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F Taguchi

Publications and source records attributed to F Taguchi.

At least 127 records · Page 7Linked to original sources
PubMed1987

Characterization of JHMV variants isolated from rat brain and cultured neural cells after wild type JHMV infection.

After intracerebral inoculation of wild type (wt) JHMV into 4 to 5 week-old Lewis rats, only variants with larger mRNA3 were selectively propagated and no wt JHMV was reisolated from the brain. Detailed analysis of a cloned virus from infected rat brain, c1-2, showed that the virus had larger mRNAs 2, 2a and 3 as compared with those of wt JHMV, while there was no such difference for other mRNAs. The E2 glycoprotein of a variant virus was also shown to be larger as compared with that of wt JHMV. Such selective replication of variants were also observed in neural cell culture after infection with wt JHMV. However, these variants isolated from the brain of infected rat (c1-2) and from infected neural cells (CNS virus) differed from each other in the amounts of mRNAs 2 and 2a as well as 65 K protein. All of these data suggest that the viruses with larger E2 glycoprotein have the growth advantage in rat brain cells, which could be responsible for acute encephalitis of rats after infection with wt JHMV.

Animals↗
PubMed1986

Characterization of a variant virus isolated from neural cell culture after infection of mouse coronavirus JHMV.

Our previous experiments showed that a variant virus with a larger envelope glycoprotein encoded by a larger mRNA3 (cl-2) multiplied predominantly in the brain of rats after wild type (wt) JHMV infection (F. Taguchi, S. Siddell, H. Wege, and V. ter Meulen, 1985, J. Virol. 54, 429-435). We could isolate similar but not identical variant virus after infection of cultured neural cells from rat brain with wt JHMV (designated CNS virus), which also had a larger mRNA3 and produced larger envelope E2 glycoprotein in infected cells. CNS virus multiplied to a higher degree in cultured astrocytes from rat than wt JHMV and cl-2. During infection with these variant viruses in neural cells, virus populations generated did not change, in contrast to consistent selection of viruses with larger mRNA3 after wt JHMV infections. CNS virus produced abundant mRNA2a as well as 65K glycoprotein while the productions of both were trace in cl-2 infected cells. The present experiments, together with our previous observation, suggest that the larger E2 glycoprotein may be of importance for the replication in rat brain cells.

Animals↗
PubMed1986

Sequence reiteration required for the efficient growth of BK virus.

Compared with wild-type BK virus DNA having tandem triplication of a 68 base pair (bp) element in its transcriptional control region, a mutant viral DNA with a single copy of the 68 bp element induced remarkably delayed virus production in human embryonic kidney (HEK) cells. We molecularly cloned the DNA of progeny viruses using plasmid vector pAT153. Nucleotide sequence analysis of representative clones revealed that all of the altered viral DNAs examined duplicated various segments extending over origin-distal portions of the 68 bp element and their flanking regions. After transfection of HEK cells, most of these rearranged viral DNAs induced viral growth slightly slower than, or at the same rate as, the wild-type viral DNA. Comparison of the structures of these rearranged viral DNAs suggests that reiteration of a 13 bp sequence, which is located in an origin-distal portion of the 68 bp element, is required for the efficient replication of BK virus.

BK Virus↗
PubMed1985

Difference in sensitivity to interferon among mouse hepatitis viruses with high and low virulence for mice.

Mouse hepatitis viruses (MHV) of different virulence for mice were studied with respect to interferon (IFN) sensitivity. The growth of low-virulent MHV-S and intermediately virulent MHV-JHM was significantly suppressed in IFN-treated L cells compared with untreated cells. However, a comparable suppression of the growth of highly virulent MHV-2 was not observed in IFN-treated cells. This differential effect of IFN treatment could also be demonstrated at the level of viral mRNA and viral proteins. In cells infected with MHV-S or MHV-JHM the amount of viral mRNAs was remarkably reduced by IFN treatment. Also the levels of the major intracellular viral proteins, in particular the E1 protein, were affected by IFN treatment. Similar effects could not be demonstrated in MHV-2-infected cells. These results suggest that during MHV-S or MHV-JHM infection IFN treatment suppresses virus replication at several stages. The significance of these results is discussed in terms of the pathogenecity of these viruses.

Animals↗
PubMed1985

Characterization of a variant virus selected in rat brains after infection by coronavirus mouse hepatitis virus JHM.

The intracerebral inoculation of Lewis rats with the murine coronavirus MHV-JHM leads in the majority of animals to acute encephalitis and death within 14 days. Viral RNAs isolated from the brains of animals 5 to 7 days after infection were compared by Northern blot analysis with the RNAs produced during the lytic infection of Sac(-) or DBT cells with wild-type MHV-JHM (wt virus). Reproducibly, the subgenomic mRNAs 2 and 3 but no other viral RNAs were significantly larger in the brain-derived material. All viruses isolated from infected brain material displayed and maintained this altered mRNA profile when cultivated in Sac(-) or DBT cells. A virus isolated from the infected brain material, MHV-JHM clone 2 (cl-2 virus), has been further characterized. This isolate grew in tissue culture and induced cytopathic effects comparable to those induced by wt virus. However, the mRNAs 2 and 3 produced in cl-2 virus-infected cells had molecular weights ca. 150,000 larger than those produced in cells infected with wt virus. There was no detectable difference in genome-sized RNA (mRNA 1) or subgenomic mRNAs 4, 5, 6, and 7 as determined by electrophoresis in agarose gels. T1-resistant oligonucleotide analysis of genomic RNA revealed one additional and one missing oligonucleotide in the fingerprint of cl-2 virus compared with wt virus. The oligonucleotide fingerprints of intracellular mRNA 3 were identical for both viruses. Pulse-labeling with [35S]methionine in the presence of tunicamycin showed that the primary translation product of mRNA 3, the E2 apoprotein, was ca. 15,000 larger in molecular weight in cl-2 virus-infected cells. These data show that viruses with larger mRNAs 2 and 3 (the latter encoding an altered E2 glycoprotein) are selected for multiplication in rat brains. Mechanisms for the generation of such variants and the possible nature of their selective advantage are considered.

