Studies in mice of the modes of immunomodification imposed by cyclophosphamide, have been extended to comparative studies with Myocrisin, l-asparaginase and interferon. It has been shown for mice infected or by an avirulent clone of SFV, that the potentiation of disease may be marked by many distinct changes in the type and rate of response.

For low doses of virus, enhancement (Myocrisin, l-asparaginase) or impairment (interferon) of the efficiency of infection may be associated with death (potentiation by Myocrisin) or protection (immunoenhancement by l-asparaginase).

For higher doses of virus the increased mortality after infection (primary potentiation) is determined within 2 or 3 days and appears to be due to inhibition of phagocytosis (Myocrisin and l-asparaginase) and of T cell functions (l-asparaginase and cyclophosphamide). The increased incidence of death after challenge (secondary potentiation) appears to be due to inhibition of B cell functions (cyclophosphamide) associated with suppression of antibody synthesis and persistence of viraemia.

These results are discussed in relation to the expression of virulence by a heterogeneous and replicating antigen. The critical cellular and humoral changes which occur within 2 or 3 days of infection are emphasized.


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