• African Swine Fever Virus is the only member of the Asfarviridae family and, as poxvirus and iridovirus, belongs to the monophyletic group of NCLDV. This virus causes a highly lethal haemorrhagic disease in domestic pigs with mortality rates up to 100%. However it’s asymptomatic in its natural host, wild pigs, warthogs, boars and soft tics. Its main cell targets are macrophages and monocytes where the intracellular enviroment after the infection might have high concentration of different oxidative agents, that may induce DNA damage.
• The ASFV pol X is encoded by the gene O174L and is the smallest naturally ocurring DNA-dependent DNA polymerase with about 21 kDa. pol X is only about one-half the size of pol-beta, and matches the structure of the palm (nucleotidyltransferase) and finger (dNTP selection) domains of DNA polymerases exceptionally well. Notably, polX lacks the 5-deoxyribose phosphate lyase and thumb domains present in pol-beta. In spite of this, its biochemical properties point to a role in a viral base excision repair pathway. [1] [2]
• During the last 10 years the level of fidelity has been debated in the literature, for some authors pol X is considered as an error-prone polymerase. This led some authors to propose a mutagenic role for the viral BER pathway, that may increase the virus genome variability and therefore, adaptation to environment. [3] [4]
• Later, a new paper demonstrated that the presence of a disulfide bond in the recombinant protein strongly decreases the insertion fidelity. however, the biological consequences of a disulfide switch as a determinant in polymerase function remain unclear. [5]
• A recent paper showed that the replication a mutant virus lacking pol X gene is impaired in swine macrophages and analysis of viral DNA shows that deletion of pol X results in an increase in the mutation frequency in macrophages [6]

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