African Horse Sickness Virus (AHSV)
A Microbial Biorealm page on the genus African Horse Sickness Virus (AHSV)
Viruses; dsRNA viruses; Reoviridae; Sedoreovirinae; Orbivirus; African Horse Sickness Virus (AHSV)
Description and significance
ASHV is a pathogenic virus that causes African Horse Sickness. It is lethal in up to 95 % of its hosts, including horses, zebras, donkeys, camels, dogs, and mules, and it is carried by two different species of arthropods. There are nine different serotypes of this virus, of which serotype 9 is the most geographically widespread, reaching most of the African continent. Serotype 4 has transgressed the African borders into Spain and Portugal, infecting many animals in the years 1987-1990.Four different forms of this disease exists: the pulmonary form, cardiac form, the acute (mixed) form, and the horsesickness fever. The disease is not contagious, yet those animals testing positive for the disease are euthanized promptly, and animals traveling from Africa must be quarantined prior to their travel to other continents as a precautionary measure (1).
The AHSV genome is 18,200-30,500 nucleotides long and is made up of 10 double-stranded RNA segments of varying sizes. Three of them are large, named L1-L3. Three of them are medium and are identified as M4-M6, and finally four of them are small, labeled S7-S10. Seven structural proteins are encoded for by 7 of the double stranded RNA segments, and four non-structural proteins are also encoded for by the additional three segments. Of these proteins, the smallest two are encoded for by the same S10 RNA segments, most likely due to different in-frame translation initiation codons. The genome for this virus is very similar to that of its genus' prototype virus, bluetongue virus (BTV) (3).
Cell structure, metabolism & life cycle
The virus particles are spherical and have a icosahedreal symmetry, meaning that they are very similar in shape to a soccer ball. The icosahedron is made up pf twenty equilateral triangles with sixty different subunits. The virus' capsid is 40-60 nm in length, and overall the virius is composed of an inner and outer capsid, a core, and a nucleoprotein complex. The life cycle of this virus is as follows; the virus looses its outer membrane when it enters the host. Next, the virus binds to a cell surface, and transcription and protein synthesis occurs. Within structures known as virus inclusion bodies, mRNA is synthesized, the genome is replicated, resulting in the assembling of a particle, which is then inserted in the cytoplasm of the host cell. Within the cytoplasm, new virions are self-assembled. These virus particles are released from the host cell by budding, during which the virions form a short-lived lipid envelope. The host cells are lysed in order to release the newly formed virus. The capsid of the virus is protease resistant; therefore, it cannot be destroyed by the host cells, providing one reason why the virus is fatal in many of its hosts (3).
Ecology (including pathogenesis)
The disease usually follows seasons of heavy rain, alternating with hot and dry conditions, which is why Africa is its primary geographical range. The virus can be deactivated by exposing it to radiation, pH above 12, pH below 6, formalin, β-propiolactone, and circulatory impairment. The transmission of the virus occurs using an arthropod vector, Cuclicodes, and these insects favor the warm, moist conditions previously mentioned. The disease can also be carried by common ticks and mosquitoes. The role that these arthropods play in the disease transmission is still unknown. The respiratory form of this disease has the following symptoms and is usually fatal within one week: fever of 104-105 °F for one to two days followed by dyspnea, spasmodic coughing, and dilated nostrils. The cause of death is usually noxia, or depletion of oxygen. One giveaway symptom is frothing from the nostrils and mouth(1,3).
As mentioned before, the AHSV is morphologically very similar to the bluetongue virus (BTV). BTV is a member of the same genus and is also non-contagious with an arthropod vector. This virus infects ruminants instead of equines and canines. As presented in a recent study, complete nucleotide sequencing revealed that the inner most of the four capsid proteins in both viruses is the most conserved and the outermost capsid protein the most variable. Of all the nucleotides in the RNA segment encoding for the inner protein, 57-58% of the nucleotides are identical. It is suggested that these similarities account for the similar morphological characterisitcs of the viruses(2).
1)"African Horse Sickness"."The Merck Veterinary Dictionary". 2011.Merck Sharp & Dohme Corp. 2) Iwata, H., Yamagaw M., Roy, P. "Evolutionary relationships among the Gnat-transmitted orbiviruses that cause African horse sickness, bluetongue, and epizootic hemorrhagic disease as evidenced by their capsid protein sequences"."Virology". 1992. Volume 191. p. 251-262. 3)[ http://www.ncbi.nlm.nih.gov/pubmed/8001348] Roy, P., Mertens, PP, Casal, I. "African horse sickness virus structure"." Comp Immunol Microbiol Infect Dis". 1994. Volume 17. p. 243-73.