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Biomedical subjects

K Maeno

Publications and source records attributed to K Maeno.

At least 73 records · Page 4Linked to original sources
PubMed1983

Detection of cellular receptors for Sendai virus in mouse tissue sections.

We have established a method for detecting virus receptors in the tissue sections and have been able to clarify the distribution of cellular receptors for Sendai virus in various mouse organs, including trachea, esophagus, large intestine and cerebrum. The virus receptors were detected in ciliated cells of the trachea, as to be expected for a pneumotropic virus. The lamina propria and connective tissue of the mouse esophagus and large intestine, immediately under the epithelium, contained an abundance at virus receptors, but very few were detected in the epithelium of these organs. In mouse cerebrum, the cells lining the ventricles had a large number of virus receptors.

Animals↗
PubMed1983

Role of the nuclear matrix in the growth of herpes simplex virus type 2.

Nuclear matrix was prepared from Vero cells infected with herpes simplex virus type 2. In the early stage of infection, both 155K and 110K viral proteins were associated with the nuclear matrix, while in the late stage, 155K protein, presumably a viral capsid protein, was predominantly associated with the matrix. Electron microscopic study showed that empty capsids were bound to the filamentous networks of the nuclear matrix of the late stage. Neither viral DNA nor viral DNA polymerase activity was associated with the nuclear matrix. These results may indicate that the nuclear matrix plays some role in the growth of herpes simplex virus, especially during the morphogenesis.

Animals↗
PubMed1983

Identification of DNA polymerase(s) involved in the repair of viral and cellular DNA in herpes simplex virus type 2-infected cells.

When human embryonic fibroblasts (HEF) were infected with herpes simplex virus type 2 (HSV-2), replicative viral DNA synthesis and some repair synthesis of cellular DNA were induced at the early stage of infection, but almost all DNA synthesis at the late stage of infection was derived from repair synthesis of cellular and viral DNA (Y. Nishiyama and F. Rapp, Virology 110, 466-475, 1981). In this study, we have assessed the effects of DNA polymerase inhibitors on repair DNA synthesis HSV-2-infected HEF. Both viral and cellular DNA syntheses during the late stage of infection were extremely resistant to aphidicolin and phosphonoacetic acid but partially sensitive to high concentrations of 1-beta-D-arabinofuranosylcytosine, while replicative viral DNA synthesis during the early stage of infection was very sensitive to all of those inhibitors. The results suggest that neither HSV-induced DNA polymerase nor cellular DNA polymerase alpha was involved in the repair synthesis of viral and cellular DNA but that cellular DNA polymerase beta was.

Aphidicolin↗
PubMed1983

Mechanism of uncoating of influenza B virus in MDCK cells: action of chloroquine.

Exposure of influenza B virus-infected MDCK cells to chloroquine at the time of infection resulted in significant inhibition of infection. The appearance of input virus in the intracellular vesicles was not affected in the presence of the drug, but primary transcription of the virus genome did not occur. Chloroquine caused a rapid rise in the pH inside the lysosomes of MDCK cells, to 6.5 from the physiological pH 5.6. In contrast, exposure of infected cells incubated in acidic medium (pH 6.0) to chloroquine did not cause an increase in lysosomal pH and this low pH treatment during the chloroquine-sensitive phase was followed by virus production. Influenza B virus induced haemolysis of chick erythrocytes at low pH values (5.0 to 5.9) which was associated with cell-cell membrane fusion. It is likely that chloroquine prevents the uncoating of influenza B virus by increasing the lysosomal pH above the critical value required for inducing fusion between the virus envelope and the lysosomal membrane.

Animals↗
PubMed1983

Effect of high salt treatment on influenza B viral protein synthesis in MDCK cells.

Based on the information that high salt inhibits the initiation of cellular mRNA translation which depends on the function of the 5'-terminal structure of mRNA, we compared the effect of high salt on translation of host cellular mRNAs and influenza viral mRNAs, both of which are of 5'-terminal structure. Brief exposure of influenza B virus-infected MDCK cells to high salt medium resulted in a dose-dependent inhibition of viral polypeptide synthesis as well as of cellular polypeptide synthesis, but it had less effect on synthesis of viral polypeptides, particularly nonstructural protein (NS). Under these conditions the Na+ content of the infected cells was significantly increased. A similar salt effect on in vitro translation of viral and cellular mRNAs extracted from infected cells was also observed. There was no significant difference in sensitivity to hypertonic block of in vivo translation of influenza viral mRNAs and vesicular stomatitis virus mRNAs, the latter of which possess a virus-directed structure at the 5'-terminus.

