Bystander virus infection prolongs activated T cell survival

In animals, T cells often die rapidly after activation, unless activation o ccurs in the presence of inflammatory factors. To understand how such activ ated cells survive to participate in immune responses, we studied the effec ts of viral infection on T cells responding to an unrelated superantigen, N ormal T cells activated by superantigen in uninfected mice died as a result of their activation, whereas T cells that were activated during vaccinia i nfection survived longer in vivo and in culture, This bystander effect of v iral infection on activated T cells was independent of effects on the magni tude of the initial T cell response, on induction of Bcl-2 and Bcl-x, on T cell proliferation, and on Fas killing, The failure of such effects to pred ict the fate of activated T cells in vivo indicates that virus infections s hape T cell responses via mechanisms that differ from those described previ ously. These mechanisms may contribute to the ability of viral infections t o induce autoimmunity.