Hostname: page-component-7bb8b95d7b-l4ctd Total loading time: 0 Render date: 2024-09-26T21:40:46.290Z Has data issue: false hasContentIssue false
  • English
  • Français

The influence of the age of the host on local virus multiplication and on the resistance to virus infections

Published online by Cambridge University Press:  15 May 2009

Anne Mclaren  and
F. K. Sanders
Anne Mclaren
Affiliation:
Royal Veterinary College, University of London
F. K. Sanders
Affiliation:
M.R.C. Virus Research Group, London School of Hygiene and Tropical Medicine
Rights & Permissions [Opens in a new window]

Extract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. The susceptibility of mice of different ages to intramuscular, intraperitoneal, and oral administration of EMC virus, and to intracerebral and intramuscular injection of both the Texas and the Connecticut-5 strains of Coxsackie virus have been studied. In all cases susceptibility decreases with age. The development of resistance to a given virus may vary in rate and extent according to the route by which the virus is given.

2. The multiplication of small amounts of EMC virus in muscle, and of the Texas and Connecticut-5 strains of Coxsackie virus in both muscle and brain, has been studied in mice of different ages. A very high degree of multiplication of all three viruses was observed in both muscle and brain of young mice, but no significant multiplication of the EMC virus in older muscle could be detected with these small inocula, nor of either of the Coxsackie strains in older muscle or brain.

3. Multiplication of EMC virus in young mice was shown to take place within the muscle itself. Haemagglutination tests showed that less haemagglutinin, as well as less infective virus, was produced in the muscles of older mice following the injection of small amounts of virus.

4. Multiplication of EMC and GDVII viruses could be demonstrated even in older mice if a sufficiently large amount of virus was inoculated initially.

5. The rapid initial disappearance of infectivity from the site of inoculation was shown to be mainly due to dispersal of inoculated virus around the body.

6. The simplest hypothesis which will accommodate the observed data on virus multiplication and on the development of resistance with age appears to be that the accessibility of the host cell to virus decreases with age. We found no evidence that the ability of the host cell to support virus multiplication declines with age.

This work was done in the Department of Zoology, Oxford University. One of us was in receipt of a Medical Research Council training grant. The expenses of the research were met by a grant from the Nuffield Foundation, to whom we should like to express our gratitude.

Type
Research Article
Information
Journal of Hygiene , Volume 57 , Issue 1 , March 1959 , pp. 106 - 122
Copyright
Copyright © Cambridge University Press 1959

References

REFERENCES

Cairns, H. J. F. (1950). Intracerebral inoculation of mice: fate of the inoculum. Nature, Lond., 166, 910.CrossRefGoogle ScholarPubMed
Culbertson, J. T. (1939). The immunization of rats of different age groups against Trypanosoma lewisi by the administration of specific antiserum per os. J. Parasit. 25, 181.CrossRefGoogle Scholar
Dalldorf, G., Sickles, G. M., Plager, H. & Gifford, R. (1949). A virus recovered from the faeces of ‘poliomyelitis’ patients pathogenic for suckling mice. J. exp. Med. 89, 567.CrossRefGoogle ScholarPubMed
Fisher, R. A. (1950). Statistical Methods for Research Workers. Edinburgh: Oliver and Boyd.Google Scholar
Gard, S. (1940). Encephalomyelitis of mice: II. A method for the measurement of virus activity. J. exp. Med. 72, 69.CrossRefGoogle Scholar
Gard, S. & Heller, L. (1951). Hemagglutination by Col-MM-virus. Proc. Soc. exp. Biol., N.Y., 76, 68.CrossRefGoogle ScholarPubMed
Godman, G. C., Bunting, H. & Melnick, J. L. (1952). The histopathology of Coxsackie virus infection in mice. I. Morphologic observations with four different viral types. Amer. J. Path. 28, 223.Google ScholarPubMed
Greig, M. E. & Mayberry, T. C. (1951). The relationship between cholinesterase activity and brain permeability. J. Pharmacol. 102, 1.Google ScholarPubMed
Helvig, F. L. & Schmidt, E. C. H. (1945). A filter-passing agent producing interstitial myocarditis in anthropoid apes and small animals. Science, 102, 31.Google Scholar
Lahelle, O. & Horsfall, F. L. (1949). Hemagglutination with the GD VII strain of mouse encephalomyelitis virus. Proc. Soc. exp. Biol., N.Y., 71, 713.CrossRefGoogle Scholar
MacDonald, F. & Sanders, F. K. (1959). In preparation.Google Scholar
Melnick, J. L. & Curnen, E. C. (1952). Viral and Rickettsial Infections of Man, The Coxsackie group, chap. 14, p. 338. Ed. Rivers, T. M., Publ., J. B.Lippincott.Google Scholar
Melnick, J. L., Shaw, E. W. & Curnen, E. C. (1949). A virus isolated from patients diagnosed as non-paralytic poliomyelitis or aseptic meningitis. Proc. Soc. exp. Biol., N.Y., 71, 344.CrossRefGoogle ScholarPubMed
Morgan, I. M. (1941). Influence of age on susceptibility and on immune response of mice to Eastern equine encephalomyelitis virus. J. exp. Med. 74, 115.CrossRefGoogle ScholarPubMed
Olitsky, P. K., Sabin, A. B. & Cox, H. R. (1936). An acquired resistance of growing animals to certain neurotropic viruses in the absence of humoral antibodies or previous exposure to infection. J. exp. Med. 64, 723.CrossRefGoogle ScholarPubMed
Pappenheimer, A. M., Kunz, L. J. & Richardson, S. (1951). Passage of Coxsackie virus (Connecticut-5 strain) in adult mice with production of pancreatic disease. J. exp. Med. 94, 45.CrossRefGoogle ScholarPubMed
Reed, L. J. & Muench, H. (1938). A simple method of estimating fifty per cent endpoints. Amer. J. Hyg. 27, 493.Google Scholar
Rowe, W. P. (1953). Propagation of Group A Coxsackie viruses in denervated adult mouse muscle. Science, 117, 710.CrossRefGoogle Scholar
Rustigian, R. & Pappenheimer, A. M. (1949). Myositis in mice following intramuscular injection of viruses of the mouse encephalomyelitis group and of certain other neurotropic viruses. J. exp. Med. 89, 69.CrossRefGoogle ScholarPubMed
Sabin, A. B. (1941). Constitutional barriers to the involvement of the nervous system by certain viruses, with special reference to the role of nutrition. J. Pediat. 19, 596.CrossRefGoogle Scholar
Sigel, M. M. (1952). Influence of age on susceptibility to virus infections with particular reference to laboratory animals. Annu. Rev. Microbiol. 6, 247.CrossRefGoogle ScholarPubMed
Theiler, M. & Gard, S. (1940). Encephalomyelitis of mice. I. Characteristics and pathogenesis of the virus. J. exp. Med. 72, 49.CrossRefGoogle ScholarPubMed
Von Magnus, H. & Von Magnus, P. (1949). Breeding of a colony of white mice free of encephalomyelitis virus. Acta pathl. microbiol. scand. 26, 175.CrossRefGoogle ScholarPubMed
Warren, J., Smadel, J. E. & Russ, S. B. (1949). The family relationship of encephalomyocarditis, Columbia-SK, M.M., and Mengo encephalomyelitis viruses. J. Immunol. 62, 387.CrossRefGoogle ScholarPubMed