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Biomedical subjects

O Narayan

Publications and source records attributed to O Narayan.

At least 199 records · Page 11Linked to original sources
PubMed1980

Pathogenesis of human poliovirus infection in mice. I. Clinical and pathological studies.

Human poliovirus infection in mice was studied to determine the similarities to human poliomyelitis, the selective vulnerability of neurons to infection, the role of the immune response in age-dependent susceptibility, and possible viral persistence. Mice inoculated intracerebrally (ic) with the Lansing type 2 poliovirus developed a disease with clinical, pathological, and age-dependent features resembling human poliomyelitis. Adult mice had a shorter incubation period (50% paralysis, Day 8 vs. Day 13) and a higher incidence of paralysis (97% vs. 79%) than newborns. Only paralyzed animals had pathologic changes in the spinal cord, and these corresponded to the degree of paralysis. Fluorescent antibody staining showed that selective infection of neurons was most intense in the anterior horn motor neurons of the spinal cord. There was no extraneural virus replication and no systemic neutralizing antibody response. Cyclophosphamide immunosuppression enhanced rather than diminished disease, indicating that maturation of immune responses did not explain the relative resistance of newborns to paralysis.

Animals↗
PubMed1980

Pathogenesis of human poliovirus infection in mice. II. Age-dependency of paralysis.

The mechanism of resistance of newborn mice to poliovirus-induced paralysis was studied by comparing regional virus replication in the adult and in the newborn central nervous systems (CNS) after intracerebral (ic) and intraspinal inoculation. Initial virus replication in the brains was similar in both age groups. Paralysis correlated with replication of virus in the spinal cord to a constant threshold, and this replication in newborns was delayed. Intraspinal inoculation of newborns eliminated the delay, indicating that neonatal anterior horn motor neurons were fully susceptible to infection. Cordectomy prevented the spread of virus, despite patent cerebrospinal fluid (CSF) pathways. Thus, poliovirus appeared to spread within the CNS via an axonal transport system. Known maturational changes in the fast transport system may explain the relative resistance of immature mice to poliovirus-induced paralysis.

Age Factors↗
PubMed1980

Biological characterization of the virus causing leukoencephalitis and arthritis in goats.

This study describes the biological properties of a strain of virus isolated from tissues of a goat with leukoencephalomyelitis-arthritis. The agent is a retrovirus, having a virion-associated reverse transcriptase enzyme and an antigenic determinant(s) which cross-reacts with the p30 of visna-maedi viruses. Morphogenesis of the virus is also similar to visna virus in terms of virus assembly and the multinucleated giant cell formation which accompanies replication of the latter virus. Despite its cytopathogenic property the goat agent was not lytic in goat cell culture, causing instead a productive infection which persisted through multiple subcultures of the cells. The virus replicated incompletely in sheep cell cultures but could be rescued from the latter, weeks after inoculation, by co-cultivation with goat cells. Our data suggest that this strain of goat leukoencephalitis virus is a variant of the ovine retroviruses with a host range limited to the goat.

Animal Diseases↗
PubMed1980

Biochemical characterization of the virus causing leukoencephalitis and arthritis in goats.

Goat leukoencephalitis-arthritis virus (GLV) has the density of a retrovirus in sucrose and contains an endogenous RNA-dependent DNA polymerase (reverse transcriptase). The virion reverse transcriptase utilizes the synthetic RNA template poly(rA). (dT)12 but not the synthetic DNA template poly(dA). (dT)12. A high mol. wt. RNA similar in size to visna virus RNA was isolated from 3H-uridine-labelled virions. The major structural protein of GLV has the same mol. wt. as that of visna virus. From these data the GLV appears to be a retrovirus.

Animal Diseases↗
PubMed1980

Visna-maedi-like disease associated with an ovine retrovirus infection in a Corriedale sheep.

A visna-maedi-like disease was found in a Corriedale sheep from which a retrovirus sharing the group antigen of visna-progressive pneumonia virus was isolated from lung, brain, and spleen. Clinically, the sheep had acute neurologic signs and dyspnea. Pathologic examination showed lesions similar to both visna and maedi. In the lung, there was a patchy interstitial pneumonia with marked lymphoid hyperplasia. Changes in the central nervous system were necrotizing nonsuppurative encephalitis of the brain stem, poliomyelitis of the cervical cord, and ependymitis and subependymal gliosis of the ventricles. Histologically, the central nervous system lesions seemed to have arisen sequentially, perhaps in response to bursts of virus replication as the agent underwent possible antigenic mutation. The severe lesions in both the central nervous system and lungs suggested a virus strain with dual tropism.

Animals↗
PubMed1980

The pathogenesis of viral leukoencephalomyelitis-arthritis of goats. I. Persistent viral infection with progressive pathologic changes.

