Circumstantial evidence has been presented which supports the view that the fatal LCM virus infection is due to an immunological conflict in the host animal. Hitherto, this outcome of the infection has only been observed in intracerebrally infected mice. In the present study, the intraperitoneal infection in young mice was investigated and the results revealed a new example of this immunological conflict. In mice infected a few days after birth, concentrations of the virus in the brain are high, while the CMI response is non‐measurable. If the infection is induced when the mice are 28 days old or more, there is little virus in the CNS, but a strong CMI response can be demonstrated. All the mice in these two age groups survive. If mice are infected when they are 17–19 days old, however, they raise a moderate CMI response nine days after infection and, at the same time, their brains contain virus in high titres. The mortality among mice infected at this age is 100 per cent, indicating that this combination is fatal. The lives of these animals can be saved by anti theta serum or if they are transplanted with syngeneic lymphoid cells sensitized to LCM virus. Our results strongly suggest an interplay between, on the one hand, the spread and the magnitude of the virus infection in the brain and, on the other, the cell mediated immune response. This interplay seems to be decisive for the clinical outcome of the LCM infection in m