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  • Title: Expression of virus-associated antigens and immune cell functions during spontaneous regression of the Friend viral murine leukemia.
    Author: Cerny J, Essex M, Rich MA, Hardy WD.
    Journal: Int J Cancer; 1975 Feb 15; 15(2):351-65. PubMed ID: 47847.
    Abstract:
    Spontaneous regression and/or remission of Friend virus (FV)-induced splenic erythroblastic leukemia was observed in CD-1 mice infected with several isolates of FV. Regression of splenic tumor was accompanied by the loss of both specific FV-induced cell membrane antigen (FVMA) and virus group-specific antigens (gsa) from the spleen cells. The frequency (percentage) of immunoglobulin-positive cells (B) and thetapositive cells (T) in the spleen was markedly decreased during leukemia progression, but there was a subsequent increase during regression. The appearance of gsa-positive (gsa+) cells in peripheral blood correlated well with the early progressive and regressive phase of leukemia (up to 7 weeks after infection). Later, the presence of these cells became unpredictable in regard to status of disease. Gsa+ blood cells reappeared in most mice with regressed splenic tumors, suggesting persistence of the virus complex in the animals. Antibody responsiveness as determined by the numbers of hemolytic plaque-forming cells, PFC, after a single immunization with sheep red blood cells (SRBC), was suppressed in leukemia progression and recovered, spontaneously, during regression of leukemia. However, hemolytic PFC elicited by antigen in both progressors and regressors expressed the specific virus-induced membrane antigen, FVMA, detectable by the PFC-inhibition test with specific antiserum and complement. Recovery of immunological responsiveness also included the spontaneous appearance of virus-neutralizing antibody to FV. However, this was not paralleled by the appearance of antibody to FVMA. Traces of anti-FVMA antibody activity were occasionally detectable in serum of both progressors and regressors and did not correlate with virus neutralization, in individual mice; This may explain the susceptibility of regressors to secondary relapse and to reinfection.
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