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Chapter 22 : Rosetting

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Abstract:

The discovery that -infected erythrocytes can bind to uninfected erythrocytes to form rosette-like clumps of cells was first made in the late 1980s. Some of the parasite ligands and host uninfected erythrocyte receptors that mediate rosette formation have been identified, and work has begun to determine the potential for a rosette-inhibiting antidisease vaccine. Despite this progress, the function of rosetting remains unknown, and the exact role of rosetting in the pathogenesis of severe malaria remains controversial. In falciparum malaria it may be the combination of rosetting and cytoadherence, together with high parasite burdens, that is particularly obstructive to microvascular blood flow and could lead to hypoxia, tissue damage, and severe malaria. Skeptics of rosetting claim that there is no evidence that rosettes form in vivo. A number of different red blood cell rosetting receptors have been described, including CR1, heparan sulfate-like molecules, ABO blood group sugars, and CD36. The CD36 glycoprotein, which is an important endothelial receptor for cytoadherence, is expressed at low levels on red blood cells but only rarely acts as a rosetting receptor in field isolates. The development of rosette-inhibiting immune responses in natural malaria infections has received relatively little attention. There is lack of proof that rosetting causes severe malaria. However, evidence does support a direct role for rosetting in the pathogenesis of some cases of life-threatening malaria.

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22

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Relapsing Fever
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Plasmodium falciparum
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Plasmodium malariae
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FIGURE 1

rosettes viewed by microscopy. The parasite-infected erythrocytes can be identified by the dark spot of pigment within the cell.

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22
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Image of FIGURE 2
FIGURE 2

Rosetting and malaria severity in Kenya. Each point on the graph represents the rosette frequency (percentage of mature-infected erythrocytes in rosettes) of a single isolate. (Reproduced from the [ ] with permission from the publisher.)

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22
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Image of FIGURE 3
FIGURE 3

Rosetting and cytoadherence together cause greater obstruction to microvascular blood flow than cytoadherence alone.

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22
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FIGURE 4

Summary of the molecular mechanisms of rosetting.

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22
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Tables

Generic image for table
TABLE 1

Rosetting and severe malaria in Africa

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22
Generic image for table
TABLE 2

Rosetting and severe malaria in Thailand

Citation: Rowe J. 2005. Rosetting, p 416-426. In Sherman I (ed), Molecular Approaches to Malaria. ASM Press, Washington, DC. doi: 10.1128/9781555817558.ch22

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