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Biomedical subjects

F Taguchi

Publications and source records attributed to F Taguchi.

At least 145 records · Page 8Linked to original sources
PubMed1983

Characterization of small plaque mutants of mouse hepatitis virus, JHM strain.

Two small plaque mutants designated as 1a and 2c were isolated from DBT cells persistently infected with the JHM strain of mouse hepatitis virus. Unlike the wild type JHM, these two mutant viruses grew more slowly with no prominent cell fusion. The buoyant densities of the mutants were slightly lower and 2c was revealed to have fewer peplomers than JHM by electron microscopy. The purified JHM contained five polypeptides with molecular weights (M.W.) of 260,000, 105,000 (GP105), 65,000, 60,000 (P60), and 23,000 (GP23). In addition to two polypeptides, P60 and GP23, which were common to JHM and the mutants, 1a was found to contain three other specific polypeptides with M.W. of 180,000 (GP180), 110,000, and 95,000 (GP95), while 2c had GP180, GP105, GP95, and one with a M.W. of 175,000. All of these polypeptides were shown to be glycosylated except for P60. After bromelain treatment, all these viruses lost the peplomers and contained P60 and another new 18,000 dalton polypeptide.

Animals↗
PubMed1983

Replication of mouse hepatitis viruses with high and low virulence in cultured hepatocytes.

Ten strains of mouse hepatitis virus with different levels of virulence and hepatotropism were examined for the ability to replicate in cultured mouse hepatocytes. All of these viruses multiplied well in hepatocytes, attaining a maximum of 10(5) to 10(7) PFU per 0.2 ml, with cytopathic effects characterized by the formation of polykaryocytes. However, in nonparenchymal adherent cells of the liver (liver macrophages), highly virulent mouse hepatitis virus type 2 multiplied to a titer 1,000 times higher than that of mouse hepatitis virus S with a low virulence. These results suggest that the virulence of mouse hepatitis virus in infected mice is determined by its potential for replication not in hepatocytes, but in macrophages, including Kupffer cells in the liver.

Animals↗
PubMed1983

Induction and enhancement of endocytosis in HeLa cells by use of liposomes and Sendai virus envelopes.

Phosphatidylserine liposomes were interacted with cultured HeLa cells to investigate the ingestion of the liposomes into the cells. It was shown by electron microscopy that great enhancement in entrappment of the liposomes into the cells was induced by adding reassembled Sendai virus envelopes. In the presence of the reassembled virus envelopes the ratio of liposome-endocytic cells was over the half of the examined cells in thin sections. To differentiate the entrapped vesicles from cell-originated intracytoplasmic vesicles, uninfective virus particle was introduced as a mark and it was shown that the uninfective virus particle was entrapped with the liposomes into the cells. These results may suggest that reconstituted Sendai virus envelopes could change HeLa cell membranes to endocytic ones.

Animals↗
PubMed1982

Prevalence rate and age of acquisition of antibodies against JC virus and BK virus in human sera.

A total of 480 serum samples from donors including 384 children up to 10 years of age were examined by the hemagglutination-inhibition (HI) test for the rates of prevalence and age of acquisition of HI antibodies against JC virus and BK virus. Among 136 serum samples from various age groups, there were five (4%) with no detectable antibodies against BK or JC virus, 75 (55%) with antibodies against both viruses, 41 (30.1%) with antibodies against only BK virus and 26 (19%) with antibodies against only JC virus. The prevalence of antibodies against JC and BK viruses was 70.5% and 80.8%, respectively, and the mean HI titers (4 x 2n,n greater than or equal to 1) were 4.90 and 4.30. About 50% of the children had acquired antibodies against BK virus by 3 years of age and against JC virus by 6 years of age. These results indicate that dual latent infections with both viruses are common, although independent infections with either virus are predominant in the human population.

Adolescent↗
PubMed1982

Heterologous response of antiserum-treated cell clones from a persistently infected DBT cell line to mouse hepatitis virus.

