Evidence for the type of nucleic acid in African swine fever virus

Summary The growth of African swine fever virus (ASFV) in pig kidney cells (PK-15) was inhibited by 5-iodo- and 5-bromo-2-deoxyuridine (IUDR and BUDR), whereas the fluoro-compound was inactive in this respect. In another cell line of the same origin (PK-C) virus inhibition occurred with as little as 1g/ml. of BUDR. The inhibitory effect was reduced when the compound was added more than 6 hours after infection, i.e. about 4 hours preceding the first appearance of progeny virus and was completely reversed in the presence of excess thymidine. Cultures in which virus multiplication was completely inhibited showed no cytopathic effects. Actinomycin-D also suppressed the growth and cytopathogenicity of ASFV in PK-C cells, the minimal inhibitory concentration being 0.2g/ml.; the antibiotic-sensitive phase of virus multiplication was 2–6 hours after infection.The growth of pseudorabies virus was inhibited in parallel with that of ASFV but the multiplication of foot-and-mouth disease virus in PK-C cells was not affected by these compounds.When ASFV was grown in the presence of¹⁴C-thymidine, followed by centrifugal concentration, enzymatic treatment and fractionation in sucrose density gradients, a peak of radioactivity coinciding with that of viral infectivity was obtained. No such peak occurred when the virus was grown in the presence of¹⁴C-uridine.It is concluded that ASFV is a DNA virus and should no longer be considered as a possible myxovirus.