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Biomedical subjects

D L Camenga

Publications and source records attributed to D L Camenga.

3 recordsLinked to original sources

Anticonvulsant prolongation of survival in adult murine lymphocytic choriomeningitis. I. Drug treatment and virologic studies.

Lymphocytic choriomeningitis virus-induced central nervous system disease is characterized by death during a seizure approximately seven days after intracerebral inoculation. This process is mediated by thymus dependent lymphocytes, sensitized against viral antigens. Various forms of immunosuppressive treatment prevent the seizure death and produce persistently infected survivors. In this study, anticonvulsant treatment (particularly diazepam treatment) of LCM virus infected mice prolonged survival without affecting viral replication, or suppressing immune responsiveness. This prolongation of life did not lead to a reversal of pathologic processes and there were no survivors. However, anticonvulsant treatment permitted study of more advanced stages of the choriomeningitis than has previously been possible.

Animals

Anticonvulsant prolongation of survival in adult murine lymphocytic choriomeningitis. II. Ultrastructural observations of pathogenetic events.

Because previous ultrastructural studies of murine lymphocytic choriomeningitis (LCM) had revealed only mononuclear cell infiltration with no cytopathology of target cells in the choroid plexus, ependyma, and leptomeninges, diazepam treatment was used to prolong survival for characterization of late pathogenetic events. Mice which were treated with diazepam and sacrificed 8, 9, and 10 days after intracerebral inoculation with LCM virus showed an increasing amount of inflammatory infiltration into choroid plexuses, leptomeninges, Virchow-Robin spaces, and ependyma. Mononuclear cells, lymphocytes, and polymorphonuclear (PMN) leukocytes increased in number as compared with terminally infected mice sacrificed 7 days after inoculation. Ultrastructurally, choroidal epithelial cells showed cytopathological changes varying from dilated endoplasmic reticulum through necrosis. Greater numbers of PMN leukocytes, macrophages, and activated macrophages and fewer undifferentiated mononuclear cells were seen in choroid plexuses of the drug-treated survivors. Virions and larger, more numerous arenavirus inclusions were present in choroid plexus and ependyma. Ultrastructurally the leptomeningitis was characterized by large numbers of activated macrophages. Choroidal epithelial necrosis appears to be the in vivo correlate of T-cell-mediated cytotoxicity in vitro.

Animals

An immunopathologic component in experimental togavirus encephalitis.

The effects of immune manipulation upon survival and histopathology in two experimental group B togavirus encephalitides were studied in inbred mice. The median survival time 8 days after intracerebral injection of Langat virus increased to 10 days with an immunosuppressive course of cyclophosphamide, with concomitant reduction in the inflammatory response. Adoptive immunization with immune lymphoid cells or serum also tended to prolong Langat virus survival while increasing inflammation. Survival following intracerebral West Nile virus (7 days) was unaffected by immunosuppression or adoptive transfer, although suppression was associated with less severe CNS lesions, and immune serum with less necrosis. These findings indicate that the immune response may be both protective and pathology-inducing in some togarvirus encephalitides. The differences in host response to these two related agents suggest caution in generalizing about the role of the immune response in viral infections.

Animals