Search PubMed⌕ Search

Biomedical subjects

O Narayan

Publications and source records attributed to O Narayan.

At least 217 records · Page 12Linked to original sources
PubMed1977

Induction of brain tumors in hamsters with BK virus, a human papovavirus.

The oncogenicity of BK virus for the central nervous system was studied in newborn hamsters. The virus was weakly oncogenic after intracerebral inoculation. Two of 45 hamsters treated with antithymocyte serum developed tumors whereas no untreated hamsters developed tumors. Both tumors were choroid plexus papillomas by histologic and electron microscopic examination. Cells cultured from one tumor had growth characteristics of transformed cells and had intranuclear T antigen; but infectious virus could not be rescued. Cultured tumor cells were weakly oncogenic for hamsters, but theoncogenicity of these cells was enhanced when the recipient animals were treated with antithymocyte serum. The possible role of host immune response as a basis for the weak oncogenicity of BK virus is discussed.

Animals↗
PubMed1976

Studies of human papovavirus tumor antigen in experimental and human cerebral neoplasms.

Three types of papovaviruses (JC, BK, and SV40) have been isolated from man. All three are oncogenic in hamsters, cause frequent infection of man, and share a common T antigen. Augmentation of the expression of T antigen by in vitro cultivation of SV40-induced tumors of hamsters suggested that growing human brain tumors in vitro might provide an effective screening technique for the SV40 virus. In a series of human brain tumors examined in cryostat sections and in tissue culture, T antigen could not be demonstrated, suggesting that by this immunofluorescent technique SV40 was not implicated in the etiology of these tumors.

Animals↗
PubMed1976

Acute encephalopathy caused by defective virus infection. I. Studies of Newcastle disease virus infections in newborn and adult mice.

An acute encephalopathy caused by a defective paramyxovirus infection was studied. Newcastle disease virus (ndv), given intracerebrally, caused neurologic disease and death in mice. Infected newborn mice died by the fourth day after inoculation, and abundant amounts of virus were recovered from their brains. Infected 4-week-old mice died by the eighth day, but only minimal amounts of virus, if any, were recovered. The brains of many moribund 4-week-old mice were histologically normal and contained no NDV antigen on fluorescent antibody staining. No serum antibody to NDV was detected. These features make this infection difficult to distinguish from a metabolic encephalopathy.

Age Factors↗
PubMed1975

Virus-induced abortion. Studies of equine herpesvirus 1 (abortion virus) in hamsters.

A hamster-adapted strain of equine herpesvirus-1 (equine abortion virus) caused severe hepatic degeneration in both pregnant and nonpregnant hamsters and, in addition, regularly induced abortion in pregnant hamsters inoculated at midgestation. In nonpregnant hamsters, the only consistently affected organ was the liver despite a prolonged viremia. Newborn animals usually died 1 to 2 days after inoculation; adults died 5 to 9 days after inoculation. In pregnant hamsters, the virus had a tropism for the placenta as well as the liver. The placental infection was confined almost exclusively to one cell type in the fetal portion of the placenta: the trophoblast cells of the syncytiotrophoblast zone. Necrosis of this zone led to fetal death and abortion. Infection of the fetus did not occur.

Abortion, Spontaneous↗
PubMed1974

Visna virus infection of American lambs.

Random-bred fetal and 4-week-old American lambs, inoculated intracerebrally with visna virus, developed a persistent infection in the brain and sometimes in the lung. The pathologic changes present in these lambs were similar to the early lesions of visna in Icelandic sheep, thus providing a possible model for the study of virus-induced demyelinating disease.

Animals↗
PubMed1974

Biological properties of two strains of Simian virus 40 isolated from patients with progressive multifocal leukoencephalopathy.

Biological properties of two strains of simian virus 40 (SV40) from brains of two patients with progressive multifocal leukoencephalopathy (PML) have been compared to those of a standard laboratory strain of SV40. Infectivity of both SV40-PML viruses was resistant to treatment with chloroform, low pH, and 50 C for 120 min. African green monkey kidney and BSC-1 cells were the most sensitive for viral replication, and cytopathology in these cultures was indistinguishable from that caused by SV40. Both viruses formed plaques in these cells. but, in African green monkey kidney cells, strain 1 virus produced plaques measuring 2 mm in diameter whereas strain 2 virus produced pleomorphic plaques varying from 1 to 10 mm in diameter. Hamster cells were not permissive for viral replication, and infection resulted only in viral transformation. Inoculation of human fetal glial cells resulted in a permissive lytic infection of one cell type and a persistent infection with only partial expression of the viral genome in the other. No morphological evidence of transformation was evident in the latter cells. Both strains of SV40-PML viruses were neutralized by commercial anti-SV40 serum, but in reciprocal kinetic neutralization tests differences in K values were noted when each was compared to SV40. Both viruses showed oncogenicity for hamsters, producing undifferentiated sarcomas when injected subcutaneously and choroid plexus papillomas after intracerebral inoculation. All hamster tumor cells contained intranuclear immunofluorescent tumor antigen. This was indistinguishable from SV40 T antigen in reciprocal staining reactions using hamster anti-T antibody induced by the two SV40-PML agents and SV40. These two human agents appear therefore to be new variants of simian virus 40.

Animals↗
PubMed1974

Age dependence of viral expression: comparative pathogenesis of two rodent-adapted strains of measles virus in mice.

The pathogenesis of two rodent-adapted strains of measles virus was studied in 1- to 2-day-old suckling and 4-week-old weanling BALB/c mice. Both the mouse-adapted Edmonston (MAEd) strain and the hamster-neurotropic (HNT) strain caused necrotizing giant-cell encephalitis with a 90 to 100% mortality after intracerebral inoculation into suckling mice. After intracerebral inoculation into weanling mice, MAEd virus caused fatal disease in 20% of the mice; HNT virus caused fatal disease in 30%, but an additional 35% of these mice developed disease and then recovered. Even when mice were moribund there was little histological evidence of disease in weanling mice inoculated intracerebrally with either strain of virus. Fluorescent-antibody staining showed extensive measles virus antigen in the suckling mouse brain and focal areas of measles virus antigen in the weanling mouse brain. Infectious virus was recovered easily from the brains of suckling mice by plaquing on Vero cells, but no infectious virus could be recovered similarly from weanling mice. However, virus could be recovered by intracerebral inoculation of weanling mouse tissue homogenates into suckling animals. The immune response appeared to play no role in the recovery from infection or in these age-related differences in disease. It appears that maturation of the cells of the mouse central nervous system converted the production of measles virus from the infectious form in the suckling mouse to a primarily defective infection in the weanling mouse.

Age Factors↗
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↗