Animals↗
PubMed1985

Presence of interferon and antibodies to BK virus in amniotic fluid of normal pregnant women.

Paired samples of maternal sera, umbilical cord sera and amniotic fluids were tested for antibodies to BK virus (BKV) and for interferon content. It was found that two out of 14 pregnant women were antibody negative, the latter were estimated to be susceptible to BKV primary infection. In contrast, there was no foetal case among those which were at risk of foetal infection with BKV as judged from the presence of BKV antibody in maternal sera and interferon in the placentas. It might be hypothesized that BKV may be transmitted to the foetus only in the case of BKV primary infection of antibody-negative pregnant women with undetectable amount of interferon (IFN) in the placenta.

Amniotic Fluid↗
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↗
PubMed1984

Defective interfering particles of mouse hepatitis virus.

After six to eight serial undiluted passages of mouse hepatitis virus (JHM strain) in DBT cell culture, a decrease in the yield of infectious virus occurred, and with further passages fluctuating yields of infectious virus were observed. The serially passaged virus interfered with the multiplication of the standard JHM virus, but not with vesicular stomatitis virus. After sucrose equilibrium centrifugation of high passage virus, a single peak contained both infectious virus and interfering activity. This virus population resembled the original JHM virus in its structural proteins, but it contained an increased proportion of a protein with a molecular weight of 65 X 10(3). Genomic RNA from standard JHM virus contained a single species of RNA with a molecular weight of 5.4 X 10(6). After five undiluted passages, however, the virion population contained two RNA species with molecular weights of 5.4 X 10(6) and 5.2 X 10(6). RNase T1 resistant oligonucleotide finger-printing of these RNAs showed that the lower molecular weight RNA had lost several oligonucleotide spots that were present in the genomic RNA of the standard JHM virus. After several serial diluted passages of passage 10 virus, a single virus population was obtained which again had only standard virus RNA with a molecular weight of 5.4 X 10(6) and lacked interfering activity. These results indicated that defective interfering particles were generated by serial undiluted passages of JHM virus.

Animals↗
PubMed1983

Effects of a heat-labile factor(s) in normal serum on the interferon-inducing activity of Newcastle disease virus (NDV). Brief report.

The effect of fresh serum on the interferon-inducing activity of Newcastle disease virus (NDV) was studied. Infectivity in fertile eggs, hemolytic activity in human erythrocytes and interferon-inducing activity in mouse L cells and mouse spleen cells were all reduced by treatment of NDV with fresh serum from humans or guinea pigs, while hemagglutinating (HA) activity remained unchanged. The interferon-inducing ability of UV-inactivated NDV was also similarly reduced after treatment with serum. The serum effects were decreased by heating at 56 degrees C for 30 minutes or the addition of 10 mM EDTA. These results suggest that a heat-labile serum factor(s) such as complement or certain enzyme(s) reduced the hemolytic activity and consequently the penetrating activity of NDV, and that interferon-inducing activity was related to the hemolytic but not to the HA activity of NDV particles. Thus, it was concluded that the hemolytic activity of NDV was necessary for interferon induction in both mouse L cells and mouse spleen cells.

Animals↗
PubMed1983

Growth of Tyzzer's organism in primary monolayer cultures of adult mouse hepatocytes.

The Tyzzer's disease organism was grown in primary monolayer cultures of adult mouse hepatocytes prepared by collagenase perfusion. The organisms produced a plaque-like cytopathic effect involving almost the whole culture around 72 h post-infection when the bacterial growth reached a maximum. The organisms showed specific immunofluorescence, and electron microscopy revealed that intracellular organisms had peritrichous flagella and underwent cell division. After intravenous inoculation of the infected cell culture into mice, necrotic hepatitis was produced and the organisms, recovered from the liver lesion, could be propagated in primary culture of mouse hepatocytes.

Animals↗
PubMed1983

Plaque formation by Tyzzer's organism in primary monolayer culture of mouse hepatocytes.

Tyzzer's disease organism propagated on primary monolayer cultures of mouse hepatocytes and produced definite plaques. In phase contrast microscopy, the organisms were motile in the plaques. Plaque formation was inhibited by antiserum. After serial plaque cloning the organisms still had virulence in mice. To establish a standard plaquing procedure, factors affecting plaque formation were studied. The critical factors in plaque formation were the culture period of host cells before inoculation, medium for suspending the organisms, and temperature and time of infection. A 24 to 36 hr-preculture of host cells and trypticase soy broth (BBL) as the suspending medium gave the best results. The optimal conditions for infection were 37 C for 90 min. The plaquing efficiency was higher when a larger volume of inoculum was applied to host cell monolayers, suggesting that the organism played an active role in the initial stage of infection.

Animals↗