Arch Virol (1987) 95:225-235 Archives of Virology © by Springer-Verlag 1987 Transformation of rabbit arterial smooth muscle cells with Simian virus 40 M. Nachtigal, P. Greenspan, L. Terracio, and S.D. Fowler Depa,rtments of Pattlology and Anatomy, School of Medicine, UniversitsT of South Carolina, Columbia., South Carolina, U.S.A. Accepted January 28, 1987 Summary In vitro studies were carried out to induce viral transformation of vascular smooth muscle cells. Cultured rabbit arterial smooth muscle cells were infected with simian virus 40 (SV 40), and transformed cultures were produced that exhibit altered morphology, increased growth rate and plat- ing efficiency, growth on semi-solid substrate, and chromosomM abnor- malities. Nuclear SV 40 T-antigen was detected in all cells of these cultures. Muscle-specific actin was identified by a specific monoclonal antibody suggesting retention of smooth muscle cell characteristics by the trans- formed cells. Significant cytoplasmic lipid accumulation occurred in trans- formed cells incubated with p-very low density lipoprotein, as revealed both by chemical analyses and Nile Red lipid staining of the cultures. The trans- formed smooth muscle cells grow permanently in cell culture. Our investiga- tions show that arterial smooth muscle ceils transformed with SV 40 virus exhibit altered phenotypic properties distinct from that of normal arterial smooth muscle ceils. Introduction Evidence has accumulated that viruses are present in the human vascular wall, sometimes in association with pathological changes (3, 12, 17). However, the relationship of viruses with vascular smooth muscle cells and their pathogenic roles remains unclear. It is known that c~%ol~%ic infection can be obtained in cultured vascular smooth muscle cells with herpes simplex virus t~pes i and 2 (3), and cyt~)megMovirus (28). Moreover, infec- tion of cultured chicken vascular smooth muscle cells with Marek's disease herpesvirus resulted in cytopathic effects and accumulation of cholesterol and cholesteryI ester (7) in association with altered cellular lipid metabolism (13, 14). Arterial injury as a results of a direct cytopathic effect of viruses on