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The analysis of blood leucocyte chromosomes has been carried out on 60 patients with different infectious diseases (influenza, measles, scarlet fever, and disentery), and on 47 patients immunized against measles, tick-born encephalitis, typhoid fever and brucellosis. The mutagenic influence of viruses on the genital cells of mice and on the human somatic cells in vitro was studied. Both viruses and bacteria appeared to be able to bring about different breaks in human and animal cells.

A limited number of passages (up to 10) in human diploid cells (HDC) does not lead to changes in the phenotypic markers indicating the degree of attenuation of the vaccine strains of measles virus (Schwarz, Leningrad-16, Edmonston-Zagreb). At the same time, the increase in virus titer and the acquiring of immunogenicity when administered by nonparenteral (conjunctival, nasal) routes represent the prerequisites of a convenient form of application of the measles vaccine prepared in HDC.

Moustached marmosets (Saguinus mystax) were infected intranasally with either of two low-passaged, wildlike strains of measles virus, strain Edmonston or strain JM. The infection resulted in 25 and 100% mortality, respectively, 12 to 14 days after infection. Clinical signs, gross pathological findings, and histology lacked the characteristic features of measles in other primates. A deficient immune response and widespread gastroenterocolitis appeared to be the main causes for the fatal outcome. Fluorescent-antibody staining detected large amounts of measles antigen in lymphatic tissues, the gastrointestinal and respiratory tracts, the salivary glands, pancreas, liver, kidney, and other visceral tissues. Live attenuated or inactivated measles vaccine proved equally effective in preventing fatal measles in marmosets. Challenge with live virus of animals which were primed 1 year previously with inactivated alum-absorbed vaccine resulted in a precipitous response, with a 100- to 1,000-fold increase in antibody titers. This vigorous booster response suggests the existence of a primary deficiency in lymphocyte cooperation in marmosets, which upon adequate priming is followed by extensive clonal expansion and antibody synthesis. Marmosets appear to be the most susceptible primate species to measles infection. They are capable of distinguishing differences in virulence of virus strains with a level of sensitivity not available in other animals.

Chronic measles encephalitis was induced in C57BL/6 mice with the hamster neurotropic strain of measles virus when virus which had been passaged at low dilution in the brains of suckling C57BL/6 mice was inoculated intracerebrally into 1- to 6-month-old mice. One-third to two-thirds of mice surviving the acute infection were consistently found to develop chronic neurologic dysfunction within 3 weeks to 1 year post-infection. The acute mortality was higher in males than in females and showed a slight decline with increasing age in males. Indirect immunofluorescence (IF) studies using measles virus-specific sera from a subacute sclerosing panencephalitis patient and from a hyperimmune rabbit demonstrated abundant viral antigen in regions of telencephalon and diencephalon correlated with the appearance of typical central nervous system signs in both acute and chronic disease. Viral antigen was found in infected neurons in the grey matter. Deposition of immune complexes was minimal as observed in adjacent brain sections stained with goat anti-mouse antibody by direct IF. Occasional necrotic foci and perivascular cuffing were observed in brains from chronically infected mice.

Measles virus-infected hamster brain tissue remained viable when frozen slowly in medium containing dimethyl sulfoxide. This procedure was essential for isolation of neurotropic measles virus from tissue specimens stored frozen.

The time of appearance of a lysosomal enzyme, beta-glucuronidase, in the medium of cells infected with either measles virus or echovirus 6 varied with the host cell system. Replication and release of virus preceded leakage of beta-glucuronidase from green monkey kidney cells. In contrast, extracellular enzyme appeared before replication and release of virus in human amnion cells. Hydrocortisone depressed enzyme leakage but did not retard replication of measles virus or viral-induced cytopathology. The intracellular distribution of beta-glucuronidase in uninfected and measles virus-infected cells was also studied. Measles virus infection altered the position of particulate-bound beta-glucuronidase in linear sucrose gradients prior to substantial release of this enzyme intra- and extracellularly. At early stages in infection, most of the cell-associated virus banded with particulate-bound enzyme in the middle of the gradient. As infection progressed, separation of measles virus infectivity from enzyme activity occurred, and intracellular virus was recovered near the meniscus of sucrose gradients.

The morphogenesis of the Edmonston strain of measles is described in cultures of hamster dorsal-root ganglion maintained for as long as 63 days postinoculation. The patterns observed confirmed those previously reported in both neural and non-neural tissue. However, in the present tissue, the development of viral material could be followed chronologically within different cell types such as neurons and Schwann cells. Active replication was visualized up to 63 days postinoculation. The appearance of cytoplasmic nucleocapsid preceded that of intranuclear nucleocapsid, the latter occurring after 14 days. These intranuclear inclusions were formed after the transformation of the nucleoli into bizarre pleomorphic bodies which eventually segregated into clumps of nucleocapsid. These intranuclear inclusions mimic those seen in subacute sclerosing panencephalitis, now known to be etiologically related to a measles-like virus.