Importantly, increased host Bcl-2 expression in transitional B cells complemented the lack of vBcl-2 expression during MHV68 infection, demonstrating that (a) MHV68 vBcl-2 mutants are competent for developing B cell infection, and (b) vBcl-2 carries out functions that are normally associated with host Bcl-2 activity. The gene discussed is BCL2; the disease is infection.