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Biomedical subjects

F Taguchi

Publications and source records attributed to F Taguchi.

At least 163 records · Page 9Linked to original sources
PubMed1979

Factors involved in the age-dependent resistance of mice infected with low-virulence mouse hepatitis virus.

Four-week-old weanling mice survived, whereas 1-week-old suckling mice died, after intraperitoneal inoculation of mouse hepatitis virus, MHV-S strain. The factors involved in this difference in susceptibility were studied. After virus inoculation, differences in virus growth in the liver and spleen were observed, which correlated with the susceptibility of animals to the virus. Interferon, detected at an early stage of infection, was considerably lower in suckling mice than in weanling mice. Titers of MHV-S in peritoneal cells from infected animals were at least 100 times greater in suckling than in weanling mice, and a similar, but less prominent difference in virus growth was also found in the corresponding cultured macrophages. After transfer of peritoneal cells from weanling to suckling mice, a decrease in mortality of infected suckling mice was observed. These results suggest that both interferon and macrophages may be important in the age-dependent resistance of mice to MHV-S infection.

Aging↗
PubMed1979

Induction of lytic plaques by murine leukemia virus in murine sarcoma virus-transformed nonproducer mouse cells persistently infected with mouse hepatitis virus MHV-S.

Kirsten murine sarcoma virus-transformed, nonproducer BALB3T3 (K-BALB) cells were persistently infected with mouse hepatitis virus, MHV-S. The cultures developed plaques after infection with murine leukemia viruses. If the murine leukemia virus-infected cultures were further submitted to the UV-XC assay, comparable numbers of XC plaques were obtained. The sensitivity to murine leukemia viruses, as determined by the UV-XC assay, was higher in MHV-S-infected cells as compared to uninfected K-BALB cells.

Animals↗
PubMed1979

T lymphocyte-dependent difference in susceptibility between DDD and C3H mice to mouse hepatitis virus, MHV-3.

After intraperitoneal inculation with a virulent mouse hepatitis virus, MHV-3, 50% lethal dose in DDD mice was about 7 log10 higher than that in C3H mice. Histopathologically, splenic lymphocytes especially of the thymus-dependent area were more severely affected in susceptible C3H mice than in DDD mice. In the liver of C3H mice, virus multiplied exponentially after inoculation, attaining 10(6) PFU at moribund stage, while virus multiplication in DDD mice was much less prominent decreasing remarkably at day 5 or later. The virus could multiply in the primary culture of spleen cells from C3H mice but not in those from DDD mice, and cells supporting virus growth seemed to be a theta-positive population of lymphocytes. No difference was observed between the two strains of mice in the ability of peritoneal macrophages to support virus growth in vitro as well as serum interferon levels after infection.

Animals↗
PubMed1978

Concanavalin A-mediated agglutination of 3T3 cells after exposure to UV-irradiated herpes simplex virus.

Studies were made to determine the effect of UV-irradiation of herpes simplex virus (HSV) on Concanavalin A (Con-A)-mediated agglutination of 3T3 cells. There were three different phases of agglutination by Con-A of cells infected with HSV. The agglutinability began to increase from 3 or 4 hr, or 72 hr after exposure of cells to HSV. The early-appearing agglutinability was further divided into two phases, based on its sensitivity to metabolic inhibitors. These were tentatively called "Early 1 or inhibitor sensitive", "Early 2 or inhibitor insensitive" and "Late" agglutinability. "Early 1" agglutination, detected from 3 hr post infection (pi), was induced by treating cells with HSV, either active or UV-irradiated for less than 5 min and was inhibited when actinomycin D (1 microgram/ml) or cycloheximide (50 microgram/ml) was added to the cultures. "Early 2" agglutination began to increase from 4 hr pi when cells were inoculated with HSV irradiated for 7 to 20 min and was not affected by either inhibitor. HSV irradiated for 6 min failed to induce either agglutinability. "Late" agglutination, observed 72 hr pi, was detected in cultures which had been treated with HSV irradiated for 4 to 15 min. Among those, virus irradiated for 6 to 8 min was most efficient. HSV-transformed cells were also agglutinated without exception by low concentrations of Con-A.

Agglutination↗
PubMed1978

Isolation of mouse hepatitis virus from infant mice with fatal diarrhea.