Animals↗
PubMed1982

Comparative studies on the distribution mode of orthomyxo-virus and paramyxo-virus receptor possessing cells in mice and birds.

Many experimental studies have shown that orthomyxo- and para-myxoviruses may be pneumotropic, but not enterotropic in mammals. On the other hand, these viruses are both pneumotropic and enterotropic in avian species. We have devised a new method for detecting virus receptor possessing cells (VRPC) in tissue sections. VRPC could be detected in the cells lining the airways of both mice and birds. The mode of distribution of VRPC in mouse digestive system differed remarkedly from that in avian digestive system. VRPC were not found in the epithelium of mouse digestive systems whereas the epithelium of bird digestive system were abundant in VRPC. When the large intestines from mice or duck undergoing laparotomy and inoculated directly into intestine with influenza virus were examined, viral antigen was detected in the epithelial cell of duck colon, but not in mouse intestines. From the study utilizing the new method, it could be concluded that the distribution mode of VRPC is one of the most important factors determining the virus tissue specificity.

Animals↗
PubMed1982

Role of viral glycoproteins in haemolysis by influenza B virus.

Influenza B virus exhibited haemolytic activity at low pH, but the pH profile for its activity varied from strain to strain. The results of selective heat-inactivation of the enzyme activity of neuraminidase (NA) or elimination from virions of the enzyme-active portion of the NA molecule by trypsin digestion, suggest that proteolytically cleaved haemagglutinin, but not enzyme activity of NA, is essential for haemolysis by influenza B virus.

Animals↗
PubMed1982

Interferon production in mouse spleen cells and mouse fibroblasts (L cells) stimulated by various strains of Newcastle disease virus.

Interferon production in mouse spleen cells and mouse fibroblasts (L cells) stimulated by three strains of Newcastle disease virus (NDV), Italian, La Sota and Ulster, was investigated. Strain Italian was fully infectious and highly virulent; strain Ulster exhibited very low infectivity and very low virulence; strain La Sota was between these extremes. All of these strains of MDBK cell-grown NDV could induce interferon in mouse spleen cells, and it was concluded that proteolytic cleavage of F0 protein of NDV and, consequently, virus penetration are not necessary for interferon induction in these cells. On the other hand, NDV with uncleaved F0, which was characterized by an apparent lack of haemolytic and cell fusion activity and infectivity for tissue culture cells, had no interferon-inducing ability in L cells. The cleavage of F0 protein was paralleled by an appearance of interferon-inducing activity in L cells.

Animals↗
PubMed1982

Gamma interferon production in allogeneic stimulation: antigenicity that is sufficient to cause interferon production.

Spleen cells obtained from allogeneic cell-primed mice produced immune interferon when cocultivated with the antigenic cells. The purpose of this study was to clarify the antigenic determinants for immune interferon production in this allogeneic stimulation system. An incompatibility at the K end alone or at the D end alone of the H-2 complex was sufficient for immune interferon induction. No interferon production was observed in the combinations between strains of mice that differ for the non-H-2 regions, including the M locus. Immune interferon-producing cells (IIPC), induced by difference of the H-2K or H-2D regions, recognized the specificities controlled by the H-2K or H-2D regions, respectively; namely, there was no cross-reaction between the two regions. The difference between H-2d and H-2b did not cause interferon production in the combinations of which non-H-2 regions were very similar to each other. IIPC were not induced in the combination, but when IIPC were properly induced in B6 spleen cells, the IIPC could recognize the specificities controlled by the H-2d region (B10D2) and produced immune interferon.

Animals↗
PubMed1981

Analysis of nuclear accumulation of influenza NP antigen in von Magnus virus-infected cells.

When 1-5C-4 cells were infected with von Magnus virus derived from influenza A/RI/5+ virus by successive undiluted passages in chick embryos, virus-specific proteins were synthesized but production of infectious virus was inhibited. In these cells the synthesis of viral RNA was suppressed and the nucleoprotein (NP) antigen was found predominantly in the nucleus in contrast to standard virus-infected cells in which the antigen was distributed throughout the whole cell. The intracellular location and migration of NP were determined by isotope labeling and sucrose gradient centrifugation of subcellular fractions. In standard virus-infected cell NP polypeptide was present predominantly in the cytoplasm in the form of viral ribonucleoprotein (RNP) and intranuclear RNP was detected in reduced amounts. In contrast, in von Magnus virus-infected cells NP polypeptide was present predominantly in the nucleus in a nonassembled, soluble from and the amount of cytoplasmic RNP was considerably reduced. After short-pulse labeling NP was detected exclusively in the cytoplasm in a soluble form and after a chase a large proportion of such soluble NP was seen in the nucleus. It is suggested that a large proportion of the NP synthesized in von Magnus virus-infected cells in not assembled into cytoplasmic RNP because of the lack of available RNA and the NP migrated into the nucleus and remained there.

