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Article contents

Immunity to an attenuated variant of Plasmodium berghei: role of some non-specific factors

Published online by Cambridge University Press:  06 April 2009

Seiji waki
Affiliation:
Department of Parasitology, Gunma University School of Medicine, Maebashi 371, Japan
Shushke Nakazawa
Affiliation:
Department of Parasitology, Gunma University School of Medicine, Maebashi 371, Japan
Janice Taverne
Affiliation:
Department of Immunology, Middlesex Hospital Medical School, London W1P 9PG
G. A. T. Targett
Affiliation:
Department of Medical Protozoology, London School of Hygiene and Tropical Medicine, London WC1E 7HT
J. H. L. Playfair
Affiliation:
Department of Immunology, Middlesex Hospital Medical School, London W1P 9PG

Extract

Plasmodium berghei XAT, an attenuated variant of lethal P. berghei, causes a resolving infection in Balb/c mice from which they recover in about 3 weeks. The parasitaemia displays an early peak at about 5 days, followed by a steep drop in parasite number associated with the appearance of degenerating forms inside mature erythrocytes; the parasites remaining are inside reticulocytes. By contrast, no degenerating parasites were seen in infections caused by the virulent parent, which was mainly confined to mature erythrocytes. However, P. berghei XAT was no more sensitive to reactive O2 metabolites, generated by alloxan, or to tumour necrosis serum, than its virulent parent. Furthermore, its early drop in parasitaemia was unaffected by silica. The drop still occurred in the absence of T cells, although the infection was then ultimately lethal, and it was not mediated by NK cells since it occurred in nude mice treated with anti-asialo GM1 serum to abolish NK cell activity. However, it was absent in splenectomized mice, in which P. berghei XAT infection was lethal. Thus, the attenuation of P. berghei XAT infection is not due to increased susceptibility to some of the agents thought to cause parasite destruction, but to some other mechanism in which the spleen is involved.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1985

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References

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