1887

Abstract

SUMMARY

Depending on passage history, strain WE infectious LCM virus either damages L cells more or less severely or leaves them morphologically intact. Correspondingly, the plaques which are formed on L cell monolayers are of different appearance, ranging from intensely turbid to clear. Multiplication of LCM virus in certain mouse organs profoundly affects plaque characteristics. The brain, for instance, favours lytic variants while the spleen supports the replication of virus which forms turbid plaques. This statement holds if virus taken from organs of persistently infected mice or virus passaged from mouse to mouse is analysed and is true also if the initial preparation contains virus forming predominantly either clear or turbid plaques on L cell monolayers. Selection is not rapid and not absolute. It may take months of multiplication before a final state is reached, and even then the number of characteristic plaques is usually in great excess of the rest but never reaches 100%. Cloning procedures may alter the proportions, but with our experimental conditions no plaque has ever been isolated which would retain its characteristics upon passage. Differences of plaque type morphology were not reflected in differences of pathogenic properties, and both clear and turbid variants caused persistent infection if used to infect newborn mice and led to disease with signs of neurological involvement and death if inoculated intracerebrally into adult animals.

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/content/journal/jgv/10.1099/0022-1317-30-1-113
1976-01-01
2024-05-04
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References

  1. Eagle H. 1959; Amino acid metabolism in mammalian cell cultures. Science, New York 130:432–437
    [Google Scholar]
  2. Gori G. B., Lee D. Y. 1964; A method for eradication of Mycoplasma infections in cell cultures. Proceedings of the Society for Experimental Biology and Medicine 117:918–921
    [Google Scholar]
  3. Hotchin J., Benson L. M., Seamer J. 1962; Factors affecting the induction of persistent tolerant infection of newborn mice with lymphocytic choriomeningitis. Virology 18:71–78
    [Google Scholar]
  4. Hotchin J., Kinch W., Benson L. 1971; Lytic and turbid plaque-type mutants of lymphocytic choriomeningitis virus as a cause of neurological disease or persistent infection. Infection and Immunity 4:281–286
    [Google Scholar]
  5. Lehmann-Grube F. 1967; A carrier state of lymphocytic choriomeningitis virus in Lcell cultures. Nature, London 213:770–773
    [Google Scholar]
  6. Lehmann-Grube F. 1971; Lymphocytic choriomeningitis virus. Virology Monographs vol 10 Wien and New York: Springer-Verlag;
    [Google Scholar]
  7. Lockart R. Z., Eagle H. 1959; Requirements for growth of single human cells. Science, New York 129:252–254
    [Google Scholar]
  8. Rivers T. M., scott T. F. M. 1936; Meningitis in man caused by a filterable virus. II. Identification of the etiological agent. Journal of Experimental Medicine 63:415–432
    [Google Scholar]
  9. Sanford K. K., Earle W. R., Likely G. D. 1948–9; The growth in vitro of single isolated tissue cells. Journal of the National Cancer Institute 9:229–246
    [Google Scholar]
  10. Traub E. 1937; Immunization of guinea pigs with a modified strain of lymphocytic choriomeningitis virus. Journal of Experimental Medicine 66:317–324
    [Google Scholar]
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