Armstrong – Table of Contents

“In view of the shorter incubation period of this virus in monkeys as compared to that of
encephalitis strains, it would seem logical to expect that in the transfer of a mixed
infection the choriomeningitis might ultimately displace the encephalitis strains. This
result has actually been observed during the transfers from monkeys synchronously
inoculated with the two strains. In mice, however, the opposite was observed for the
encephalitis, with its shorter incubation period, after a few transfers supplanted the
choriomeningitis strain.
“It is to be remembered, however, that monkey 37 was apparently immune to encephalitis
(Freeman strain) but not to the choriomeningitis, a condition calculated to suppress the
encephalitis virus to the advantage of the latter (choriomeningitis) should both have been
present”.
Armstrong further discussed the fact that lymphocytic choriomenungitis
(henceforth referred to as LCM) was not a commonly occurring spontaneous disease in
monkeys since he had encountered no naturally immune monkeys. He also wondered
whether this virus might be present in the human population since the clinical disease in
monkeys closely resembled recently described (22) cases of so-called “lymphocytic or
aseptic meningitis” for which no infectious agent had been isolated. He also indicated the
initiation of future studies utilizing neutralization tests of human sera against the viruses
of St. Louis encephalitis and LCM to determine the prevalence of human exposure
against these agents.
In order to demonstrate that LCM was a previously undescribed virus and distinct from
St. Louis encephalitis strains and other agents, Armstrong showed that: 1) Cebus
monkeys and guinea pigs refractory to encephalitis strains succumbed to LCM strains. 2)