Role of CR1 Knops polymorphism in the pathophysiology of malaria: Indian scenario.
Role of CR1 Knops polymorphism in the pathophysiology of malaria: Indian scenario.
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发表时间：
2009-12
影响因子：
0.5
通讯作者：
M. Gandhi;Arpita Singh;V. Dev;T. Adak;A. P. Dashd;H. Joshi
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作者：
M. Gandhi;Arpita Singh;V. Dev;T. Adak;A. P. Dashd;H. Joshi
恶性疟原虫（Plasmodium falciparum）是死亡的主要原因，并且引起与隔离有关的脑型疟疾，隔离是由滋养体和疟原虫感染的红细胞粘附到脑中深部血管床的内皮细胞引起的。疟疾的病理生理学因玫瑰花结而复杂化。玫瑰花结是未感染的红细胞与感染成熟无性寄生虫的红细胞结合的过程，并由红细胞表面补体受体1（CR 1）的表达控制。已知CR 1的各种多态性形式，包括分子量多态性、红细胞表达水平/密度多态性和Knops（KN）多态性。Knops血型包括几个等位基因对：Knops a和B（Kna和Knb）、麦考伊a和B（McCa、McCB）、Swain-Langley（Sla）和Villien（Vil）。已发现Knops表型Sl（a-）比Sl（a+）玫瑰花结效率低，因此建议更具有保护性。与过去几年疟疾病例总数的减少相比，恶性疟原虫病例并没有减少多少。此外，恶性疟原虫是印度所有死亡率和大部分发病率的主要原因。因此，我们研究了CR 1 Knops多态性在印度人群疟疾病理生理学中的作用。方法采用病例对照研究方法。采用CAPS（Cleaved Amplified Polymorphic Sequence）方法。本研究共招募了100名正常个体（无任何疾病）和100名患有恶性疟原虫感染（无并发症疟疾）的个体。结果在印度人群（正常人和恶性疟原虫感染者）中，仅存在野生型等位基因。解释与结论我们的结论是，在印度的背景下，玫瑰花结的过程中可能会发生独立的Knops多态性的影响，并在一定程度上可以控制由其他多态性的CR 1基因（密度和结构多态性）。
BACKGROUND & OBJECTIVES Plasmodium falciparum is the leading cause of mortality and causes cerebral malaria associated with sequestration caused by cytoadherence of the trophozoite and schizont-infected erythrocytes to the endothelial cells of the deep vascular beds in the brain. Pathophysiology of malaria is complicated by rosetting. Rosetting is a process of binding of uninfected erythrocytes to the erythrocytes infected with mature asexual parasites and is controlled by expression of complement receptor 1 (CR1) on RBC surface. Various polymorphic forms of CR1 are known including molecular weight polymorphism, red blood cell expression levels/density polymorphism and Knops (KN) polymorphism. The Knops blood group includes several allelic pairs; Knops a and b (Kna and Knb), McCoy a and b (McCa, McCb), Swain-Langley (Sla), and Villien (Vil). Knops phenotype Sl (a-) has been found to rosette less effectively than Sl (a+) and hence suggested to be more protective. P. falciparum cases have not reduced much as compared to the reduction in the total number of malaria cases in the past few years. In addition, P. falciparum is the leading cause for all mortality and most of the morbidity in India. We, therefore, investigated the role of CR1 Knops polymorphism in the pathophysiology of malaria in Indian population. METHODS A case control approach was used for this study. CAPS (Cleaved amplified polymorphic sequence) methodology was adopted. A total of 100 normal individuals (free from any ailment) and 100 individuals suffering from P. falciparum infection (uncomplicated malaria) were recruited for this study. RESULTS We found that in Indian population (normal individuals and P. falciparum-infected individuals), only the wild type allele is present. INTERPRETATION & CONCLUSION We concluded that the process of rosetting in the Indian context could be occurring independently of the effect of Knops polymorphism and in part could be controlled by other polymorphisms of the CR1 gene (density and structural polymorphism).