From DBT cells persistently infected with mouse hepatitis virus JHM strain (JHM-CC), a cell line producing neither infectious virus nor intracellular viral antigen was obtained after two passages in the presence of antiserum. In addition, 11 cell clones were manipulated from JHM-CC and found to be also free from the virus. These newly obtained cell line and 4 of 11 cell clones were shown to be resistant to JHM and the virus recovered from JHM-CC (JHM-CCV), while the other 7 cell clones were susceptible to both JHM and JHM-CCV as well as vesicular stomatitis virus. The susceptibility of all the cell clones and the newly obtained cell line to JHM and JHM-CCV became higher with passages. The observations were discussed in relation to the viral persistency in JHM-CC.

Animals↗
PubMed1981

Correlation between growth potential of mouse hepatitis viruses in macrophages and their virulence for mice.

Correlation between the virulence of mouse hepatitis virus (MHV) for mice and the growth potential of the virus in peritoneal adherent cells was observed for highly virulent MHV-2 and avirulent MHV-1, JHM, and MHV-S strains. However, this phenomenon was not observed in strain MHV-3, which multiplied to almost the same degree in peritoneal adherent cells from susceptible and resistant mouse strains.

Animals↗
PubMed1981

Selective antiviral activity of the antibiotic 2'-amino-2'-deoxyribofuranosyl adenine.

The effect of new anti-mycoplasmal antibiotic, 2'-amino-2-deoxy-9-beta-D-ribofuranosyl adenine (2-AA) on virus multiplication was investigated. The 2-AA inhibited only the multiplication of measles virus among the viruses tested; i.e., herpes simplex virus, BK virus, vesicular stomatitis virus, measles virus and Echo virus. At a concentration of 5 micrograms/ml of 2-AA, the inhibition of measles virus replication was complete, i.e., no infectious virus nor viral antigen detected. In contrast, 9-beta-D-arabinofuranosyl adenine (50 micrograms/ml) was active to herpes simplex virus and BK virus, and was inactive to measles virus, vesicular stomatitis virus and Echo virus. Results described herein may suggest that 2-AA affects the late function (perhaps the translation step) of the replication of measles virus.

Anti-Bacterial Agents↗
PubMed1980

Resistance to highly virulent mouse hepatitis virus acquired by mice after low-virulence infection: enhanced antiviral activity of macrophages.

As early as 1 to 2 days after intranasal inoculation with a mouse hepatitis virus of low virulence, MHV-S, susceptible DDD mice became fully resistant to a normally lethal challenge with a highly virulent MHV-2. The resistance of MHV-S-pretreated mice was correlated with significantly decreased MHV-2 multiplication in the liver, spleen, and brain. Infection with MHV-S did not induce a high level of interferon in DDD mice, and no neutralizing antibody against MHV-2 was detected in the sera of mice until day 6 of MHV-S infection. The multiplication of MHV-2 was suppressed in peritoneal cells (PC) in vivo and peritoneal adherent cells (PAC) in vitro of MHV-S-pretreated mice was compared with those of normal mice. This suppression of virus multiplication was demonstrated in PAC collected during days 1 to 3 of infection but not in PAC collected from day 5 on. PC from MHV-S-pretreated mice were also suppressive to MHV-2 growth in DK cells as compared with PC from normal mice. By treatment of MHV-S-pretreated mice with silica, suppression of virus growth in the liver was partially diminished. These findings suggest that increased suppression of MHV-2 growth in PAC (mostly macrophages) of MHV-S-pretreated mice is responsible for resistance.

Animals↗
PubMed1979

Asymptomatic infection of mouse hepatitis virus in the rat. Brief report.

After intranasal inoculation of suckling rats mouse hepatitis virus multiplied mostly in the nasal epithelium; though there were no symptoms, antibodies were produced. Antibodies were also demonstrated in adult rats. These findings suggest that the rat may be a natural host for the virus.

Animals↗