Antigenic variation during malaria infection—the contribution from the murine parasite <i>Plasmodium chabaudi</i>

Phillips, R. S.; Brannan, L R; Balmer, Paul; Neuville, Pascal

doi:10.1046/j.1365-3024.1997.d01-239.x

Cited by 45 publications

(41 citation statements)

References 25 publications

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“…It is possible that the immune system of the host might respond differently to infection with slow-or fast-growing strains of parasite. Another possibility is that clonal antigenic switching of variant surface antigens may have occurred, as reported previously (1,14). Antigenic switching, possibly mediated by P. chabaudi cir genes (10), would enable a small number of parasites to survive strong immunity targeted against other antigens that do not switch.…”

Section: Discussionmentioning

confidence: 90%

Mixed Strain Infections and Strain-Specific Protective Immunity in the Rodent Malaria Parasite Plasmodium chabaudi chabaudi in Mice

2006

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Important to malaria vaccine design is the phenomenon of "strain-specific" immunity. Using an accurate and sensitive assay of parasite genotype, real-time quantitative PCR, we have investigated protective immunity against mixed infections of genetically distinct cloned "strains" of the rodent malaria parasite Plasmodium chabaudi chabaudi in mice. Four strains of P. c. chabaudi, AS, AJ, AQ, and CB, were studied. One round of blood infection and drug cure with a single strain resulted in a partial reduction in parasitemia, compared with levels for naïve mice, in challenge infections with mixed inocula of the immunizing (homologous) strain and a heterologous strain. In all cases, the numbers of blood-stage parasites of each genotype were reduced to similar degrees. After a second, homologous round of infection and drug cure followed by challenge with homologous and heterologous strains, the parasitemias were reduced even further. In these circumstances, moreover, the homologous strain was reduced much faster than the heterologous strain in all of the combinations tested. That the immunity induced by a single infection did not show "strain specificity," while the immunity following a second, homologous infection did, suggests that the "strain-specific" component of protective immunity in malaria may be dependent upon immune memory. The results show that strong, protective immunity induced by and effective against malaria parasites from a single parasite species has a significant "strain-specific" component and that this immunity operates differentially against genetically distinct parasites within the same infection.

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Section: Discussionmentioning

confidence: 90%

Mixed Strain Infections and Strain-Specific Protective Immunity in the Rodent Malaria Parasite Plasmodium chabaudi chabaudi in Mice

2006

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“…The molecular weights of these recombinant antigens expressed in Sf 9 cells transfected with recombinant baculovirus or in E. coli were smaller than those of naive antigen. The difference of molecular weight between naive and recombinant antigens may be explained by the difference in parasite strains, the antigenic variation [2,12], or the lack of glycosilation of recombinant antigen. It should be noted that the gene sequence coding for the p26 was originally obtained from the Antwerp strain [16], whereas the genomic DNA used for PCR in the present study was obtained from the Australian strain.…”

Section: Discussionmentioning

confidence: 99%

Immunization with Recombinant Surface Antigens p26 with Freund's Adjuvants against Babesia rodhaini Infection.

Igarashi

Asaba

Xuan

et al. 2000

The Journal of Veterinary Medical Science

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ABSTRACT. The surface proteins of Babesia rodhaini have previously been shown to induce a high degree of protective immunity. In the present study, one of those proteins, B. rodhaini antigen p26 was expressed in Escherichia coli and in insect cells infected with a recombinant baculovirus. These proteins were recognized by immune serum from a drug-cured BALB/c mouse. While BALB/c mice immunized with both recombinant antigens and Freund's adjuvants showed 40-100% survival rate against challenge infection with B. rodhaini, saponin failed to induce protection, although significant levels of B. rodhaini-specific antibodies were produced in both immunized mice (1:1,000-2,000 by indirect immunofluorescent antibody test). The immunization of IFN-γ-deficient mice with the recombinant proteins was not protective against B. rodhaini infection, indicating that IFN-γ is one of the important factors for the survival against lethal B. rodhaini infection.

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“…Cytoadherence aside, there is strong evidence that antigenic variation per se allows the parasite to persist in the face of immunity (reviewed in Brown et al 1986;Phillips et al 1997). By expressing a novel antigen, the immune system is unable to recognize and destroy the parasite.…”

Section: (B) Antigenic Variationmentioning

confidence: 99%

Virulence in malaria: an evolutionary viewpoint

Mackinnon

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2004

Phil. Trans. R. Soc. Lond. B

227

205

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Malaria parasites cause much morbidity and mortality to their human hosts. From our evolutionary perspective, this is because virulence is positively associated with parasite transmission rate. Natural selection therefore drives virulence upwards, but only to the point where the cost to transmission caused by host death begins to outweigh the transmission benefits. In this review, we summarize data from the laboratory rodent malaria model, Plasmodium chabaudi, and field data on the human malaria parasite, P. falciparum, in relation to this virulence trade-off hypothesis. The data from both species show strong positive correlations between asexual multiplication, transmission rate, infection length, morbidity and mortality, and therefore support the underlying assumptions of the hypothesis. Moreover, the P. falciparum data show that expected total lifetime transmission of the parasite is maximized in young children in whom the fitness cost of host mortality balances the fitness benefits of higher transmission rates and slower clearance rates, thus exhibiting the hypothesized virulence trade-off. This evolutionary explanation of virulence appears to accord well with the clinical and molecular explanations of pathogenesis that involve cytoadherence, red cell invasion and immune evasion, although direct evidence of the fitness advantages of these mechanisms is scarce. One implication of this evolutionary view of virulence is that parasite populations are expected to evolve new levels of virulence in response to medical interventions such as vaccines and drugs.

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Antigenic variation during malaria infection—the contribution from the murine parasite Plasmodium chabaudi

Cited by 45 publications

References 25 publications

Mixed Strain Infections and Strain-Specific Protective Immunity in the Rodent Malaria Parasite Plasmodium chabaudi chabaudi in Mice

Mixed Strain Infections and Strain-Specific Protective Immunity in the Rodent Malaria Parasite Plasmodium chabaudi chabaudi in Mice

Immunization with Recombinant Surface Antigens p26 with Freund's Adjuvants against Babesia rodhaini Infection.

Virulence in malaria: an evolutionary viewpoint

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