It has been established that resting lymphocytes are unable to replicate a variety of RNA viruses, while lymphocytes activated by mitogens or antigens rapidly acquire the ability to do so. We have developed an assay for enumerating activated lymphocytes based on this principle, in which lymphocytes are stimulated by antigen, infected with vesicular stomatitis virus and those lymphocytes which have been activated are capable of producing infectious centers and are described as virus-plaque forming cells. In the mouse, V-PFC are produced by Con A and PHA, but not LPS, and spleen cells treated with anti-thy 1 plus C are unable to make V-PFC. The principle goals in the coming year of this grant are to define which subpopulation of T-lymphocytes is capable of producing virus-killer cells, helper T-cells, etc., particularly using anti Ly sera to discriminate between functional subpopulations. Secondly, we have established that resting lymphocytes are indeed capable of being infected by VSV and that until the cells are activated by antigen or mitogen the infection remains a latent one. We are currently studying the duration of latency of viruses within lymphocytes, the effect on the functioning of latently virus-infected lymphocytes and their surface markers. Lastly, detailed studies of the virus plaque assay on human cell populations, activated B-cells and T-cells will be carried out to establish whether this assay is selective only for activated T-cells, or whether preliminary removal of non-T-cells is required to permit enumeration of activated T-cells.