SummaryBrain tissues of newborn mice infected intracerebrally with Junin virus were examined by light and electron microscopy in order to elucidate the pathogenesis of Junln virus infection as well as the effect of antithymocyte serum (ATS) on the development of the disease.The most prominent brain lesions caused by Junin virus in mice consisted in microglial activation, perivascular cuffs with mononuelear cells and demyelinating processes. Animals pretreated with ATS and subsequently infected with gunln virus showed no neurologic disorders and only minimal or no lesions in their brain.It is concluded that Junln virus encephalitis might have an immunological basis similar to that described in experimental allergic encephalitis. This assumption is supported by the inhibiting effect of ATS which is known to be a potent suppressor of delayed type hypersensitivity.

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In 1963 Murphy found that the inbred mouse strain SJL/J had a high incidence (up to 91%) of reticulum cell neoplasms at a mean age of 13 months (Murphy, 1963). The basic histological pattern of the neoplasms was that of type B according to Dunn's classification of mouse neoplasms (Dunn, 1954). Later, Murphy, (1964-65) described the tumors as " multicellular reticulum cell neoplasms " and stressed their close microscopic resemblance to Hodgkin's disease in humans. The susceptibility of SJL/J mice to spontaneous development of reticulum cell neoplasms of type B, as well as to the induction of lymphatic leukemia and myeloid leukemia by different leukemogenic agents, was studied more recently by Haran-Ghera et al. (1967). The pathogenesis of spontaneous reticulum cell sarcoma in SJL/J mice was described by Siegler and Rich (1968) who found that the neoplasm arose in the mesenteric lymph nodes and Peyer's patches.

Despite extensive studies, the correlation between the morphology and pathogenicity of murine leukemia viruses (MLV) has not yet been clarified. The virus particles found in the plasma of leukemic mice belong to 2 distinct groups, 1 or 2% of them being enveloped A particles and the vast majority being of type C. It is generally believed that these 2 types of particles represent different phases in the development of the same virus. Particles of type A have been thought to be an earlier form of type C particles. One of the tissue culture lines established from Friend leukemia solid tumors has provided the material for the present study. The supernatant fluid of the line designated C-1A contains an almost pure population of A particles as illustrated in Figure 1. The ratio is, therefore, the reverse of what is unvariably observed in the plasma of leukemic mice where C particles predominate.