The Molecular Biology of Yaba Tumour Pox Virus: Analysis of Lipids, Proteins and DNA

Abstract
Cytopathological studies have shown that Yaba tumor pox virus (Yaba virus) infection leads to the accumulation of large lipid vacuoles. The rate of accumulation of these vacuoles increased as the infection proceeded. These lipid vacuoles were not seen in control cells or in cells infected with monkeypox virus (MPV) but were seen during Yaba virus infection in the presence of cytosine arabinofuranoside (100 .mu.g/ml). Yaba virus also failed to inhibit host protein synthesis as infection proceeded for prolonged periods. Yaba virus proteins were shown to be substantially different from those of MPV when analyzed by 2-dimensional electrophoresis. The genome of Yaba virus gave restriction enzyme fragments which differed from those of the MPV genome when cleaved with the enzymes HindIII and XhoI. Yaba virus DNA hybridized to the HindIII fragments K, L and M and to the XhoI fragments A, B, C, E and G of MPV DNA. [Monkey kidney cells were used in this study.].