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Bovine Diarrhea Virus
The Bovine Viral Diarrheal Virus (BVDV) is the most prevalent enzootic virus that infects both wild and domestic types of bovine animals and other ruminants, such as goats, pigs, camelids, and cervids. There is a relation to other pathogens known to have caused the Border Disease of Sheep and Classical Swine Fever (1). It is a highly successful disease that can be present in many geographical regions and can have a wide range of negative impacts on animal owners and the respective economies around the world (2). In the impacted milk and beef sectors, significant financial losses can be expected. Both direct and indirect (3) economic losses are to occur; directly through losses in production and indirectly through the costs of mitigative control and treatment programmes.
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In a random meta-analysis(4), 6.5 million cows were inspected to conceive an estimate for the frequency of incidence of BVDV of antibody-positive, persistently infected and viraemic animals in herds. There is a 60-80% seroprevalence in herd levels in two example regions, the European Union (5) and North America. The ratio is 9:1 for BVDV Type 1 to BVDV Type 2 in the EU, whereas, in North America, the ratio is instead 1:1. In Australia, approximately 70% of herds are currently experiencing viral infection, which is statistically significant.
The virus is made up of four species, all within the genus Pestivirus, and is included in the Flaviviridae family, its taxonomical name is, therefore, Flavividae pestivirus. It is understood that it is also teratogenic(6). The disease cause is dynamic, eliciting various medical symptoms, including mucosal disease. Acute (transient) and chronic (persistent) infections occur.
In terms of the structure of the viruses in this genus of pestivirus(7), they are spherical in shape and their capsids are enveloped. These virions have an approximate diameter ranging from 40 to 50 nm.
Their shape resembles an icosahedral (composed of equal subunits that form equilateral triangles organized symmetrically) form. Pseudo T=3 the symmetrical structure of the virus, so, in other words, they are T=3 icosahedral capsid protein virions.
They have a cubic genomic structure and are monopartite in their genomic segmentation. In contrast to a capsid protein, mature virions contain three membrane proteins encoded by viruses. Such membrane proteins produced by viruses are Erns, E1 and E2. They are an RNA virus with a single strand. The disease takes place through two genotypes. Type 1- or Type 2 BVDV, with each of these having varied subtypes. Variants of BVDV with the same hereditary constitutions, i.e. biotypes, are cytopathogenic (CP) and non-cytopathogenic (NPC). In terms of the gene expression of this virus, the RNA of the virion itself will cause infection, as it acts as the messenger RNA as well as the genome.
The virus will replicate by attaching itself to a host’s receptors of the virus’s envelope. Protein E will assist internalisation into the host cell with endocytosis mediated by clathrinid, i.e. the host’s endosomal membrane is incorporated into the virus’s membrane. The genome of RNA is distributed into the cytoplasm. The positive-sense genomic ssRNA is converted into a polyprotein that is separated into all structural and non-structural proteins (to produce the proteins for viral replication, i.e. spreading).
Viral influencing factors comprise of biotypical variability, genotypical variation, and heterogeneity in antigens. It is important to note that both BVDV 1 and BVDV 2 viruses can be implicated in the entire spectrum of medical diseases when explaining the clinical forms of BVDV. Infection with bovine viral diarrhoea virus in cattle may contribute to a wide range of medical symptoms from subclinical to fatal diseases(9). After review, the clinical manifestations can be viewed in three subcategories.
The first being BVDV infection in cattle which are immunocompetent, the second being the repercussions of BVDV on a foetus, e.g. infection of the foetus, and lastly, BVDV infection in cattle which are immunotolerant, causing mucosal disease (always fatal). For contraction to occur(10), a host must either be infected via nose to nose contact, i.e. via nasal secretions, with a carrier of the virus, or through a dam to an unborn child, or lastly through contaminated stud semen (11). Clinical effects are based on the interaction of a host’s impacting factors, as in, the rates of environmental stress, and viral factors.
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During gestation(12) , an infection with Bovine Viral Diarrhoea may be transferred from cows to unborn calves, resulting in malformation, miscarriage or calves that serve as unnoticed sources for further spread of the BVD virus.
Persistently infected animals (PI animals)()(13) may be asymptomatic and therefore go ignored, spreading the disease between herds more easily and therefore frequently. PI animals must be immediately destroyed. Persistently infected animals occur when a foetus is infected during the first three to four months of pregnancy(14). If the foetus survives the infection, they will remain a carrier of the disease. It may develop symptoms later in life and is likely to be smaller at birth. Infection after four months allows for a stronger, more competent immune system, which means that the animal can create antibodies and will not be a carrier. Clinical abnormalities may, however, still arise because of the infection.
Environmental factors affecting the viral infection results include the status of immunity function, pregnancy, foetal gestational age at the time of infection, and whether the environment is allowing for a functioning immune system. Skeletal and neurological defects that result from exposure to susceptible dams to the virus during days 75 to 170 of pregnancy. Neurological and structural abnormalities cause hydrocephalus, brachygnathism, hydranencephaly, porencephaly, hypoplasia of the cerebellar, microencephaly, demyelination and brachygnathism, impaired development and infancy, thymic aplasia and pulmonary hypoplasia. Retinal dysplasia or atrophy, optic atrophy, cataract, microphthalmia or recurrent pupillary membrane in the ear, and alopecia hypotrichosis are ocular abnormalities also found with BVD (15) .
Biosecurity, immediate PI livestock disposal, and acute BVD treatment must be performed(16). Blood testing must be executed regularly. Modified live virus and killed virus vaccines are available for mitigative purposes. No treatment to completely eradicate BVDV is currently available( (17).
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