522 Antigenic Modulation of Friend Erythroleukemic

In the tumor dormant state, small numbers of tumor cells persist in the host without outgrowth to overt neoplasia. The cancer l i t e ra ture contains numerous reports describing recurrence of solid tumors and leukemias years after apparent successful t r ea tmen t of the pr imary neoplasia (1). These reports suggest tha t residual tumor cells can persist in a dormant s ta te during the prolonged clinical remission. Few exper imental models have been developed to study the tumor dormant state. In this laboratory we have been invest igat ing a murine model in which the rapidly fatal Fr iend virus e ry thro leukemia can be suppressed to a dormant s ta te by t rea tment with statolon, an extract of mycophage-infected Penici l l ium stoloniferum cultures (2-4), or the double-stranded RNA extracted from statolon (5). This report describes our continuing analysis of host mechanisms involved in maintenance of Fr iend leukemia virus (FLV) ~ in a dormant state. Infection of DBA/2 mice with FLV causes a depression in humoral (6) and cel lular immuni ty (7) and macrophage functions (8) followed by the development of a fatal e ry thro leukemia (2). Trea tment of FLV-infected mice with statolon abrogates the depression of humoral immuni ty and macrophage functions (6, 8). Between 50 and 70% of these mice ma in ta in immunocompetence and survive, suppressing the ery thro leukemia to a dormant state, which lasts for the normal lifespan of most of these mice (2-4, 9). However, late in life, some of these mice develop ery thro leukemia from which FLV can be isolated (2, 3). Mice with dormant FLV infections contain antibodies tha t complex FLV virion polypeptides and are cytotoxic for FLV-transformed cells, and these antibodies appear to be crucial for leukemosuppression and maintenance of the virus in a dormant state (9-11). Serum from mice with dormant l%V infections is referred to as dormant FLV-immune serum (FVIS). The precise mechanism by which FLV antibodies suppress FLV ery thro leukemia and main ta in the virus in a dormant s ta te is not known. DBA/2 mice are deficient in the fifth component of complement (C5) (12) which is required for ant ibody-mediated complementdependent immune cytolysis (13). Carlson and Terres demonstrated ant ibody-dependent ki l l ing of syngeneic lymphomas by the DBA/2 mouse in vivo (14). The mechanism involved in this destruction of the lymphomas was most l ikely ant ibody-dependent cell-