Visna virus synthesized in absence of host-cell division and DNA synthesis.
Visna virus is similar to the avian and the murine oncornaviruses. Oncornavirus replication is dependent upon the provirus being integrated into the host cell's DNA but integration and subsequent oncornavirus synthesis is blocked when the host cells are prevented from synthesizing cellular DNA or dividing. The synthesis of visna virus is restricted in vivo and may be dependent upon the host cell's ability to synthesize cellular DNA or divide. Treatment of sheep choroid plexus (SCP) cells with ultraviolet light or with mitomycin C prior to infection irreversibly inhibited plexus (ScP) cells with ultraviolet light or with mitomycin C prior to infection irreversibly inhibited both cell division and cellular nucleic acid synthesis but did not inhibit visna virus synthesis. Similarly, the synthesis of visna virus in cultures of SCP cells which had been prevented from dividing by being deprived of serum and in cultures of SCP cells which were incapable of synthesizing host cell nucleic acids by being treated with miracil D or sodium hexachloroiridate was equivalent to the synthesis of visna virus in cultures of SCP cells which were allowed to both synthesize cellular nucleic acids and divide. The synthesis of visna virus in the presence of ethidium bromide further demonstrated that integration of the visna provirus into the host cell's DNA is not required for visna virus synthesis to occur.
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002831:Choroid Plexus; D046508:Culture Techniques; D004247:DNA / Q000096:biosynthesis; D004996:Ethidium / Q000494:pharmacology; D008937:Mitomycins / Q000494:pharmacology; D012756:Sheep; D014779:Virus Replication; D014790:Visna-maedi virus / Q000254:growth & development*
D008937:Mitomycins; D004247:DNA; D004996:Ethidium