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Biomedical subjects

R T Johnson

Publications and source records attributed to R T Johnson.

At least 271 records · Page 15Linked to original sources
PubMed1972

Virions from progressive multifocal leukoencephalopathy: rapid serological identification by electron microscopy.

Virions were extracted directly from the brain of a patient with progressive multifocal leukoencephalopathy (PML). They were treated with antiserum to SV40, with rabbit antiserum to previous PML isolates, or with serum from another patient with the same disease and observed directly by electron microscopy. This procedure could be used for the rapid identification of the antigenic nature of virions in cases of PML.

Agglutination↗
PubMed1972

Specificity of the inflammatory response in viral encephalitis. I. Adoptive immunization of immunosuppressed mice infected with Sindbis virus.

The viral-induced perivascular inflammatory response in Sindbis virus encephalitis of mice was shown to be immunologically specific. Mice were inoculated intracerebrally with Sindbis virus, and 24 hr later a single dose of cyclophosphamide was given which ablated the inflammatory response. 3 days after virus inoculation, cells and/or sera from specifically and nonspecifically sensitized donor mice were given, and the inflammatory reactions, virus content, and antibody response of recipients were examined 5 days later. Reconstitution of the viral inflammatory response required virus-specific sensitized lymph node cells and was enhanced when these lymph node cells were combined with bone marrow cells. Reconstitution was not achieved with Sindbis virus immune serum even when combined with nonspecifically sensitized cells. Combination of immune serum with Sindbis virus-sensitized cells did not produce an accentuation of the reaction. In distinction, reconstitution of the inflammatory reaction surrounding the stab wound was reconstituted with bone marrow cells from mice inoculated with Sindbis virus or control antigens. Reconstitution of the perivascular reaction was associated with a reduction in brain virus content. Although the transfer of Sindbis virus-sensitized lymph node cells and bone marrow cells resulted in the limited production of neutralizing antibody in the immunosuppressed recipient, the reduction in virus was significantly greater with the transfers of Sindbis virus-sensitized lymph node cells than with the passive transfer of immune serum alone.

Animals↗
PubMed1972

Effects of viral infection on nervous system development. II. Attempts to modify bluetongue-virus-induced malformations with cyclophosphamide and antithymocyte serum.

Treatment with cyclophosphamide and antithymocyte serum (ATS) did not significantly increase the susceptibility of mice to bluetongue virus infections of the nervous system. Cyclophosphamide actually inhibited virus growth in newborn and 2-week-old mice and, in newborn mice, diminished the severity of virus-induced pathologic sequelae. Autoradiographic studies suggested this inhibition resulted from the effect of cyclophosphamide on the immature cells of the subventricular zone which were the cell population selectively infected by bluetongue virus. In newborn mice ATS inhibited the inflammatory reaction and development of antibody, but did not result in alterations in mortality, initial virus growth and localization or early necrosis of cells in the subventricular zone. Antithymocyte serum only caused longer persistence of virus and slight extension of late pathologic lesions. The failure of cyclophosphamide and ATS treatment to induce more extensive lesions in older mice show that the age-dependency of bluetongue lesions is not determined by the immaturity of immune responses.

Age Factors↗
PubMed1972

Effects of viral infection on nervous system development. I. Pathogenesis of bluetongue virus infection in mice.

Bluetongue vaccine virus was adapted to mice by serial intracerebral passage. The adapted virus was found to multiply selectively in immature cells of the subventricular zone of the forebrain and spread along cell migratory pathways to the olfactory bulbs, caudate/putamen, hippocampus and areas of cerebral cortex. Symmetrical, mineralized, partially cavitated lesions developed in these areas as a sequela of the infection. Infection of fetal mice led to more severe cerebral malformation, and infection of 2-week-old mice resulted in very limited multiplication without sequelae. The pattern of infection correlated with the maturation and migration of cells within the developing telencephalon.

Age Factors↗
PubMed1972

Granular ependymitis. Occurrence in myxovirus infected rodents and prevalence in man.

Intracerebral inoculation of neuropathic and nonneuropathic strains of mumps virus into adult hamsters resulted in an acute focal infection of ependymal cells followed by focal ependymal denuding. Similar lesions followed defective infection with influenza A in both hamsters and mice; when a large amount of influenza A was inoculated, aqueductal stenosis and hydrocephalus developed in some adult animals as a sequela of widespread ependymal cell loss. A survey of 100 consecutive adult human brains showed that 65% had granular ependymitis which had many of the characteristics found in the focal ependymal lesions produced in rodents. These studies suggest that human CNS mumps infections may produce granular ependymitis.

Adult↗