Editing Bluetongue disease (section)

== Evolution ==
The viral genome is replicated via structural protein VP1, an RNA-dependent RNA polymerase.<ref name="Rodríguez-Martín_2021" />  The lack of proof-reading abilities results in high levels of transcription errors, resulting in single nucleotide mutations. Despite this, the BTV genome is quite stable, exhibiting a low rate of variants arising in populations.<ref name="Kopanke_2020">{{cite journal | vauthors = Kopanke JH, Lee JS, Stenglein MD, Mayo CE | title = The Genetic Diversification of a Single Bluetongue Virus Strain Using an In Vitro Model of Alternating-Host Transmission | journal = Viruses | volume = 12 | issue = 9 | pages = 1038 | date = September 2020 | pmid = 32961886 | pmc = 7551957 | doi = 10.3390/v12091038 | doi-access = free }}</ref> Evidence suggests this is due to purifying selection across the genome as the virus is transmitted alternately through its insect and animal hosts.<ref name="Kopanke_2020" /> However, individual gene segments undergo different selective pressures and some, particularly segments 4 and 5, are subject to positive selection.<ref name="Kopanke_2020" />

The BTV genome exhibits rapid evolution through genetic drift, reassortment of genome segments (genetic shift), and intragenic recombination. This evolutionary process, in conjunction with the random fixation of quasispecies variants during transmission between susceptible animals and vectors, is postulated to be the primary driver of the genetic diversity observed in BTV field strains.<ref>{{cite journal | vauthors = Niedbalski W | title = The evolution of bluetongue virus: genetic and phenotypic diversity of field strains | journal = Polish Journal of Veterinary Sciences | volume = 16 | issue = 3 | pages = 611–616 | date = 2013-09-01 | pmid = 24195303 | doi = 10.2478/pjvs-2013-0086 }}</ref>  Reassortment can lead to a rapid shift in phenotypes independent of the slow rate of mutation. During this process, gene segments are not randomly reassorted. Rather, there appears to be a mechanism for selecting for or against certain segments from the parental serotypes present.<ref>{{cite journal | vauthors = Kopanke J, Lee J, Stenglein M, Mayo C | title = In Vitro Reassortment between Endemic Bluetongue Viruses Features Global Shifts in Segment Frequencies and Preferred Segment Combinations | journal = Microorganisms | volume = 9 | issue = 2 | pages = 405 | date = February 2021 | pmid = 33669284 | pmc = 7920030 | doi = 10.3390/microorganisms9020405 | doi-access = free }}</ref>  However, this selective mechanism is still poorly understood.

To date, BTV serotypes 25 and above have been identified as the causative agents of infection in small ruminants. The infection is subclinical, which likely explains why these serotypes, which are less or non-virulent, have not been identified earlier through laboratory diagnosis studies. It is noteworthy that BTV serotypes 25 and higher are transmitted without midges, indicating that direct contact between sheep or goats may be a potential vector.<ref name="Saminathan_2020" /><ref name="Wageningen_University" />