Key result
Deletion of the ASFV Pol X gene impaired viral growth in swine macrophages at low multiplicity of infection and increased mutation frequency, indicating its role in maintaining viral genome stability.
ASFV Pol X plays a biological role in preserving viral genetic information and repairing accumulated DNA damage during infection in macrophages.
Pol X supports ASFV fitness in swine macrophages; leaves open its utility as a live-vaccine target pending in vivo validation.
The function of the African swine fever virus (ASFV) reparative DNA polymerase, Pol X, was investigated in the context of virus infection. Pol X is a late structural protein that localizes at cytoplasmic viral factories during DNA replication. Using an ASFV deletion mutant lacking the Pol X gene, we have shown that Pol X is not required for virus growth in Vero cells or swine macrophages under one-step growth conditions. However, at a low multiplicity of infection, when multiple rounds of replication occur, the growth of the mutant virus is impaired in swine macrophages but not in Vero cells, suggesting that Pol X is needed to repair the accumulated DNA damage. The replication of the mutant virus in Vero cells presents sensitivity to oxidative damage, and mutational analysis of viral DNA shows that deletion of Pol X results in an increase in the mutation frequency in macrophages. Therefore, our data reveal a biological role for ASFV Pol X in the context of the infected cell in the preservation of viral genetic information.
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Redrejo‐Rodríguez et al. (2013) studied African swine fever virus (ASFV) infection. ASFV deletion mutant lacking the Pol X gene vs. Wild-type ASFV was evaluated on Virus growth and mutation frequency in Vero cells and swine macrophages. Deletion of the ASFV Pol X gene impaired viral growth in swine macrophages at low multiplicity of infection and increased mutation frequency, indicating its role in maintaining viral genome stability.
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