The simian virus 40 small-t (ST) antigen plays a key role in permissive and nonpermissive infections, increasing virus yields in lytic cycles of primate cells and enhancing the ability of large-T (LT) to transform rodent or even human cells. In the absence of ST, tumors in rodent model systems appear primarily in lymphoid and other proliferative tissues and transformation is reduced in several in vitro systems. The functions of ST largely reflect its binding and inhibition of protein phosphatase 2A, although a recently described dnaJ domain also contributes to its biology. The dnaJ domain is present in LT and a third early gene product, the 17kT protein, for which a potential role in transformation deserves further evaluation.
Copyright 2001 Academic Press.