MANY neurotropic viral infections are accompanied by inflammatory cellular infiltrates of the central nervous system. With some of these viruses, notably lymphocytic choriomeningitis (LCM), the cellular response is believed to be responsible for the morbidity and mortality associated with infection1, and suppression of the lymphocytic response by treatment with anti-thymocyte serum prevents clinical signs of disease2,3. Yellow fever infection caused by the 17-D virus in mice is characterized by a diffuse encephalomyelitis consisting of mononuclear cell infiltration of leptomeninges and perivascular areas, as well as neuronal degeneration and glial proliferation4. We have used rabbit anti-mouse thymocyte (RAMT) serum to prevent cellular responsiveness to 11-D virus, in order to evaluate the role of delayed hypersensitivity in the pathogenesis of experimental yellow fever.
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