An epizootic of fatal diarrhea occurred in mice which were approximately 10 days of age. The enteric lesions were similar to those reported in lethal intestinal virus of infant mice, but many diseased mice also had necrotic hepatitis. Mouse hepatitis virus antigen was demonstrated in the affected intestine and liver, and a virus that produced syncitium formation in mouse brain tumor cell culture was isolated from the intestines, livers, and brains. The virus was capable of producing intestinal and hepatic lesions similar to the naturally occurring disease after inoculation into suckling mice. Electron microscopy revealed viral particles within affected intestinal epithelial cells of the inoculated mice.

Animals↗
PubMed1978

Vertical transmission of mouse hepatitis virus infection in mice.

Transplacental infection with mouse hepatitis virus, JHM strain was studied by intravenous inoculation of pregnant dams. Inoculation on day 9 or 12 of gestation brought about the death of more than 50% of the fetuses at 4 days postinfection while inoculation on day 6 or 15 of gestation effected the death of 12% of fetuses or neonates. Inoculation of day 12 of gestation resulted in markedly higher virus titers. At 72 h postinfection in the placentas, fetal membranes and fetuses than in the maternal livers and blood. Virus-specific antigen and virus particles were noted in the placentas, visceral yolk sac and fetal livers by immunofluorescence and electron microscopy. Histopathology revealed degenerative and necrotic changes in these tissues and in the fetal bone marrow.

Animals↗
PubMed1977

Persistent infection with mouse hepatitis virus of low virulence in nude mice.

A persisting type of infection with wasting syndrome was established in congenitally athymic nude mice after intraperitoneal inoculation with a mouse hepatitis virus which was not fully pathogenic for heterozygous haired littermates. From the liver, spleen, lymph nodes, and brain of most infected nude mice, the virus was detected at high titers during aperiod from 6 to 35 days postinfection, occurrence of degenerative and necrotic lesions being correlated with virus titers in these organs. The titer of serum neutralizing antibody remained undetectable or very low in most diseases nude mice, whereas some animals resisting the infection could produce antibody at a later stage. In heterozygous haired mice, some lesions were detectable at a very early stage of infection in the spleen and liver, but they seemed to disappear with a marked elevation of the neutralizing antibody titer. Nude mice were able to resist the virus infection when they had previously received transfer of thymocytes from weanling heterozygous littermates.

Animals↗
PubMed1977

Age-dependent response of mice to a mouse hepatitis virus, MHV-S.

To a mouse hepatitis virus strain MHV-S, 4 week-old ICR mice were shown to be fully resistant irrespective of route and dose of inoculation, and fatal infection was produced only with cortisone treatment. Two-week-old mice also showed high resistance to MHV-S except for after intracerebral inoculation, and 60% of infected mice died. Mice aged 1 week or less, however, died after intracerebral, intraperitoneal, subcutaneous and intranasal inoculation, while some of them survived after peroral inoculation. Between mice aged 4 weeks and those aged 1 week or less, there was a significant difference in viral growth in the liver after intranasal inoculation, whereas almost the same degree of viral multiplication was seen in the brain of both age groups. Such age-dependent difference in susceptibility to a low-virulent mouse hepatitis virus especially after nasal inoculation is discussed in relation to natural infection in mouse breeding colonies.

Age Factors↗
PubMed1976

Difference in response to mouse hepatitis virus among susceptible mouse strains.

After intraperitoneal inoculation with a high-virulent mouse hepatitis virus (MHV) a significant difference was seen in survival time between DDD and CDF1 (BALB/c X DDD) mice, while 50% lethal doses were not significantly different. With 3 X 10(3) PFU of the virus CDF1 and DDD mice died in 45 and 120 hr, respectively, on the average. This difference of susceptibility between DDD and CDF1 mice was first demonstrable at the age of 1 week and was more pronounced at the age of 4 weeks but showed no dependence of the sex. Virus titers ran 2 to 3 log higher in the liver and blood of CDF1 than in those of DDD mice, while being only 1 log higher in the spleen. At an early stage of infection viral antigen was demonstrable by immunofluorescence in sinusoidal lining cells of the liver more prominently in VDF1 than in DDD mice. Interferon production occurring in parallel with virus growth was significantly higher in CDF1 than in DDD mice. In DDD mice, liver lesions were rather focal with some accumulation of round cells, while they were confluent with poor cellular response in CDF1 mice. Viral growth in cultured peritoneal macrophages from CDF1 mice was 1 log higher than in those from DDD mice. The results suggest that the divergence in response to MHV among susceptible mice greatly depends upon the susceptibility of macrophages and reticuloendothelial cells which constitute primary targets of the virus.

Animals↗