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Otherwise resistant adult mice were rendered susceptible to intracerebral Junin virus (JV) infection only when a staggered cyclophosphamide (CY) schedule was used. Forty-five-day old Balb/c mice, intracerebrally JV-infected and immunosuppressed with four 50 mg/kg body weight CY doses at days -1, +1, +4, +6 (day 0: viral infection) developed a lethal disease (86.6 per cent mortality) with high CNS viral titers and brain lesions. Neutralizing antibodies were absent throughout, while immunofluorescent antibody levels were considerably diminished. The transfer of hyperimmune serum conferred partial though significant protection on CY-treated animals but no correlation was found between CNS viral titers and mortality since in both infected CY-treated and untreated mice similar brain viral content was found. This was also confirmed by immune spleen cell transfer at day 0 where the clearance achieved was unable to modify the time course of the disease. Feasible mechanisms explaining recovery from JV infection by means of the protective effect of antibodies and the cell-mediated clearance are discussed.

The adult mouse model had been considered resistant to Junin virus (JV) infection. However, we found that C3H/HeJ murine strain proved highly susceptible up to 5 months of age to intracerebral inoculation with the prototype XJ JV strain, showing neurological signs and 80-90% mortality within 13 days. Neutralizing antibodies (Nt Ab) were absent, but low immunofluorescent Ab levels (1:5) were detected as from day +7. The virus could only be rescued by coculture of brain samples with Vero cells. Histopathological findings were consistent with the suckling mouse model and with a delayed-type hypersensitivity reaction. XJ inoculation by extraneural routes failed to cause disease, however, it induced Nt Abs. Ic infection with XJCL3 strain of JV attenuated for man and guinea pig, but not for mouse, induced high Nt Ab levels but not mortality. In either case, mice resisted ic XJ challenge. Thus, C3H/HeJ is the first adult mouse model susceptible to JV.