In neonatal or congenital lymphocytic choriomeningitis (LCM) virus carrier mice, low numbers of T lymphocytes were always infected, but attempts to infect resting or stimulated T lymphocytes in previously uninfected adult mice have consistently failed. Only T cells in newborn mice were susceptible to LCM virus and their infection persisted when the animals grew older. Infectibility declined with increasing age of the mice. Initially, the majority was demonstrated among thymocytes, but later more splenic cells were infected. In contrast to neonatal carrier mice, in drug-induced carriers (in which persistent infection had been established later in life by immuno-suppression after infection) spleens and thymi contained initially no or a few infectious T lymphocytes; their numbers increased with the age of the mice but remained relatively low and erratic. We follow the hypothesis that LCM virus-specific immunological tolerance of carrier mice is due to age-dependent virus susceptibility of T lymphocytes and propose that murine T lymphocytes in general lack viral receptors for LCM virus, but that the few that carry LCM virus-specific immunological receptors bind the virus. If this occurs during an early stage of cellular development, infection results and functional inactivation is the consequence.


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