly increased from 8.2% in the year 2003, suggestive of a slow but active infection taking place. This notion was supported by the detection of VP1 gene nucleic acid from whole blood in six out of 29 seropositive goats by reverse transcription–polymerase chain reaction. However, no new virus strain was isolated from embryonating chicken embryos (ECEs) inoculation. Alignment of VP7 amino acid sequences revealed that Taiwan and Japan isolates possessed three specific amino acids on sites No. 82 (arginine), No. 328 (aspartate), and No. 336 (glutamine), which are different from many countries. In a three-dimensional model, these amino acids were located closely on the middle lateral surface of VP7 trimers. Since VP7 is a major outer protein engaged in entry into insect cells and a strong T cell response inducer, these differences likely indicate the result of positive selection of local vectors and hosts in Taiwan.

Bluetongue.

Summary Bluetongue (BT) is an arthropod-transmitted viral disease of non-African ungulates, principally sheep. The disease results from vascular injury analogous to that of human haemorrhagic viral fevers, with characteristic tissue infarction, haemorrhage, vascular leakage, oedema, and hypovolaemic shock. Importantly, BT is not zoonotic. Bluetongue virus (BTV) infection of ruminants and vector Culicoides midges is endemic throughout many tropical and temperate regions of the world; however, within this global range the virus exists within relatively discrete ecosystems (syn. episystems) where specific constellations of BTV serotypes are spread by different species of biting Culicoides midges. Recently discovered goat-associated BTVs, notably BTV serotype 25 (BTV-25) in central Europe, appear to have distinctive biological properties and an epidemiology that is not reliant on Culicoides midges as vectors for virus transmission. Bluetongue virus infection of ruminants is often subclinical, but outbreaks of severe disease occur regularly at the upper and lower limits of the virus's global range, where infection is distinctly seasonal. There have been recent regional alterations in the global distribution of BTV infection, particularly in Europe. It is proposed that climate change is responsible for these events through its impact on vector midges. However, the role of anthropogenic factors in mediating emergence of BTV into new areas remains poorly defined; for example, it is not clear to what extent anthropogenic factors were responsible for the recent translocation to northern and eastern Europe of live attenuated vaccine viruses and an especially virulent strain of BTV-8 with distinctive properties. Without thorough characterisation of all environmental and anthropogenic drivers of the recent emergence of BT in northern Europe and elsewhere, it is difficult to predict what the future holds in terms of global emergence of BTV infection. Accurate and convenient laboratory tests are available for the sensitive and specific serological and virological diagnosis of BTV infection and confirmation of BT in animals. Prevention and control strategies for BT are largely reactive in nature, and typically are reliant on vaccination of susceptible livestock and restrictions on animal trade and movement.

Cross-sectional study of bluetongue virus serotype 8 infection in South American camelids in Germany (2008/2009)

Bluetongue (BT) is a major disease of ruminant livestock that can have a substantial impact on income and animal welfare. In South American camelids (SAC), fatalities related to bluetongue virus (BTV) infection were reported in Germany and France during the recent BTV-8 and BTV-1 epizootics, which raised concern about the role of SAC in the epidemiology of BTV.Therefore, a large-scale serological and virological study was conducted in Germany from autumn 2008 to spring 2009. Risk factors associated with BTV infection were analysed by multiple logistic regression. These included age, species, gender and housing arrangements of SAC as well as the location of the herds and the presence of ruminants on farms.Altogether, 249 (14.3%) of 1742 SAC were found seropositive by BTV ELISA, and 43 (47.3%) of the 91 herds had at least one BTV-seropositive SAC. However, no BTV RNA was detected in any of the seropositive samples. Seroprevalence depended on the sampling region and probably on age, but not on any other analysed risk factors associated with BTV infection in ruminants. The highest seroprevalence was found in the west of Germany where the BTV-8 epizootic started in 2006. Recorded BTV-8 related disease and fatalities are discussed. Although the prevalence of BTV-8 antibodies was high in some regions, the virological results indicate that SAC play a negligible role in the epidemiology of this virus infection.

Bluetongue: History, global epidemiology, and pathogenesis

Bluetongue is an arthropod-transmitted viral disease of ruminants and certain other animals that was recognized and described more than 100 years ago in southern Africa. Bluetongue virus (BTV) infection of ruminants and vector Culicoides insects is enzootic throughout tropical and temperate regions of the world; however, there have been drastic recent regional alterations in the global distribution of BTV infection, particularly in Europe since 1998. Multiple novel BTV serotypes also have been detected since 1998 in the south-eastern United States, apparently encroaching from the adjacent Caribbean ecosystem, and novel serotypes of BTV have been identified recently in other historically enzootic regions of the world, including the Middle East and Australia. It has been proposed, but certainly not proven, that global climate change is responsible for these events. BTV infection of ruminants is often subclinical, but outbreaks of severe disease occur with regular frequency especially at the upper and lower limits of the virus’ global range where infection is highly seasonal - occurring in the late summer and autumn. Bluetongue disease results from vascular injury, likely through a process analogous to that of human hemorrhagic viral fevers in which production of vasoactive mediators from virus-infected macrophages and dendritic cells results in enhanced endothelial paracellular permeability with subsequent vascular leakage and hypovolemic shock.

The pathogenesis and immunology of bluetongue virus infection of ruminants

Bluetongue (BLU) virus is transmitted from infected to susceptible ruminants by hematophagous vector midges ( Culicoides species). Cattle are important reservoir hosts of the virus because infection typically is asymptomatic and characterized by prolonged cell associated viremia, and because at least some species of insect vector preferentially feed on cattle. Interaction of BLU virus with the cell membrane of erythrocytes in infected cattle likely facilitates both prolonged viremia as well as infection of the insect vector. BLU disease is most common in sheep and some wildlife species. A variety of host, agent and environmental factors clearly can influence expression of disease in these species. The pathogenesis of BLU virus infection of cattle and sheep is remarkably similar, thus the basis for expression of disease in sheep but not cattle remains to be firmly established. Some difference in susceptibility of endothelial cells to infection in the two species is one potential explanation. Ruminants develop a variety of antiviral responses after BLU virus infection. Antibodies to outer capsid protein VP2 are responsible for virus neutralization, and confer resistance to reinfection with the homologous serotype of BLU virus. Antibodies to epitopes on proteins which are common to all viruses of the BLU serogroup form the basis of current diagnostic serologic tests. Cell mediated responses have been incompletely characterized, in part because BLU virus replicates within dividing lymphocytes and virus-mediated cytolysis inhibits in vitro blastogenesis. Immunological competence of ruminants to BLU virus arises prior to midgestation, and suggestions that persistent immune tolerant BLU virus infection occurs after in utero exposure of cattle have not been substantiated and are not consistent with recent findings.