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Bluetongue virus is a species of the genus Orbivirus, within the Reoviridae family. The Reoviridae are non-enveloped and possess a double-stranded RNA genome contained in an outer-shelled icosohedral capsid. The BTV genome is arranged into 10 segments and encodes 7 structural and 4 non-structural viral proteins². The BTV receptor is currently unknown, but is proposed to included sialic acid and junctional adhesion molecules. After interaction with this receptor, the virus enters an endolysosome where the capsid is partially digested to allow the genome into the cell. Replication begins at this partially uncoated stage since the virus particles contain all the necessary enzymes⁵. First, the dsRNA is transcribed to form positive sense RNA, of which some is delivered to cytoplasm for ribosomal translation and the remainder is packaged into partially assembled virions. Complementary negative sense RNA is then formed in the virions, to give a dsRNA genome. Complete virus particles are released from the cell.

Bluetongue virus is a species of the genus Orbivirus, within the Reoviridae family. The Reoviridae are non-enveloped and possess a double-stranded RNA genome contained in an outer-shelled icosohedral capsid. The BTV genome is arranged into 10 segments and encodes 7 structural and 4 non-structural viral proteins². The BTV receptor is currently unknown, but is proposed to included sialic acid and junctional adhesion molecules. After interaction with this receptor, the virus enters an endolysosome where the capsid is partially digested to allow the genome into the cell. Replication begins at this partially uncoated stage since the virus particles contain all the necessary enzymes⁵. First, the dsRNA is transcribed to form positive sense RNA, of which some is delivered to cytoplasm for ribosomal translation and the remainder is packaged into partially assembled virions. Complementary negative sense RNA is then formed in the virions, to give a dsRNA genome. Complete virus particles are released from the cell.

The 24 distinct serotypes of BTV are distinguished by epitopes on the outer capsid protein VP2, although VP5 also can influence neutralization through its conformational influence on VP2 [11]. The L2 gene, which encodes VP2, is the only serotype-specific BTV gene and there is considerable variation amongst all 10 genome segments of field strains of BTV within endemic areas such as California [15,25]. This variation of BTV genes in field strains of the virus has arisen as a consequence of both drift and reassortment of individual viral genes. Reassortment of BTV genes has been demonstrated after infection of either the ruminant host or insect vector with different strains or serotypes of BTV [29,30]. Individual BTV gene segments evolve and reassort independently of serotype in the field. Genetic drift of individual BTV genes occurs by the selective acquisition and amplification in vector insects of specific variants from the quasispecies virus population that arises in the blood of infected ruminants (founder effect; 6,7).

There are 24 distinct serotypes of BTV, which are are distinguished by epitopes on the outer capsid protein VP2², encoded by L2, the only serotype-specific BTV gene.  

There are 24 serotypes worldwide, although not all serotypes exist in any one geographic area, eg, only 5 serotypes (2, 10, 11, 13, and 17) have been reported in the USA. Distribution throughout the world parallels the spatial and temporal distribution of vector species of Culicoides biting midges, which are the only significant natural transmitters of the virus. Of more than 1,400 Culicoides species worldwide, fewer than 20 are actual or possible vectors of bluetongue virus. Continued cycling of the virus among competent Culicoides vectors and susceptible ruminants is critical to viral ecology. In the USA, the principal biologic vector is C variipennis sonorensis , which limits distribution of the virus to southern and western regions. In Australia the principal vector is C brevitarsis , while in Africa, Europe, and the Middle East it is C imicola . In each geographic region, secondary vector species may attain local importance. Vectors become infected with bluetongue virus by imbibing blood from infected vertebrates; transovarial transmission has not been reported. High affinity of the virus to blood cells, especially the sequestering of viral particles in invaginations of RBC membranes, contributes to prolonged viremia in the presence of neutralizing antibody. The extended viremia in cattle (up to 9 wk), and the host preference of most vector species of Culicoides for cattle, provides a mechanism for year-round transmission in domestic ruminants. Mechanical transmission by other bloodsucking insects is of minor significance. Bluetongue virus is not contagious, and concentrations in secretions and excretions are minimal, making oral or aerosol transmission unlikely. However, semen from viremic bulls can serve as a source of infection for cows through natural service or artificial insemination. Embryo transfer is regarded as safe, provided that donors are not viremic and an appropriate washing procedure for embryos is used. Accidental infection has been reported in dogs in the USA following administration of a modified live virus vaccine that was contaminated with the virus. Serologic evidence of infection with bluetongue virus has been found in large carnivores in Africa, perhaps as a result of ingesting virus-infected viscera.

There are 24 serotypes worldwide, although not all serotypes exist in any one geographic area, eg, only 5 serotypes (2, 10, 11, 13, and 17) have been reported in the USA. Distribution throughout the world parallels the spatial and temporal distribution of vector species of Culicoides biting midges, which are the only significant natural transmitters of the virus. Of more than 1,400 Culicoides species worldwide, fewer than 20 are actual or possible vectors of bluetongue virus. Continued cycling of the virus among competent Culicoides vectors and susceptible ruminants is critical to viral ecology. In the USA, the principal biologic vector is C variipennis sonorensis , which limits distribution of the virus to southern and western regions. In Australia the principal vector is C brevitarsis , while in Africa, Europe, and the Middle East it is C imicola . In each geographic region, secondary vector species may attain local importance. Vectors become infected with bluetongue virus by imbibing blood from infected vertebrates; transovarial transmission has not been reported. High affinity of the virus to blood cells, especially the sequestering of viral particles in invaginations of RBC membranes, contributes to prolonged viremia in the presence of neutralizing antibody. The extended viremia in cattle (up to 9 wk), and the host preference of most vector species of Culicoides for cattle, provides a mechanism for year-round transmission in domestic ruminants. Mechanical transmission by other bloodsucking insects is of minor significance. Bluetongue virus is not contagious, and concentrations in secretions and excretions are minimal, making oral or aerosol transmission unlikely. However, semen from viremic bulls can serve as a source of infection for cows through natural service or artificial insemination. Embryo transfer is regarded as safe, provided that donors are not viremic and an appropriate washing procedure for embryos is used. Accidental infection has been reported in dogs in the USA following administration of a modified live virus vaccine that was contaminated with the virus. Serologic evidence of infection with bluetongue virus has been found in large carnivores in Africa, perhaps as a result of ingesting virus-infected viscera.