Antigens, Viral↗
PubMed1981

Analysis of the inhibitory effect of canavanine on the replication of influenza RI/5+ virus. II. Interaction of M protein with the plasma membrane.

When influenza A/RI/5+ virus-infected cells were incubated in medium to which 2 micrograms of canavanine (arginine analog) per ml had been added 4 hr after infection, all viral polypeptides were synthesized but the budding-like process with the appearance of extracellular virus was completely inhibited. The plasma membrane isolated from these cells contained exclusively hemagglutinin (HA), and membrane (M) protein and nucleoprotein (NP) appeared to be associated with the nucleus, in contrast to untreated cells whose plasma membrane contained abundant HA, M protein, and NP. Disruption of canavanine-treated cells by freeze-thawing generated a number of hemagglutinating membranous vesicles or fragments containing exclusively HA. By isotope labeling it was found that the M protein synthesized in the presence of canavanine, together with HA and NP, is a canavanine-substituted polypeptide. It is suggested that canavanine inhibits the formation of the mature envelope of influenza RI/5+, because of the inability of M protein to associate with the plasma membrane.

Animals↗
PubMed1981

Natural interferon-producing cells in mice.

When mouse lymphoid cells derived from untreated C57BL/6 mice were cocultivated in liquid cultures with L-cell monolayers for 3 h, overlaid with soft agar, and then further incubated for 12 h, protected foci of L cells against vesicular stomatitis virus infection were formed. Many strains of mice have been found to have the protected focus-forming cells on the L-cell monolayers. The formation of the protected foci was completely suppressed by addition of cycloheximide into soft agar. When anti-interferon (type I) antiserum was added to soft agar, there was a decrease in focus counts of about 80%. These experimental results indicated that the formation of protected foci by untreated mouse lymphoid cells was mediated for the most part by type I interferon that was produced without addition of special inducer. We have designated these focus-forming cells as natural interferon-producing cells (NIPC). NIPC belong to the glass-adherent fraction, and Thy-1 antigen, immunoglobulin, and Ia antigen could not be detected on the surface of the NIPC. NIPC were detected in congenitally athymic nude mice. These findings suggest that NIPC belong to the Ia-negative macrophages. Mouse lymphoid cells obtained from germfree mice could form the protected foci on L-cell monolayers and could produce interferon without the addition of a special inducer. NIPC are considered to be a cellular background for spontaneous interferon production.

Animals↗
PubMed1981

Mechanism of immune interferon production in vitro: interaction between immune interferon-producing cells and antigenic cells.

Various processes of in vitro immune interferon production by sensitized spleen cells stimulated with allogeneic cells were investigated. When L cells, an interferon-inducing antigen, were fixed with methyl alcohol or paraformaldehyde, the ability to induce immune interferon disappeared. In this immune interferon production system, the majority of sensitized spleen cells adhered to target cells within 1 h of cocultivation. Adherence of immune interferon-producing cells to target cells was observed only when L cell-sensitized spleen cells were cocultured with L cells or with mouse embryo cells derived from C3H mice. Fixation of antigenic cells with methyl alcohol or paraformaldehyde significantly reduced cell adherence. When L cells alone or sensitized spleen cells alone were pretreated separately with cytochalasin D, neither cell type could bind to partner cells. Specific adherence did not take place at 4 degrees C, nor in the presence of dinitrophenol or sodium azide. Continuous protein synthesis in both cells was not required for immune cell adherence. Divalent cations, Ca2+ or Mg2+, were required for this immune specific adherence to take place. However, once stable adherence was established, treatment with cytochalasin D, ethylenediaminetetraacetic acid, or sodium azide, or simple reduction of temperature, did not disrupt the binding. Interaction between immune interferon-producing cells and antigenic cells can be subdivided into two phases according to the requirement for divalent cations: (i) lymphocytes and antigenic cells interact transiently, and divalent cations are required to maintain the binding; (ii) lymphocytes and antigenic cells form a stable interaction, and deprivation of divalent cations does not disrupt the binding. Colchicine showed an inhibitory effect in the period after cell-to-cell adherence. Colchicine did not inhibit the release of interferon. On the other hand, vinblastine, another antimicrotubule agent inhibited the secretion of immune interferon. Since interferon synthesis was not stopped immediately after addition of cycloheximide, continued protein synthesis of sensitized spleen cells was not required for interferon secretion. The present study showed that adherence of immune interferon-producing cells to antigenic cells was a complex phenomenon involving a series of successive events.

Animals↗