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S Hotta

Publications and source records attributed to S Hotta.

At least 55 records · Page 3Linked to original sources
PubMed1984

Dengue type 2 virus infection in human peripheral blood monocyte cultures.

Dengue type 2 virus (D2V) infection in cultured human monocytes was studied. D2V permissiveness of the monocytes was enhanced when the cells were inoculated with D2V in the presence of either polyclonal or type-specific monoclonal anti-dengue antibody. The enhancement of D2V permissiveness mediated by the antibodies was more clearly demonstrated when the monocytes had been treated with trypsin before virus inoculation, though treatment of the cells with trypsin alone decreased D2V permissiveness. The enhancement of infection by type-specific neutralizing monoclonal antibody suggests that the D2V particles possess at least two antigenic determinants closely associated with virus infectivity. Infectious center assays revealed that the infection enhancement in the presence of the antibodies was due primarily to an increase in the number of D2V-infected cells, and that only a small proportion of the monocyte population supported D2V replication. The virus-permissive monocytes did not bear HLA-DR antigens on their cell surface. The presence of nonadherent lymphocytes in the monocyte cultures before D2V inoculation did not affect the D2V permissiveness of the monocytes. Treatment of cultured monocytes with the synthetic adjuvants N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) and its lipophilic derivative, [B30]-MDP, did not significantly affect the D2V permissiveness of the cells.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Antibody-mediated enhancement of dengue virus infection in mouse macrophage cell lines, Mk1 and Mm1.

Antibody-mediated enhancement of dengue type 2 virus (D2V) replication in murine macrophage cell lines (Mk1 and Mm1) was studied. While both Mk1 and Mm1 supported D2V replication in the absence of enhancing antibodies, virus production was enhanced when both cell lines were inoculated with D2V in the presence of dengue type 1 virus (D1V)-hyperimmune rabbit IgG, D1V-hyperimmune mouse ascitic fluids, or D2V-hyperimmune mouse ascitic fluids at subneutralizing concentrations. The enhancement ratios were greater in Mk1 than in Mm1. Type-specific neutralizing monoclonal anti-D2V antibody also mediated D2V replication enhancement in Mk1 to the same extent as mediated by three other enhancing antibodies described above. In contrast, however, the same monoclonal antibody mediated only a slight and smaller magnitude of D2V replication enhancement in Mm1 than did the other enhancing antibodies. Fluorescent antibody observations revealed that virus replication enhancement in both Mk1 and Mm1 was due primarily to an increase in the numbers of virus-infected cells. D2V infection enhancement in Mk1 by the anti-D2V mouse ascitic fluids at a dilution showing nearly 50% plaque-reduction activity was markedly suppressed by addition of complement to the inocula, whereas that by the monoclonal antibody, which has been identified as mouse IgG1, was not. Phagocytoses of tritiated thymidine-labeled bacteria by Mk1 and Mm1 were also enhanced when the bacteria had been opsonized with antibody. The phagocytosis enhancement ratios were again greater in Mk1 than in Mm1.

Animals↗
PubMed1984

Effect of interferons on dengue virus multiplication in cultured monocytes/macrophages.

The effects of interferons on dengue virus multiplication in cultured human and mouse monocytes/macrophages were studied. Interferon treatment before, but not after virus inoculation suppressed virus multiplication dose-dependently. Recombinant human leukocyte A interferon was as effective as ordinary human fibroblast interferon in suppressing dengue virus multiplication in cultured human monocytes. Human monocytes, a population of non-proliferating cell lineage, maintained their interferon-mediated antiviral state for a few days after removal of the interferons.

Animals↗
PubMed1983

Enhancement of dengue virus type 2 replication in mouse macrophage cultures by bacterial cell walls, peptidoglycans, and a polymer of peptidoglycan subunits.

The effects of bacterial cell walls, peptidoglycans, and a water-soluble polymer of peptidoglycan subunits on dengue virus type 2 replication in cultured mouse peritoneal macrophages were studied. Pretreatment of macrophage cultures with all of test cell walls isolated from seven bacterial species for 3 days significantly enhanced the virus production in the cultures. Peptidoglycans prepared from four of the above cell walls also exerted the virus production-enhancing effects in a similar manner as the walls. A water-soluble polymer of peptidoglycan subunits which was prepared by treatment of Staphylococcus epidermidis wall peptidoglycan with an interpeptide bridge-splitting enzyme (endopeptidase) also definitely enhanced the virus production in macrophage cultures, although its activity was weaker than that of the original wall and peptidoglycan. Macrophage cultures from athymic nude mice, when treated with cell walls and peptidoglycans of S. epidermidis and Lactobacillus plantarum for 3 days, also showed an increased ability to support dengue virus type 2 replication. The infectious center assay demonstrated that the virus replication enhancement by S. epidermidis cell wall and peptidoglycan was primarily due to an increase in the number of virus-infected cells. This finding did not seem to be in conflict with the observation that macrophages treated with the above cell wall or peptidoglycan phagocytized more latex particles than did untreated macrophages. The conclusions based on the above experiments are that the treatment of mouse peritoneal macrophage cultures with bacterial cell walls and their components increases the take of dengue virus type 2 by macrophages and thus raises the virus production in the macrophage cultures.

Animals↗
PubMed1982

Dengue virus multiplication in cultures of mouse peritoneal macrophages: effects of macrophage activators.

