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Langat virus encephalitis in mice II. The effect of irradiation

Published online by Cambridge University Press:  15 May 2009

H. E. Webb ,
D. G. D. Wight ,
G. Wiernik ,
G. S. Platt  and
C. E. G. Smith
H. E. Webb
Affiliation:
St Thomas's Hospital, London, S.E. 1
D. G. D. Wight
Affiliation:
St Thomas's Hospital, London, S.E. 1
G. Wiernik
Affiliation:
St Thomas's Hospital, London, S.E. 1
G. S. Platt
Affiliation:
Microbiological Research Establishment, Porton, Salisbury, Wilts
C. E. G. Smith
Affiliation:
Microbiological Research Establishment, Porton, Salisbury, Wilts
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Summary

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1. Irradiation in a whole body dose of 200 rads or more increased the sensitivity of mice to intraperitoneal infection with Langat virus so that the LD 50 was increased to about the intracerebral LD 50.

2. In mice given 500 rads before infection: (a) viraemia was prolonged by about 5 days; (b) the IgM response was depressed; (c) the IgG response was delayed by about 3 days and depressed in titre; (d) virus concentration in the brain rose continuously until death on about the tenth day while in the controls it reached a peak on the fifth day then subsided; (e) histological changes in the CNS were delayed and minimal even at death; (f) irradiated mice died with little evidence of paralysis while the controls died with severe paralysis.

3. In irradiated mice, protection was observed when antibody was administered on the third day following infection. Antibody given on the 3 days after infection to control mice aggravated the disease.

4. The results in this and the preceding paper are discussed in relation to the pathogenesis of encephalitis. It is concluded that neuronal damage is caused both by virus multiplication in neurones and by damage superimposed by inflammatory changes with associated oedema and hypoxia. The inflammatory changes appear to be due to an allergic reaction to virus-antibody complexes formed in the circulation and in the central nervous system.

We are grateful to Miss S. J. Illavia, B.Sc., and Miss G. E. Fairbairn for their skilled technical assistance; to the Department of Radiotherapy at St Thomas's Hospital for providing time and staff to help with the irradiation experiments; and to Mr S. Peto of the Microbiological Research Establishment for statistical advice.

This work was made possible by a generous grant from the Wellcome Trust and the Endowment Funds of St Thomas's Hospital.

Type
Original Articles
Information
Journal of Hygiene , Volume 66 , Issue 3 , September 1968 , pp. 355 - 364
Copyright
Copyright © Cambridge University Press 1968

References

Ashe, W. K. & Notkins, A. L. (1966). Neutralization of an infectious herpes simplex virus-antibody complex by anti-γ-globulin. Proc. natn Acad. Sci. U.S.A. 56, 447–51.CrossRefGoogle ScholarPubMed
Chang, S. S. (1965). Stress-induced suppression of interferon production in virus-infected mice. Nature, Lond. 205, 623–4.CrossRefGoogle Scholar
Imam, I. Z. E. & Hammon, W. Mcd. (1957). Susceptibility of hamsters to peripherally inoculated Japanese B and St Louis viruses following cortisone, X-ray and trauma. Proc. Soc. exp. Biol. Med. 95, 6–11.CrossRefGoogle Scholar
Julien, P. & De Maeyer, E. (1966). Interferon synthesis in X-irradiated animals: I Depression of circulating interferon in C3H mice after total body irradiation. Int. J. Radiat. Biol. 11, 567–76.Google Scholar
Kundin, W. D. (1966). Pathogenesis of Venezuelan equine encephalomyelitis virus. II. Infection in young adult mice. J. Immun. 96, 49–58.CrossRefGoogle ScholarPubMed
Litt, M. (1964). Studies in experimental eosinophilia. VII. Eosinophils in lymph nodes during the first 24 hours following primary antigen stimulation. J. Immun. 93, 807–13.CrossRefGoogle Scholar
Litt, M. (1967). Primary antibody in guinea-pig lymph node 10 minutes after introduction of chicken red blood cells (C.RBC). Fedn Proc. Fedn Am. Socs exp. Biol. 26, Abstr. 2767, 752.Google Scholar
Malkova, D. (1962). The effect of X-irradiation on the spread of tick-borne encephalitis virus through the regional lymphatic system. Acta Virol., Prague 6, 475–8.Google Scholar
Malkova, D. & Frankova, V. (1959). The lymphatic system in the development of experimental tick-borne encephalitis in mice. Acta Virol., Prague 3, 210–3.Google ScholarPubMed
Najjar, V. A., Robinson, J. P., Lawton, A. R. & Fidalgo, B. P. (1967). The physiological role of the lymphoid system, I. An extension of the mechanism of antibody-antigen reaction. Bull. Johns Hopkins Hosp. 120, 63–77.Google Scholar
Notkins, A. L., Mahar, S., Scheele, C. & Goffman, J. (1966). Infectious virus-antibody complex in the blood of chronically infected mice. J. exp. Med. 124, 81–97.CrossRefGoogle ScholarPubMed
Quilligan, J. J., Boche, R. D., Carruthers, E. J., Axtell, S. L. & Trivedi, J. C. (1963). Continuous cobalt60 irradiation and immunity to influenza virus. J. Immun. 90, 506–11.CrossRefGoogle ScholarPubMed
Schneck, L. & Berkovitch, S. (1965). X-irradiation and Coxsackie B virus infection in neonatal rats. Proc. Soc. exp. Biol. Med. 118, 658–61.CrossRefGoogle Scholar
Taliaferro, W. H. (1957). Modification of immune response by X-irradiation and cortisone. Ann. N.Y. Acad. Sci. 69, 745–64.CrossRefGoogle Scholar
Tasker, J. B., Miesse, M. L. & Berge, T. O. (1962). Studies on the virus of Venezuelan equine encephalomyelitis III. Distribution in tissues of experimentally infected mice. Am. J. trop. Med. Hyg. 11, 844–50.CrossRefGoogle ScholarPubMed
Webb, H. E., Wight, D. G. D., Platt, G. S. & Smith, C. E. G. (1968). Langat virus encephalitis in mice. I. The effect of the administration of specific antiserum. J. Hyg., Camb. 66, 343–54.CrossRefGoogle ScholarPubMed