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Rabbit anti-mouse thymocyte serum (ATS) administrated as late as 7 days after infection suppressed host cell-mediated responsiveness to intracerebrally injected Junín virus, thereby diminishing the morbility and mortality of this infection. It did not affect either the humoral antibody response or the virus titer in brain. This findings suggest that: a) in mouse brain cells, Junín virus infection is basically non-cytopathic: b) cell-mediated immunity is responsible for morbility and mortality and does not clear up virus from brain as in other viral encephalitides; and c) ATS may be of therapeutic interest by suppressing or diminishing the cell-mediated response to Junín virus.

As previously postulated, the pathological changes which develop in 1-4 day old mice after intracerebral inoculation of 1-1000 DL50 of Junín virus prototype strain (XJ), was designated as experimental hemorrhagic fever of the mouse EHFm. In this paper, virus distribution, hematological alterations, interferon and circulating antibody responses are described. A mortality of 93.45% occurred between 9 and 20 days post-infection (p.i.), with 81.6% of death occurring between 11 and 18 days p.i. This last period can be considered to be the critical period of the disease. The study of virus distribution shows that the brain, where the virus was inoculated, was the only place where virus could be detected 48 hs, p.i. Four days p.i., the titer in the brain increased remarkably and virus was detected in the blood. Virus, within the same values, could be isolated up to the 10th. day. Invasion of liver and spleen occurred on the 10th. and 15th. days p.i., respectively (Fig. 1). The onset of clinical symptoms coincided with widespread disemination of the virus. CF antibodies were found only 15 days p.i., with a titer of 1/64. Neutralizing antibodies remained below detection levels during the whole experiment (Fig. 1). Surviving mice (6.3%) had high circulating antibody titers 40 days p.i. This result would indicate that the morobidity of EHFm is aproximately 100% (Table 1). Poor interferon response was registered in all the organs examined, indicating a low intereron producing ability for Junin virus6. Total leukocytes and lymphocyte counts showed a slight tendecy to drop, although the values were within normal range during the first ten days (Table 2, Fig 1). On day 14 p.i., a statistically significant decrease (p less than 0.001) was found. This leuko-lymphopaenia continued until death of the animals. It is expected that the data presente here would contribute to a better understanding of the Junin virus infection in the newborn mouse, the experimental animal used.