MICROBIOLOGY and IMMUNOLOGY
Online ISSN : 1348-0421
Print ISSN : 0385-5600
ISSN-L : 0385-5600
Volume 22, Issue 7
Displaying 1-7 of 7 articles from this issue
  • Takatoshi NAGATE, Matsuhisa INOUE, Kunio INOUE, Susumu MITSUHASHI
    1978 Volume 22 Issue 7 Pages 367-375
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
    Dihydropteroate synthetase (DHPS) is specified by a substrain of Escherichia coli K12, ML1410. This enzyme activity is inhibited by sulfanilamides (Sa) and is known to be heat-stable, i.e., an Sa-sensitive normal enzyme. Another DHPS activity specified by E. coli ML1410 carrying drug resistance plasmids is Saresistant but heat-sensitive, i.e., an Sa-resistant enzyme. Most plasmids encoding single Sa or double (Sa. Tc or Sa. Sm) (Tc, tetracycline; Sm, streptomycin) resistance mediate the formation of this type of DHPS. Therefore, E.coli carrying these plasmids becomes diploid for DHPS, i.e., an Sa-resistant and an Sa-sensitive normal enzyme. The biochemical mechanism of Sa resistance mediated by plasmids encoding triple (Cm.Sm.Sa; Tc.Sm.Sa) and quadruple (Cm.Tc.Sm.Sa) resistance is not due to the formation of an altered DHPS but probably due to the decrease in permeation of the drug into the cell. The evolutionary process of the formation of Sa-resistance determinants on plasmids is discussed based on the presence of two types of Sa resistance mechanism.
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  • Norio HIRANO, Shigeo HINO, Kosaku FUJIWARA
    1978 Volume 22 Issue 7 Pages 377-390
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
    Some properties of a strain of mouse hepatitis virus, MHV-2, grown on DBT cells were determined using a plaque assay on the cells. Viral growth was not inhibited by the presence of actinomycin D or 5-iodo-2-deoxyuridine. MHV-2 was completely inactivated by ether, chloroform, sodium deoxycholate or beta-propiolactone, but showed a moderate resistance to trypsin. Heating at 56 C for 30 min did not completely abolish the virus infectivity. The virus was stable after heating at 50 C for 15 min in 1m-MgCl2 or 1m-MgSO4 as well as at 37 C for 60 min at pH 3.0 to 9.0. Infectivity was decreased to 1/100 and 1/400 after storing at 4 C for 30 days and 37 C for 24 hr, respectively. The virus passed through a 200-nm but not a 50-nm Sartorius membrane filter. The buoyant density of MHV-2 was 1.183 g/cm3 in sucrose gradient, and the fraction contained coronavirus-like particles measuring 70 to 130 nm in diameter. Survival rate was 10% after exposure to ultraviolet at 150 ergs/mm2. Freezing and thawing or sonication at 20 kc for 3 min did not affect the virus titer. No hemagglutinin was demonstrable with red blood cells of the chicken, Japanese quail, mouse, rat, hamster, guinea pig, sheep, bovine or human.
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  • Macrophage Migration Inhibition Test1
    Toshiki INADA, Hisao UETAKE
    1978 Volume 22 Issue 7 Pages 391-401
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
    Cell-mediated immunity (CMI) to mouse adenovirus (M-Ad) infection was studied by macrophage migration inhibition test (MMI) as one of in vitro correlates of CMI.
    Both direct and indirect tests showed clearly that migration of packed peritoneal exudate cells (PEC) (immune mouse or nonimmune guinea pig) was remarkably inhibited; MIF was produced by interactions between immune PEC and infected cell extracts and between immune spleen cells and infected cells or their extracts. The antigen (s) responsible for the above MMI was demonstrated in 6- to 12-hour infected ME cells, and FUdR-treated infected ME cells. Since under these conditions there is S antigen (s) synthesis but not capsid antigen synthesis, the antigen (s) concerned must be an S antigen (s). T cells sensitized to infected cells were shown to be required to induce MMI.
    The MMI is specific for M-Ad, since no cross MMI was observed between M-Ad and SV40 systems. Time course study of the development of CMI to M-Ad by MMI tests showed that CMI became detectable 4 days post-infection (pi), reached its peak level about 10 days pi, and faded away rapidly in about 10 days thereafter.