The pathogenesis of viral leukoencephalomyelitis of goats was studied in newborn and adult goats using purified, concentrated leukoencephalitis virus. The disease could be transmitted using purified leukoencephalitis virus or tissue suspensions from a goat experimentally infected with leukoencephalitis virus. As early as 1 week following inoculation, goats developed lesions in the brain, joint, and lung. Lesions persisted 8 to 21 months, were not age-dependent, and were inflammatory in character. In the brain they were accompanied by demyelination. Virus could be isolated from experimental goats by cocultivation of peripheral blood leukocytes and by explantation of tissues beginning a week after inoculation and throughout the life of the goat. These studies confirm that leukoencephalitis virus is the etiologic agent of leukoencephalitis-arthritis of goats and produces a persistent infection characterized by demyelinating encephalitis, progressive arthritis, and interstitial pneumonia.

Age Factors↗
PubMed1979

Antigenic variation in visna virus.

Two antigenic variants of visna virus were isolated sequentially from a single sheep inoculated with a plaque-purified strain of virus designated 1514. The genetically stable variants, LV1-1 and LV1-4, are of two classes: LV1-1 is partially neutralized by antibody to the inoculum strain 1514, while LV1-4 is not neutralized by antibody to 1514. The genetic mechanism responsible for generating the antigenic variants was investigated by comparing the chymotryptic and tryptic maps of the envelope glycoprotein gp135 and core polypeptides (p30, p16, p14), and by comparing the pattern of large oligonucleotides produced by digestion of the RNAs by T1 ribonuclease. We show that only the peptide maps of gp135 differ among strains, that the number of peptide fragments altered is small and that gp135 is the polypeptide that elicits neutralizing antibody. The maps of the RNAs are identical. We conclude that mutation in the glycoprotein gene rather than recombination is more probably responsible for antigenic variation, and speculate on the special aspects of visna virus replication relevant to this phenomenon.

Amino Acid Sequence↗
PubMed1978

The cerebrospinal fluid in visna, a slow viral disease of sheep.

The temporal development of the CSF abnormalities was examined in visna, a chronic neurological disease caused by a persistent viral infection of sheep. Two types of changes were observed. During the first 30 to 40 days there was an intense mononuclear pleocytosis associated with high protein and proportionately elevated IgG. Later, there was a persistent slight pleocytosis associated with mildly elevated protein which had an increased proportion of IgG and antivisna antibody. These later cellular and protein changes are similar to those found in a number of chronic neurological diseases of man.

Animals↗
PubMed1978

Virus mutation during 'slow infection': temporal development and characterization of mutants of visna virus recovered from sheep.

Visna virus could be recovered from peripheral blood leukocytes of sheep for years after intracerebral inoculation. Viruses recovered from sheep prior to and several months after development of antibody were antigenically identical to the parental strain used for inoculation. Subsequently, mutant viruses which were not neutralized by the animals' sera were obtained. Longitudinal studies of leukocyte viruses collected from two infected sheep showed that more than one strain of virus could co-exist in the animal. Virus neutralization tests using sequentially collected sera and the viruses recovered from leukocytes revealed a sequential development of antibody to parental and then to each strain of mutant virus. Characterization of two of the mutant viruses showed that they were antigenically stable, virulent in cell culture and when inoculated into new sheep, elicited antibodies which cross reacted with the parental virus from which they were derived. This continuous mutation of Visna virus in persistently infected sheep may be a mechanism for the production of chronic disease.

Animals↗
PubMed1977

Antigenic shift of visna virus in persistently infected sheep.

Visna viruses isolated from persistently infected sheep were antigenically distinct from the plaque-purified virus used for inoculation. The selection of antigenic variants under antibody pressure, thought to occur in vivo, was reproduced in sheep cell cultures inoculated with plaque-purified visna virus and maintained in antibody. Antigenic shift may be a mechanism for persistence of virus in slow or recurrent viral infections.

Animals↗
PubMed1977

Slow virus infection: replication and mechanisms of persistence of visna virus in sheep.

The influence of the age and immune status of the host on the slow replication and persistence of visna virus in sheep was studied. Twenty-five randomly bred fetal American lambs were inoculated intracerebrally with visna virus. Eight of these fetuses were immunosuppressed by thymectomy and antiserum to lymphocytes before inoculation. Fetuses were sacrificed sequentially, and tissues were processed for viral quantitation. No exponential increase of virus occurred in either the normal or immunosuppressed fetuses, and virus was recovered mainly by explanation of tissues. This finding indicated that the viral genome was present in tissue cells but that the extent of replication in the early phase of infection was restricted by factors unassociated with maturation or immune status of the host. In addition, virus isolated from the peripheral blood leukocytes of a sheep one year after inoculation was antigenically distinct from the plaque-purified virus used for inoculation. This distinction suggested that a major antigenic shift of the agent had occurred and provided another mechanism for the maintenance of the persistent infection.

Animals↗