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The Edmontson strain of measles virus was adapted to the brains of newborn white mice to which extracts from African green monkey kidney (Vero) cells used for maintenance of measles virus had been injected intracerebrally. The animals showed symptoms of involvement of the central nervous system (pareses, paralyses) which reappeared in subsequent passages.

A strain designated 42-Edmonston was isolated from the brain of a Syrian hamster 30 days after inoculation during the neonatal period with the reference "wild" measles virus strain Edmonston which produced a latent infection accompanied by production of measles antibody and insignificant pathomorphological changes. Intracerebral inoculation with the 42-Edmonston strain of newborn, one day-and 5-7-day-old Syrian hamsters resulted in the development of acute measles encephalitis with typical clinical symptoms and pathomorphological changes. It is suggested that selection and adaptation of a neurotropic measles virus variant probably had occurred in the course of virus persistence in the Syrian hamster brain.

Residual neurovirulence of measles virus vaccine strains "Leningrad-16", "Moscow-5" and of cloned variant of L-16 strain--clone 3, differing in the degree of attenuation, was studied in intracerebrally (i.c.) infected Cercopithecus aethiops monkeys, receiving cortisone and/or antilymphocyte serum (ALS). Whereas the sensitivity for detection of the potential neurovirulence of vaccine strains was not increased by cortisone treatment. ALS had such effect in detection of neurotropic properties of the L-16 strain and its cloned variants.

Persistent infection with measles virus established in a calf kidney cell line differed in some features from other measles virus carrier systems. After a variable life span, ranging from 50 to 1100 days, six of the chronically infected cell lines showed an evolution towards lytic infection. Only one of these lines, the K-2 cell line, exhibited marked morphological, growth and chromosomal alterations suggesting in vitro cellular transformation. The transformed K-2 cells released infectious measles virus with several modified biological parameters. Persistent infection was not due to the accumulation of thermosensitive mutants or defective particles. The role of the host-cell factor and of the selection of the virus population during its passage in RV cells are discussed.

Measles virus strains Edmonston and L-16 have been studied in 10 intracerebrally (i.c.) infected monkeys and in 155 guinea pigs infected into the anterior eye chamber. The strains appeared to differ in pathogenicity for monkeys and guinea pigs. The more pathogenic Edmonston strain caused encephalitis in monkeys, whereas in guinea pigs it caused iridocyclitis, keratoconjunctivitis and follicular conjunctivitis. Strain L-16 was not neurovirulent for monkeys, while in guinea pigs it caused follicular conjunctivitis. Specific pathohistological changes detected in the CNS of monkeys and in the eye teguments of guinea pigs were confirmed by virologic and serologic findings.

The lesions of CNS were examined in monkeys infected intracerebrally (i.c.) with a variant of measles virus vaccine strain L-16 isolated after prolonged persistence in human cell culture NEr-2. The persisting virus variant appeared pathogenic for monkeys. The changes which had developed in their CNS within 30 to 60 days post-infection (p.i.) were alike to acute measles encephalitis which was evidenced by giant cell formation at the injection site. Twenty-two months p.i. the chronic character of lesions was evident from the appearance of foci of neuron destruction. Based on morphologic findings it was suggested that strain L-16-H has acquired some properties characteristic of nonattenuated virus.

The neurovirulence of L-16 vaccine measles virus strains and its 9 clonal variants was investigated in intracerebrally infected Macaca mulatta monkeys. Two groups of clones were distinguished: one comprised variants that caused destructive changes of neurons in the brain and diffuse proliferative gliosis, and the second variants that caused changes of a transitory character, connected with the traumatic exposure.