ABSTRACT
The ability of a virus to kill the host cell or to inhibit normal cellular functions underlies the pathological basis for many viral diseases. The death of cells infected with various lytic animal viruses probably represents the culmination of many structural, metabolic, and biosynthetic lesions within the infected cells. Sindbis virus and Semliki Forest virus, prototypes of the alphavirus group of the togavirus family, are small, enveloped plus-stranded ribonucleic acid viruses. Virus-induced damage to the cell membrane may occur as a consequence of envelope glycoprotein insertion and virus budding. The inhibition of host macromolecular synthesis and the induction of cell injury are not necessarily independent mechanisms that lead to cell death. L. Carrasco has shown that virus infection renders the cell membrane permeable to toxins and phosphorylated intermediates of metabolism. The induction of cell injury by rhabdoviruses is primarily due to the inherent toxicity of virion components.
