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Biomedical subjects

J G Stevens

Publications and source records attributed to J G Stevens.

At least 91 records · Page 5Linked to original sources
PubMed1978

Immunosuppression reactivates and disseminates latent murine cytomegalovirus.

When searched for by standard virological methods, murine cytomegalovirus (MCMV) becomes undetectable by four months after inoculation of mice. However, a two-week regimen of immunosuppression with antilymphocyte serum and corticosteroid results in reactivation and dissemination of the virus in virtually all animals. This system should be useful in defining the pathogenesis of generalized cytomegalic disease resulting from reactivation of latent virus in immunocompromized individuals.

Animals↗
PubMed1977

Intraaxonal transport of Herpes simplex virus in the rat central nervous system.

Light and electron microscopic observation 3--4 days after microinjection of Herpes simplex virus (HSV) into the left neostriatum of rat demonstrated the following results. (1) Virus labeled nerve cells were found in the ipsilateral substantia nigra; a large number of infected neurons were in the zona compacta and some were in the zona reticulata. No virus infection was evident in the contralateral side. (2) Virus labeled neurons were found in the cortex, a greater number ipsilaterally than contralaterally, and in the dorsal raphé nuclei. Cortical microinjection of HSV led to infection of some cortical cells but no neostriatal cells. We conclude, therefore, that spread of the virus to the cortex, the substantia nigra and the dorsal raphé following neostriatal injection was by retrograde axonal transport. (3) The left neostriatum, where HSV was injected, showed a surprisingly small number of virus infected neurons. The infected neurons were mostly the large neurons; the majority of medium sized neurons were well preserved. There was massive degeneration of nerve terminals throughout the neuropil. Most of these degenerating nerve terminals are considered to be afferent fibers.

Animals↗
PubMed1977

Immunosuppression reactivates and disseminates latent murine cytomegalovirus.

When searched for by standard virological methods, murine cytomegalovirus (MCMV) becomes undetectable by 4 months after inoculation of mice. However, a 2-week regimen of immunosuppression with antilymphocyte serum and corticosteroid results in reactivation and dissemination of the virus in virtually all animals. This system should be useful in defining the pathogenesis of generalized cytomegalic disease resulting from reactivation of latent virus in immunocompromised individuals.

Animals↗
PubMed1977

Newcastle disease as a model for paramyxovirus-induced neurologic syndromes. II. Detailed characterization of the encephalitis.

All chickens infected by intranasal and conjunctival routes with a neurovirulent strain of Newcastle disease virus (NDV) developed pneumonitis by 4 days after infection. This was followed 6 to 12 days later by the appearance of severe encephalitis in a significant number of survivors. Histologically, the encephalitis was characterized by neuronal degeneration and perivascular inflammation. In addition, a proliferative vasculitis in the molecular layer of the cerebellum was noted after 30 days, and this persisted for at least 200 days. Although CNS signs were absent during the pneumonic stage, significant amounts of virus were present in the brains of all birds at this time, and viral antigens were easily demonstrable in neurons, glial cells, and endothelial cells. However, when the CNS disease became apparent, viral antigens could not be detected in brains and NDV could regularly be recovered only by application of cocultivation techniques. At this time, the agent was selectively present in birds exhibiting neurologic signs. No evidence for immunopathologic processes was obtained, although hemagglutination inhibiting antibody levels to NDV were elevated in birds with CNS disease. Studies of an avirulent strain of NDV that replicated in the CNS but produced no disease provided evidence that the histologic lesions and the neurologic disease were related to virus multiplication in the brain parenchyma. A mechanism of the pathogenesis of NDV encephalitis is proposed and the disease is discussed relative to other paramyxovirus-induced encephalitic syndromes.

Animals↗
PubMed1976

Latent herpetic infections following experimental viraemia.

The spectrum of tissues harbouring latent herpes simplex virus following intravenous inoculation of mice was defined by in vitro co-cultivation techniques. The virus could be detected in central and peripheral nervous systems (including adrenal medulla), but could not be found in any non-neural tissues. Spinal ganglia were the organs most commonly involved. The relationship of these findings to the natural history of herpetic infections is discussed.

