PubMed Health⌕ Search

Biomedical subjects

K W Rammohan

Publications and source records attributed to K W Rammohan.

26 records · Page 2Linked to original sources
PubMed1985

Oligoclonal bands in unconcentrated CSF. Silver stain for agarose gels.

Agarose gel electrophoresis (AGE) and agarose isoelectric focusing (AIEF) were performed on unconcentrated CSF from patients with multiple sclerosis and other neurological disorders. Electrophoretic profiles were examined after staining with silver. Oligoclonal distribution of immunoglobulins were observed in over 90% of patients with clinically definite multiple sclerosis and over half of all patients with possible or probable multiple sclerosis. Up to 20 samples could be simultaneously examined and required the use of only 2-20 microliter of unconcentrated CSF containing 10-100 ng of total IgG. The entire procedure from sample application to completion of staining required less than 3 h. The techniques offered exquisite resolution of abnormal immunoglobulin bands and permitted distinction of normal from abnormal CSF readily.

Electrophoresis, Agar Gel↗
PubMed1983

Antibody-mediated modification of encephalitis induced by hamster neurotropic measles virus.

The acute encephalopathy induced by hamster neurotropic (HNT) measles virus in BALB/c mice was abolished, and a subacute encephalitis was induced instead, when antibody to Edmonston (Ed) measles virus was administered three days after inoculation of HNT virus. Ascites fluid from 79XIC1, a monocolonal antibody to the hemaglutinin of strain Ed, had similar effects in vivo. However, other monoclonal antibodies to the hemagglutinin of Ed strain--79XVV17 and 80IIIB2--were ineffective in vivo at all doses tested. By viral neutralization, immunofluorescence, and radioimmunoprecipitation assays, it was shown that the hemagglutinin of HNT virus reacted with 79XIC1 antibody but lacked the epitopes recognized by 79XVV17 or 80IIIB2 antibody, a finding that explains their different reactivity in vivo. These observations also identified previously unrecognized antigenic differences between the hemagglutinin of Ed and HNT measles viruses.

Animals↗
PubMed1982

Subacute sclerosing panencephalitis after passive immunization and natural measles infection: role of antibody in persistence of measles virus.

Subacute sclerosing panencephalitis (SSPE) developed in a patient in whom natural measles infection was anteceded by immunization with measles immune serum globulin (ISG). This observation prompted experimental studies of the role of antibody in viral persistence. When Balb/c mice were infected with the hamster neurotropic measles virus, acute encephalopathy was fatal in 80% of the animals. When measles antibody was administered 3 days after virus inoculation, the acute disease was abolished and subacute encephalitis had a 30% mortality. The subacute disease was characterized by the presence of neuronal viral antigen, meningitis, and encephalitis. Induction of viral persistence was therefore a consequence of antibody transfer during viral infection. Caution is advised in human prophylaxis with immune globulin.

Animals↗
PubMed1981

Induction of subacute murine measles encephalitis by monoclonal antibody to virus haemagglutinin.

Although the events which predispose a host to measles virus persistence remain largely unknown, measles antibody has been shown to contribute to the production of a persistent infection by this virus both in vivo and in vitro. Thus, the addition of measles antibody to cells infected with measles virus promotes virus persistence. Latent measles infection occurs in newborn hamsters with maternally acquired antibody after inoculation with measles virus in the immediate neonatal period. A subacute encephalitis with measles virus persistence has been induced in weanling BALB/c mice that received antibody after virus inoculation and in measles-immune primates infected with a virus derived from a patient with subacute sclerosing panencephalitis. Measles virus consists of six polypeptides, and treatment of measles-infected cells with antibody has been shown to alter the pattern of their synthesis. As the antigenic specificity of the antibody responsible for these observations is not known, we decided to investigate the effects of monoclonal antibodies directed against the individual measles polypeptides. We report here that a monoclonal antibody directed against the virus haemagglutinin, unlike an antibody to the virus nucleocapsid protein, is able to induce a subacute encephalitis in vivo.

Animals↗
PubMed1981

Idiotypes and biological activity of murine monoclonal antibodies against the hemagglutinin of measles virus.

Three hybridomas, designated C2, V17, and B2, were produced from BALB/c mice after immunization with measles virus. All three were directed against the virus hemagglutinin (HA). The HA is a structural peptide of the virus and constitutes a major target for the host immune response during measles infection. The monoclonal anti-HA antibodies have biological functions such as (i) measles virus neutralization in vitro, (ii) binding to acutely and persistently infected cells, and (iii) inhibition of HA-mediated Rhesus monkey erythrocyte agglutination. Different idiotypes, designated HAMM-1, HAMM-2, and HAMM-3, were defined on C2, V17, and B2, respectively, by syngeneic anti-idiotype sera against those three monoclonal antibodies. A limited cross-reactivity with the HAMM-1 idiotype was detected in sera from some BALB/c mice immunized with measles virus. The anti-idiotype sera could significantly inhibit the biological functions of the HAMM-1 and HAMM-3 idiotypes bearing monoclonal anti-HA-antibodies. This suggests a possible role for auto-anti-idiotypes in the immune response after infection with measles virus.

Animals↗
PubMed1980

Chronic measles encephalitis in mice.

The intracerebral inoculation of hamster neurotropic measles virus produces a fatal acute encephalopathy in the majority of weanling BALB/c mice. The few survivors remain healthy indefinitely. In contrast, weanling SJL/J mice are relatively resistant to acute encephalopathy, and about one-third of the survivors predictably develop a chronic encephalitis many weeks after inoculation. This later illness is characterized clinically by wasting, lethargy, seizures, or focal paralysis, usually culminating in death. Pathologically, a considerable brain inflammatory response occurs in association with abundant measles viral antigen. Viral antigen and inflammation were demonstrable predominantly in the limbic system but was also present in the cerebellum and brain stem. Antibody to measles virus was readily demonstrated in all animals with chronic encephalitis. This report constitutes the first description of chronic measles encephalitis in an inbred host.

Animals↗
PubMed1979

Selective neuronal, dendritic, and postsynaptic localization of viral antigen in measles-infected mice.

The pathology of acute disease produced by intracerebral inoculation of hamster neurotropic strain of measles virus was studied in adult BALB/c mice using immunolabeling techniques at a light and electron microscopic level. Brains of animals with acute disease showed an abundance of viral antigen but no inflammatory cells, giant cells, or inclusions. Infection was limited to neurons which were rarely necrotic, indicating that the process was not cytolytic. Mapping of infected neurons identified a consistent predilection to the rhinencephalon, other components of the limbic system, and the striatum. Ultrastructural examination revealed similar findings in all of the involved areas. No evidence of viral assembly at the cell membrane was found. Viral antigen was identified in neuronal perikaryon with somatofugal spread into dendritic and synaptic sites. Unlabeled smooth nucleocapsid and labeled tubular structures were detected both in the cytoplasm and nucleus of neurons. Dendritic labeling when present was occasionally associated with the neurotubules. The most remarkable and frequent finding was identification of viral antigen in postsynaptic endings. This consisted of clumps of viral antigen and occasional staining of the postsynaptic density. This localization of viral antigen may create dysfunction of synaptic transmission, and in the absence of overt pathology, may account for clinical disease.

Animals↗