Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
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Volume 29, Issue 3
Displaying 1-18 of 18 articles from this issue
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Contents
  • Establishment of HeLa Cells Persistently Infected with Rubella Virus and their Several Properties
    MASARU SUGANUMA
    1983 Volume 29 Issue 3 Pages 330-343
    Published: September 10, 1983
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.29.330
    JOURNAL FREE ACCESS
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    It was easy to establish HeLa cells persistently infected with rubella virus (M 33 strain) without any CPE (HeLa-M 33 cells). Morphological appearances of HeLa-M 33 cells were normal, but the growth of these cells was relatively slower than that of normal ones. HeLa-M 33 cell cultures contained infectious viruses of 5-20 × 104 PFU/107 cells in their cytoplasm, 2-8 × 104 PFU/ml in their culture fluids and infective centers of 20-50%. HeLa-M 33 cell cultures interfered with the growth of measles virus, vesicular stomatitis virus (VSV) and vaccinia virus at the levels of 55% to more than 90%. This phenomenon suggests that the interference in HeLa-M 33 cell cultures was mediated by interferon, but interferon activities in their culture fluids were not detected by the ordinary VSV plaque reduction methods. Interfering activities of HeLa-M33 cells were transferred to normal HeLa cells in the mixed cultures of both cells at the rate of 1: 2-6 (HeLa-M33 cells : HeLa cells). Infectivecenter-forming levels were calculated. These levels were thought to indicate those of transferences of interfering activities. Infective-center-forming levels decreased in accordance with the time after mixing of HeLa-M33 cells with normal HeLa ones and the mixing rates of the former cells. These levels increased with treatments of the cell mixtures by actinomycin D at concentrations of 0.1 to 1.0 μg/ml. Therefore, the transferences of interfering activities of HeLa-M33 cells to normal HeLa cells were inhibited by actinomycin D. These data strongly indicate interferon-mediated interferences in HeLa-M33 cell cultures, but not intrinsic interferences by Marcus. The persistent states of HeLa-M33 cell cultures changed little with the addition of human β-interferons or anti-rubella sera to their culture fluids. It is concluded that the persistences of HeLa-M33 cell cultures have been maintained by the existences of rubella virus genomes in the persistent cells (see the following papers) and are regulated by low levels of interferons in the culture fluids.
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  • Properties of the Viruses released from HeLa Cells Persistently Infected with Rubella Virus
    MASARU SUGANUMA
    1983 Volume 29 Issue 3 Pages 344-356
    Published: September 10, 1983
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.29.344
    JOURNAL FREE ACCESS
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    Properties of the viruses (HM virus) released from HeLa cells persistently infected with rubella virus (M33 strain) were investigated for the persistency of viruses by biological methods. (1) HM virus a) HM viruses formed smaller plaques on SIRC-5E cells than the M33 wild-type strain. b) HM viruses could not replicate in the cultivated cells at the nonpermissive temperature of 39. 5°C. c) HM viruses were more labile than the M33 strain with incubation at 45°C. (2) Eight clones were isolated from HM viruses on SIRC-5E cell monolayers by plaquecloning methods. a) None of the eight clones could grow in SIRC-5E cells, BHK 7M/ 1 cells or HeLa cells with incubations at 39.5°C. (temperature sensitivity = 9.1 × 10-4 to <7.1 × 10-5) b) Five of the eight clones indicated the same thermal stability, while one was more stable and two more labile than the wild-type W4/ 1 clone. c) Viruses of all clones that were grown in BHK 7M/ 1 cells at 39. 5°C did not carry hemagglutinating activity [HA (-)]. d) Viral RNA was synthesized in the cultivated cells infected with each of the clones at 39. 5°C [RNA (-))]. e) The temperature-sensitive site of each clone was characterized as existences at 12 to 16 hours of the late function after infection. (3) HeLa cell cultures infected with W4/ 1 clone viruses possessed the persistencies at earlier times (days) after infections during the period of lower viral growth (after one to two passages). (4) The Vero-M33 cell culture that was one of the Vero cell cultures persistently infected with M33 rubella virus had synthesized infectious virions with 39. 5°C cultivations and therefore, did not express temperature sensitivity at the nonpermissive temperature. It can be concluded that the virus released from HeLa-M33 cells (HM virus) was a temperature-sensitive mutant that carried a defect (or defects) in the late functioning genomes of viral growth. But the acquisition of temperature sensitivity was not an indispensable condition, because Vero-M33 cell cultures, which were among the persistently infected cultures, were not temperature-sensitive. At the present time, the mechanism by which the temperature sensitive mutants are selected remains to be clarified.
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  • Clinical Study of Idiopathic Mitral Valve Prolapse Syndrome
    KEN MURAYAMA
    1983 Volume 29 Issue 3 Pages 357-370
    Published: September 10, 1983
    Released on J-STAGE: November 21, 2014
    DOIhttps://doi.org/10.14789/pjmj.29.357
    JOURNAL FREE ACCESS
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    Echocardiographic and clinical findings were studied in 141 patients with idiopathic mitral valve prolapse syndrome. The location and severity of mitral valve prolapse could be classified by two-dimentional echocardiography in 125 patients. Prolapse of the anterior mitral leaflet was 4.5 times more common than that of the posterior leaflet, and prolapse of midportion to posteromedial commissure site formed a large majority. Echocardiographic findings of mitral valve prolapse did not correlate with clinical severity. Ausclutatory abnormalities were noted in 77 patients; 24 had click and/or late-systolic murmur, and 53 had holosystolic murmur. The heart size was almost normal except in 15 patients, but the APDT/TDT was 36.5% on the average, suggesting the thoracic skeletal abnormalities. Electrocardiography revealed ST-T changes in 52 cases, especially 39 patients with ST-T changes in II, III and aVF. Histological findings of mitral leaflets in this study did not show myxomatous degeneration. As for clinical symptoms and signs, 10 patients had NYHA II°, and six had NYHA III°. Congestive heart failure was found in a third of the patients over 40 years of age. Infective endocarditis was observed in four. In this study, I presume that the idiopathic mitral valve prolapse syndrome is related to thoracic abnormalities, because the same mesenchymal heredity that determines the skeletal habitus also affects the mitral valve, and this abnormality influences the cardiac position, rotation and contraction as well.
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