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  • IX. Variance in Complement Requirement among IgG and IgM from Early and Late Sera under Different Sensitization Conditions
    Kamesaburo YOSHINO, Noriko ISONO
    1978 Volume 22 Issue 7 Pages 403-414
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
    Early and late sera of rabbits immunized with herpes simplex virus were fractionated into IgG and IgM, and the minimal concentration of complement (C) required for full enhancement of neutralizing activity was determined for each by the plaque reduction method. In tests employing simultaneous mixing of virus, antibody and C, C-requiring neutralizing (CRN) antibody in IgM required 2-8 times more C than that in IgG. When virus-antibody mixtures were incubated at 0 C overnight before addition of C, a marked enhancement of CRN endpoint especially of late IgG and IgM was exhibited, in contrast to materially unchanged titers of the ordinary neutralizing antibody. This result suggested an abundance of slow-reacting CRN-virus complexes. The CRN antibody so detected required about 4 times more C than that detectable by the usual test in the case of late IgG and IgM. When virus sensitized with late IgG at 0 C overnight was further incubated at 37 C for 1 hr, the C requirement changed but slightly without showing any more increase of the endpoint, whereas sensitization at 0 C for 2 to 3 days further increased the CRN antibody endpoint but the C requirement was equal to that after 1 day's sensitization at 0 C. Based on these and earlier findings, a hypothesis is proposed that binding of a single antibody molecule with virus may cause a series of changes of the virus particle or part of those changes depending on the nature of antibody and on the sensitization condition, and C added to such complexes at an appropriate stage of the changes can accelerate the procession of the changes leading eventually to inactivation.
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  • Aiko TADA, Kamesaburo YOSHINO
    1978 Volume 22 Issue 7 Pages 415-426
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
    A microplate serum neutralization test for estimation of complement-requiring neutralizing (CRN) antibody was established as the first step for simplification of typing of herpes simplex virus (HSV). When guinea pigs were immunized with type 2 HSV, the late sera could mostly differentiate the types of HSV better than hyperimmune rabbit sera, the CRN titer against the heterologous type 1 HSV being much lower than the homologous titer. Sera of guinea pigs immunized with type 1 HSV showed about the same level of cross reaction against type 2 HSV as did rabbit antisera. Guinea pig sera having minimal levels of cross reaction were selected, and their high dilution (1 : 160) and complement were added to serial 10-fold dilutions of virus in the microplate titration of virus infectivity. Selective reduction of virus titer by either antiserum could determine the type of HSV. No equivocal intermediate case was found among a number of stock strains including many fresh isolates. The typing result coincided with that determined by a modification of Yang et al's method based on virus titers obtained with Vero and primary chick embryo cells. The typing based on plaguing in chick embryo cells sometimes failed to identify type 1 HSV.
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  • Tateo IWAKU
    1978 Volume 22 Issue 7 Pages 427-436
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
    Electrocardiographic changes and cell-mediated immunity in germ-free mice sensitized with formalin-killed group A streptococci were studied. In germ-free mice sensitized with formalin-killed group A streptococci, a marked prolongation of the PQ interval in electrocardiogram (ECG) was observed at the fourth and seventh week of the sensitization, and significant increases of [3H] thymidine uptake of lymphoid cells by stimulation with phytohaemagglutinin (PHA-M), pokeweed mitogen (PWM) and streptococcal mucopeptide were ob-served at the second, third and sixth week of the sensitization. Moreover, in macrophage migration inhibition test, migration inhibition of macrophages by streptococcal mucopeptide antigen was seen at the third, fifth and sixth week, and by heat-killed streptococci at the first and third week of the sensitization. In contrast, no electrocardiographic change and slight increases of [3H] thymidine uptake of lymphoid cells by stimulation with mitogens or streptococcal antigens were observed in non-sensitized germ-free mice and also in germ-free mice sensitized with formalin-killed staphylococci or treated with physiological saline.
    In germ-free mice sensitized with streptococci, their body weight did not increase and cyanosis on lips or extremities of the mice was noted throughout the experimental period.
    Light microscopic histological examination could not reveal any changes that suggest damage of the myocardial tissue.
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  • V.K. BATISH, D.R. GHODEKAR, B. RANGANATHAN
    1978 Volume 22 Issue 7 Pages 437-441
    Published: July 20, 1978
    Released on J-STAGE: October 15, 2009
    JOURNAL FREE ACCESS
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