Adrenal Glands↗
PubMed1976

Reed Neurological Research Center, UCLA School of Medicine, Los Angeles, California.

Various clinical, virological, immunological, and morphological aspects of velogenic Newcastle disease were defined in chickens inoculated by natural routes with the Missouri-(H) Len 1950 strain. The disease initially appeared as a severe pneumonitis from which most birds recovered. Several days later, many of these birds developed severe encephalitic signs, largely referable to inflammatory changes in the cerebellum. During the pneumonic stage, virus was easily isolated in relatively high titers from the brains of all chickens, and viral products were easily detected in Purkinje neurons. However, when the encephalitis developed, virus was isolated irregularly and in low titers from brains, and morphological evidence for the presence of viral products could not longer be obtained. The encephalitic disease is discussed in relation to encephalitic syndromes induced by other neurotrophic viruses.

Animals↗
PubMed1975

Reactivation of latent Herpes simplex virus after pneumococcal pneumonia in mice.

In attempts to reactivate latent herpes simplex virus, we instilled Diplococcus pneumoniae intratracheally into mice harboring latent infections in sacrosciatic spinal ganglia. All mice developed a severe pneumonia within 24 h and were given penicillin therapy. Representative mice that survived the penumonia were sacrificed at daily intervals, and appropriate tissues were examined for evidence of viral reactivation. Herpes simplex virus was reactivated in the ganglia and appeared to travel both proximally and distally in associated nerve trunks. Clinically apparent disease due to the virus was not detected in any mice.

Animals↗
PubMed1975

Effect of cytosine arabinoside on viral-specific protein synthesis in cells infected with herpes simplex virus.

The relationship between viral DNA and protein synthesis during herpes simplex virus type 1 (HSV-1) replication in HeLa cells was examined. Treatment of infected cells with cytosine arabinoside (ara-C), which inhibited the synthesis of HSV-1 DNA beyond the level of detection, markedly affected the types and amounts of viral proteins made in the infected cell. Although early HSV-1 proteins were synthesized normally, there was a rapid decline in total viral protein synthesis beginning 3 to 4 h after infection. This is the time that viral DNA synthesis would normally have been initiated. ara-C also prevented the normal shift from early to late viral protein synthesis. Finally, it was shown that the effect of ara-C on late protein synthesis was dependent upon the time after infection that the drug was added. These results suggest that inhibition of progeny viral DNA synthesis by ara-C prevents the "turning on" of late HSV-1 protein synthesis but allows early translation to be "switched off."

Arginine↗
PubMed1975

Lifetimes of mRNA molecules directing the synthesis of viral proteins in herpes simplex virus-infected cells.

Possible variations in the functional lifetimes of herpes simplex virus type 1 mRNA molecules in infected HeLa cells were studied. As shown by the rate of decrease of radioactive amino acid incorporation into viral proteins after the addition of actinomycin, the average lifetime of early viral mRNA's are shorter than those for the late messenger species. In addition, when the viral proteins made after the addition of actinomycin were further analyzed by gel electrophoresis, it was found that messengers for individual viral proteins translated within the early or late time period also had some differences in their functional lifetimes. These results indicate that the synthesis of herpes simplex virus type 1 proteins during the replicative cycle is regulated in part by mechanisms controlling the functional lifetimes of viral mRNA's.

Cycloheximide↗
PubMed1974

Evidence that neurons harbor latent herpes simplex virus.

The cell type(s) harboring latent herpes simplex virus in the spinal ganglia of mice was investigated. Taken together, results from immunofluorescence, electron microscopic, autoradiographic, and in situ nucleic acid hybridization methods suggest strongly that, in mice, latent virus is maintained in neurons.

Animals↗
PubMed1974

Nature of the scrapie agent: evidence against a viroid.

The postulated viroid nature of scrapie agent was tested. Since the agent could not be recovered after a carefully controlled phenol extraction of infected mouse brains, it is suggested that this agent is not a viroid.

Animals↗