Dengue-2 virus multiplied in cultures of methylcellulose-induced peritoneal macrophages of BALB/c mice. The in vitro-cultivated macrophages from dengue-1 virus-immune mice produced larger amounts of dengue-2 virus than did those from nonimmune controls. The effect of macrophage activators was examined by using nonimmune macrophages. Enhanced virus production was demonstrated in cultures of macrophagges pretreated with phytohemagglutinin (PHA) or bacterial lipopolysaccharide (LPS). The number of virus-infected cells in the pretreated cultures was estimated to be about 0.01% or less of the total macrophages. Continuous treatment of macrophages with PHA before and after virus inoculation brought about the most marked enhancement of dengue-2 virus multiplication. On the other hand, treatment with concanavalin A or pokeweed mitogen showed little effect on the multiplication of the same virus. Treatment with carrageenan, a specific macrophage blocking agent, markedly suppressed dengue-2 virus production in both dengue-1 virus-immune macrophages and LPS-treated macrophages. The indirect fluorescent-antibody (FA) technique revealed dengue-2 viral antigen in the cytoplasm of infected macrophages, and the FA-positive macrophages were more numerous in PHA-treated cultures than in untreated controls. The results obtained are discussed in relation to a possible role of activated monocytes/macrophages in the pathogenesis of dengue hemorrhagic fever.

Animals↗
PubMed1981

Inoculation of dengue virus into nude mice.

When athymic nude (nu/nu) and heterozygous littermate (nu/+) mice were injected intraperitoneally (i.p.) with a mouse-adapted strain of dengue virus (DV), the following differences were noted in the course of infection. (i) The average survival time of nu/nu mice was longer than that of nu/+ mice, although the mortality ratios were not significantly different. (ii) DV persisted in some of the nu/nu mice for long periods of time without exhibiting any symptoms but they died after prolonged incubation periods. These aspects were not observed in the nu/+ mice. (iii) Infected nu/nu mice produced IgM antibody only transiently in the early stage of infection but they did not subsequently show regular IgG antibody production which normally occurred in nu/+ mice. (iv) Piamatral and perivascular mononuclear cell infiltration in the infected brain was more intense in nu/+ than in nu/nu mice. It is suggested from these data that the course of DV infection in mice is affected by the availability of thymus-derived lymphocytes (T-cells). Infectious virus was detected in various organs and tissues of infected mice. The hearts of nu/nu mice tended to show higher virus titres than those of nu/+ mice, whereas the virus concentrations in the brain, skeletal muscle and lymph node were the same in both groups of mice. Specific DV antigen was revealed by the fluorescent antibody (FA) technique in cells located in the infected tissues.

Animals↗
PubMed1980

Studies on structural proteins of Chikungunya Virus. I. Separation of three species of proteins and their preliminary characterization.

Chikungunya virus (CHIKV) was purified and subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis in discontinuous buffer systems. Three bands were revealed by staining with Coomassie blue; two of them (E1 and E2) were associated with the membrane, and one (C) with the core. Their molecular weights were estimated to be 56,000 (E1), 52,000 (E2), and 36,000 (C), irrespective of the concentration of acrylamide in the gels. The molar ratios of E1, E2, and C were almost equal when the sample buffer was Tris-HCl, whereas they were different when phosphate buffer was used.

Chikungunya virus↗
PubMed1980

On the mechanism of inactivation of Chikungunya virus by tannic acid.

The mechanism of the action of tannic acid (TA) Chikungunya virus (CHIKV) was investigated. Both infectivity and hemagglutination (HA) activity of CHIKV were reduced by treatment with TA in vitro. Aggregation of the TA-treated virus particles was observed by electron microscopy. The reaction was reversible, depending on the pH of the mixture. However, mere dilution of the TA-virus mixture or addition of other protein, such as bovine serum albumin, did not restore the lost infectivity. TA also suppressed the infectivity of RNA extracted from the virus and the HA activity of the viral membrane. The affinity between TA and CHIKV structural proteins (E1, E2, and C) was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis in a discontinuous buffer system and the order of affinity was found to be C greater than E1 greater than E2. Specific conditions for binding of TA to each of the virus proteins were investigated.

Cell Membrane↗
PubMed1979

Effects of tannic acid and its related compounds upon Chikungunya virus.

The present report describes not only the effects of tannic acid (TA; belonging to hydrolyzable tannins) and its related compounds upon the infectivity of Chikungunya virus (CHIKV) but also the mechanism involved in this phenomenon. Our data show that TA inactivates CHIKV in vitro. Since the inactivating effect turned out to be pH-dependent and was suppressed by bovine serum albumin, it is most probable that the virus-inactivating capacity of TA is attributable to its preferential binding to proteins of virus particles. Examination on the virus-inactivating capacities of some TA-related compounds and comparison of their structures indicated that the active site of TA and its analogues might be the phenolic hydroxyl groups in their molecules. It seems that the active groups interact with the proteins of virus particles, resulting in a reduction or loss of viral infectivity. Discussion is made on the specificity of the actions of tannins and the possibility of application thereof to chemicals which are useful to investigate the nature and properties of viral proteins.

Animals↗
PubMed1979

Antiplague antibodies against Yersinia pestis fraction-I antigen in serum from rodents either experimentally infected or captured in harbor areas of Japan, 1971--1977.

Antiplague indirect hemagglutination tests were investigated with Yersinia pestis fraction-I antigen and sera from experimentally infected rodents. The same tests with sera treated with acetone or acetone-2-mercaptoethanol were performed in parallel. Technical conditions were determined to insure the specificity and reproducibility of the reactions. Utilizing the methods studied, we carried out serological surveillance of plague with sera from wild rats (Rattus rattus and R. norvegicus) captured in the harbor areas of Japan during the period from 1971 to 1977. Four samples (all from R. norvegicus) out of 1,645 obtained in Kobe were positive. The public health significance of the data obtained is discussed.

Animals↗