Effect of cytosine, arabinoside, iododeoxyuridine, ethyldeoxyuridine, thiocyanatodeoxyuridine, and ribavirin on tail lesion formation in mice infected with vaccinia virus.

Mice infected intravenously with vaccinia virus develop characteristic lesions over the entire tail surface. This experimental virus infection presents a highly sensitive and reliable model for evaluating the antivaccinia activity of antiviral compounds. Ara-C (1-beta-D-arabinofuranosylcytosine), ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide), IUdR (5-iodo-2'-deoxyuridine) as well as two novel analogs of IUdR, EtUdR (5-ethyl-2'-deoxyuridine), and NCSUdR (5-thiocyanato-2'-deoxyuridine), were found to inhibit the formation of vaccinia tail lesions, when administered intraperitoneally once daily for 7 days starting immediately after virus infection. The order of (decreasing) activity was: ara-C greater than IUdR greater than NCSUdR greater than ribavirin greater than EtUdR. Various drug combinations, involving IUdR + ara-C, NCSUdR + ara-C, NCSUdR + IUdR, NSCUdR + ribavirin, etc., were evaluated but none proved more efficacious than either compound administered alone.