Sudden increase in virulence in a strain of<i>Plasmodium berghei yoelii</i>

Yoeli, Meir; Hargreaves, Bruce J.; Carter, R.; Walliker, David

doi:10.1080/00034983.1975.11686998

Cited by 110 publications

(81 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is clear that virulent and avirulent strains of P. yoelii differ in their ability to invade mature red blood cells (60,63), and this has recently been linked to differential copy number and expression patterns of genes putatively involved in erythrocyte invasion (1,18,41). Nevertheless, numerous studies from different laboratories have observed immunological differences between the two infections, including disparate IFN-␥ production, regulatory cytokine production, regulatory T-cell activation, and stromal cell activation (6,10,15,16,21,22,35,36,47,62), indicating that the virulence of P. yoelii parasites is not simply due to their erythrocyte invasion capacity.…”

Section: Discussionmentioning

confidence: 99%

Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave ofPlasmodium yoeliiParasitemia

et al. 2007

View full text Add to dashboard Cite

In most models of blood-stage malaria infection, proinflammatory immune responses are required for control of infection and elimination of parasites. We hypothesized therefore that the fulminant infections caused in mice by the lethal strain of Plasmodium yoelii (17XL) might be due to failure to activate a sufficient inflammatory response. Here we have compared the adaptive CD4 ؉ T-cell and innate immune response to P. yoelii 17XL with that induced by the self-resolving, nonlethal strain of P. yoelii, 17X(NL). During the first 7 to 9 days of infection, splenic effector CD4 ؉ T-cell responses were similar in mice with lethal and nonlethal infections with similar levels of activation in vivo and equivalent proliferation in vitro following mitogenic stimulation. Nonspecific T-cell hyporesponsiveness was observed at similar levels during both infections and was due, in part, to suppression mediated by CD11b ؉ cells. Importantly, however, RAG ؊/؊ mice were able to control the initial growth phase of nonlethal P. yoelii infection as effectively as wild-type mice, indicating that T cells and/or B cells play little, if any, role in control of the primary peak of parasitemia. Somewhat unexpectedly, we could find no clear role for either NK cells or gamma interferon (IFN-␥) in controlling primary P. yoelii infection. In contrast, depletion of monocytes/macrophages exacerbated parasite growth and anemia during both lethal and nonlethal acute P. yoelii infections, indicating that there is an IFN-␥-, NK cell-, and T-cell-independent pathway for induction of effector macrophages during acute malaria infection.

show abstract

Section: Discussionmentioning

confidence: 99%

Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave ofPlasmodium yoeliiParasitemia

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Further indirect evidence in support of the birthrate hypotheses comes from field data on severe disease: these are the positive link in P. falciparum between severe malaria and parasite multiplication potential measured in vitro (Chotivanich et al 2000), and the correlation between cytoadherence in vitro and the incidence of severe anaemia and therefore perhaps asexual multiplication rate. Laboratory studies that also support the birth-rate argument are the higher growth rate and higher sequestration in a highly virulent mutant clone of P. yoelii compared with avirulent clones (Yoeli & Hargreaves 1974;Yoeli et al 1975), and the lower acute phase growth rate and virulence in a line of P. falciparum that had lost the ability to sequester (Langreth & Peterson 1985). However, in another study of a non-sequestering line in P. chabaudi, the rate of acute phase growth was similar to that of sequestering lines (Gilks et al 1990).…”

Section: Molecular Mechanisms For Virulence In Relation To Parasite Fmentioning

confidence: 99%

“…There are two forms of evidence in relation to the importance of selectivity in invasion rates: one in species with very high red cell selectivity, and the other in species with low selectivity. In P. yoelii, which has a strong predilection for reticulocytes, a mutation that allows parasites to also infect mature red cells leads to very rapid multiplication rate and hypervirulence (Yoeli & Hargreaves 1974;Yoeli et al 1975). This has been linked to invasion proteins located in the apex of the merozoite (Freeman et al 1980;Holder & Freeman 1981;Ogun & Holder 1996;Preiser & Jarra 1998).…”

Section: (B) Antigenic Variationmentioning

confidence: 99%

Virulence in malaria: an evolutionary viewpoint

Mackinnon

Read

2004

Phil. Trans. R. Soc. Lond. B

228

205

View full text Add to dashboard Cite

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.

show abstract

“…The original description of the 17XYM line reported that fast multiplying parasites emerged in a single step during blood passage of 17X, a slowly multiplying line of P. y. yoelii (3). This suggests that a single mutation event may have been responsible for the major effect in determining the fast multiplying phenotype.…”

Section: Discussionmentioning

confidence: 99%

“…erythrocyte binding ligand protein ͉ rodent malaria ͉ linkage group selection ͉ virulence U nder clinical or laboratory conditions, different lines or strains of malaria parasites can be shown to differ in the severity of the disease that they cause in their hosts (1)(2)(3). As these differences in pathogenicity are, by and large, stable properties of the individual parasite lines, it can be assumed that they have a genetic basis.…”

mentioning

confidence: 99%

Gene encoding erythrocyte binding ligand linked to blood stage multiplication rate phenotype inPlasmodium yoelii yoelii

Pattaradilokrat

Culleton

Cheesman

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Variation in the multiplication rate of blood stage malaria parasites is often positively correlated with the severity of the disease they cause. The rodent malaria parasite Plasmodium yoelii yoelii has strains with marked differences in multiplication rate and pathogenicity in the blood. We have used genetic analysis by linkage group selection (LGS) to identify genes that determine differences in multiplication rate. Genetic crosses were generated between genetically unrelated, fast-(17XYM) and slowly multiplying (33XC) clones of P. y. yoelii. The uncloned progenies of these crosses were placed under multiplication rate selection in blood infections in mice. The selected progenies were screened for reduction in intensity of quantitative genetic markers of the slowly multiplying parent. A small number of strongly selected markers formed a linkage group on P. y. yoelii chromosome 13. Of these, that most strongly selected marked the gene encoding the P.

show abstract

Sudden increase in virulence in a strain ofPlasmodium berghei yoelii

Cited by 110 publications

References 4 publications

Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave ofPlasmodium yoeliiParasitemia

Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave ofPlasmodium yoeliiParasitemia

Virulence in malaria: an evolutionary viewpoint

Gene encoding erythrocyte binding ligand linked to blood stage multiplication rate phenotype inPlasmodium yoelii yoelii

Contact Info

Product

Resources

About