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Bovine Diarrhea Virus: Testing and Treatment

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.
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.
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).
Commission of the European Communities ‘’Agriculture Pestivirus infections of ruminants’’ Report EUR 10238 EN, 1987
Bovine Viral Diarrhea Virus: Global Status | Request PDF.
Integrated BVD Control Plans for Beef Operations –
A Meta-Analysis of Bovine Viral Diarrhoea Virus (BVDV …
Moennig, V., Houe, H.,

Sex Specific Dominance Reversal Maintains Genetic Variation for Fitness in Drosophila Melanogaster

Sex specific dominance reversal maintains genetic variation for fitness in Drosophila melanogaster.
Natural selection is a relentless force which drives beneficial alleles to fixation and eliminates deleterious ones. With the dynamism natural selection imposes, explaining the maintenance of genetic variation for fitness is an ongoing challenge in evolutionary biology [1]. Mutation-selection balance provides a partial explanation for this phenomenon, however it does not describe the extent to which genetic variation is produced [1]. Strong evidence demonstrates that balancing selection can maintain stable polymorphisms through sexually antagonistic selection, where separate sexes endure opposite fitness effects from the same alleles [2, 3]. Accordingly, opposite sex individuals are in a tug-of-war over optimal traits, allowing separate alleles to be maintained in the population, preventing fixation [3]. Recently it has been proposed that the ability of sexually antagonistic selection to maintain genetic variance in fitness is augmented by the presence of sex-specific dominance reversal (SSDR), where alleles which promote fitness in one sex, are dominant in that sex [4, 8]. On sexually antagonistic loci, it has been theoretically demonstrated that unequal dominance between the sexes causes a concavity in fitness functions near the optima, as the fitness of a heterozygote in each sex is closer in fitness to the more fit homozygote of that sex [5]. Consequently, the allele that is favoured in a sex is dominant in that sex, thereby maintaining alternative alleles for selection to act upon [5]. This theoretical data has recently allowed for the application on animal models.
Sex-specific dominance of sexually antagonistic alleles is predicted to ameliorate the fitness effects of intralocus sexual conflict, therefore dominance reversal likely plays a significant role aiding species displaying higher levels of sexual conflict [6]. The first empirical example of SSDR was investigated at a single major-effect locus controlling age at maturity of salmon. At this locus, sex-dependent dominance was found to reduce sexual conflict and maintain genetic variation [7]. In a more comprehensive study, Grieshop and Arnqvist [8] used a quantitative genetic approach, where a full diallel cross among isogenic strains of seed beetles was used to account for the polygenic nature of fitness. The study revealed genome-wide SSDR for sexually antagonistic loci affecting fitness, and presented an exciting opportunity to reproduce their experiment using an organism of higher complexity. Drosophila melanogaster has been found to exhibit ample sexually antagonistic variation, making ita respectable candidate to measure SSDR in maintaining genetic variance for fitness [5]. We hypothesize that SSDR is occurring on sexually antagonistic loci of D. melanogaster, and contributes in the maintenance of genetic variance for fitness. This is an important area of research and empirical data is limited, making it essential that dominance reversal for fitness is studied for the first time in D. melanogaster. In addition to answering an enduring enigma, this study may uncover a novel phenomenon of masking intralocus sexual conflicts in D. melanogaster [6].
The best way to test this idea is to perform a full diallel cross, following the approach taken by Grieshop and Arnqvist [8]. This technique is ideal as it probes the maintenance of genetic variance in fitness by subdividing phenotypic variance into additive genetic effects, parental effects, dominance, and epistasis [8]. Additionally, by using the full diallel cross and testing for SSDR, sexually antagonistic balancing selection can be distinguished from other forms of balancing selection [8]. To generate inbred lines, we will follow the experimental protocol outlined by Mallet and Chippindale, and use a ‘clone generator’ system of markers and chromosome translocations [9]. Using D. melanogaster from an outbred stock population maintained on a specific selection regime for roughly 30 years, hemiclone lines will be produced using ‘C’ males of an unknown genotype crossed with virgin clone generator (CG) females. A single male progeny is selected to be crossed again to a virgin CG female thus fixing a genomic paternal haplotype, which will be maintained by crossing hemiclone males to CG females. To generate inbred lines, a hemiclone male is crossed with a virgin wildtype C female with an unknown genotype. Virgin daughters produced will be crossed to hemiclone males, and the procedure is repeated 6 times to generate inbred lines for the given haplotype. Each successive cross increases the quantity of genes identical to the original haplotype by 50%, allowing isogenic strains by 6 generations [9].
The surviving inbred strains will be subject to a full diallel cross, where F1 offspring will be analyzed for sex specific competitive lifetime reproductive success (fitness) [8]. F1 male and female fitness will be assayed separately using same sex competitors with a specific visible marker. As a precaution, the experiment will be initiated using 100 lines to account for the loss of strains over multiple generations of inbreeding. It is anticipated that the fitness variance of the inbred lines of D. melanogaster is largely determined by polymorphisms under sexually antagonistic selection opposed to mutation selection balance [8]. Predictions also entail a negative correlation for dominant alleles for fitness amongst male and female flies.
If executed, this study has the potential to produce novel data indicating that SSDR contributes in maintaining genetic variance for fitness in D. melanogaster. This analysis may bring knowledge on balancing selection one step closer to resolving the enigma of outstanding genetic variance. Furthermore, if the hypothesis is upheld, it will provide a basis for further tests of SSDR in more complex organisms, and give evolutionary biologists a better understanding of how genetic variance for fitness is maintained.
Charlesworth B, Hughes KA. (2000). The maintenance of genetic variation in life-history traits. In: Singh RS, Krimbas CB, editors. Evolutionary genetics. Cambridge: Cambridge Univ Press. p. 369–392.
Connallon, T.