Search PubMed⌕ Search

Biomedical subjects

N Hirano

Publications and source records attributed to N Hirano.

At least 127 records · Page 7Linked to original sources
PubMed1988

Reactivities of 4 murine coronavirus antigens with immunized or naturally infected rat sera by enzyme linked immunosorbent assay.

Four murine coronavirus antigens, sialodacryoadenitis virus (SDAV) strain TG, Parker's rat coronavirus (PCV) strain 8190, mouse hepatitis virus (MHV) strains S and NuU, were examined for their reactivities to hyperimmunized and naturally infected rat sera by ELISA. With the immunized sera, SDAV and PCV antigens reacted best with respective homologous sera. MHV antigens reacted with all antisera, anti-SDAV, anti-PCV, and anti-MHV-S at approximately the same level, and MHV-S showed a slightly higher reactivity than MHV-NuU. The reactivities of the sera from various colonies to these antigens were in the order--from high to low--of SDAV, MHV-S, MHV-NuU, and PCV. None of sera negative for SDAV antigen reacted positively to the other antigens. Within the sera positive for SDAV, the positivities were in the order of MHV-S, MHV-NuU, and PCV. These results suggested that, although homologous antigens are best to detect SDAV or PCV infection by ELISA, MHV antigen can be used if highly cross-reactive viral strain is selected.

Animals↗
PubMed1987

A sensitive plaque assay for bovine rotavirus in cultures of the bovine cell line GBK.

The Lincoln strain of bovine rotavirus was found to replicate with cytopathic effects in cultures of GBK cells, a stable cell line derived from bovine kidney, when the cultures were maintained in the presence of trypsin. The virus was readily passaged and the infected cells were shown to contain specific viral antigen by indirect immunofluorescent staining. The virus formed plaques in GBK cell monolayers, when trypsin was incorporated in the agar overlay medium. The plaque count increased about twofold when diethylaminoethyl dextran was further included in the overlay medium. Plaque assay in GBK cells was more sensitive than that in MA-104 cells previously reported by Matsuno et al. The specificity of plaques was confirmed by specific inhibition with antiserum against the Lincoln strain.

Animals↗
PubMed1986

Pathogenesis of haemagglutinating encephalomyelitis virus (HEV) in mice experimentally infected by different routes.

Three-day-old suckling mice inoculated intracerebrally (i.c.) with the 67N strain of haemagglutinating encephalomyelitis virus (HEV) showed nervous signs and died. The virus was passaged 10 times in suckling mice and was designated the MB-67N strain. The pathogenesis of MB-67N was studied with various ages of mice and inoculation routes. All mice inoculated i.c. with a large dose of virus died regardless of age, although a smaller dose caused fatal infection only in suckling mice. By intranasal, intraperitoneal and subcutaneous inoculation, the virus also killed suckling mice under 16 days old, but not older mice, even with a large dose. The susceptibility of mice for the MB-67N strain was influenced by age and inoculation routes. High titres of virus were re-isolated from the brain of diseased mice after inoculation by any route, but not from other organs. Histologically, numerous areas of severe focal necrosis were produced in the cerebral cortex. Specific immuno-fluorescence and numerous viral particles were found in the cytoplasm of nerve cells by immuno-fluorescence staining and electron microscopy. These findings indicate that the MB-67N propagates mainly in the central nervous system and nerve cells serve as a main target of virus replication.

Animals↗
PubMed1984

Analysis of genomic and intracellular viral RNAs of small plaque mutants of mouse hepatitis virus, JHM strain.

The genomic RNA and intracellular RNA of mouse hepatitis virus, strain JHM (MHV-JHM) and two plaque mutants (1a and 2c), which have been isolated from a persistently infected culture (JHM-CC), have been analyzed by T1-resistant oligonucleotide finger-printing. The genomic RNA of the virus population (JHM-CC virus) released from different passage levels of the same persistent infection has also been analyzed. The analysis shows the locations within the genomic and intracellular RNAs of more than 45 T1-resistant oligonucleotides and confirm earlier studies (J. L. Leibowitz, K. C. Wilhelmsen, and C. W. Bond (1981), Virology 114, 39-51), showing that the six subgenomic RNAs of MHV-JHM form a 3' coterminal nested set which extends for different lengths in a 5' direction. The analysis also identifies in each subgenomic RNA those large T1 oligonucleotides derived from noncontiguous regions of the genome during mRNA synthesis. Two important conclusions can be reached from analysis of the mutant viruses. First, the virus population released from the persistent infection represents a fairly constant mixture of viruses, and the fluctuating emergence of variants as predominant species in the culture does not occur. Second, the data indicate that for particular intracellular RNAs of mutant viruses the sequence rearrangements occurring during subgenomic mRNA synthesis are different from those in the corresponding intracellular RNA of wild-type virus. The result may indicate a potential flexibility in the leader/body fusion process that has not been previously recognized.

Animals↗