The persistence of the human malaria parasite Plasmodium falciparum during blood stage proliferation in its host depends on the successive expression of variant molecules at the surface of infected erythrocytes. This variation is mediated by the differential control of a family of surface molecules termed PfEMP1 encoded by approximately 60 var genes. Each individual parasite expresses a single var gene at a time, maintaining all other members of the family in a transcriptionally silent state. PfEMP1/var enables parasitized erythrocytes to adhere within the microvasculature, resulting in severe disease. This review highlights key regulatory mechanisms thought to be critical for monoallelic expression of var genes. Antigenic variation is orchestrated by epigenetic factors including monoallelic var transcription at separate spatial domains at the nuclear periphery, differential histone marks on otherwise identical var genes, and var silencing mediated by telomeric heterochromatin. In addition, controversies surrounding var genetic elements in antigenic variation are discussed.

中文翻译：

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恶性疟原虫的抗原变异。

人类疟原虫恶性疟原虫在其宿主的血液阶段增殖过程中的持续存在取决于在感染的红细胞表面连续表达变异分子。这种差异是由大约60个var基因编码的称为PfEMP1的表面分子家族的差异控制介导的。每个寄生虫一次表达一个var基因，从而使该家族的所有其他成员保持转录沉默状态。PfEMP1 / var使被寄生的红细胞粘附在微脉管系统中，从而导致严重疾病。这篇评论强调了关键调控机制，被认为对var基因的单等位基因表达至关重要。抗原变异是由表观遗传因素精心策划的，包括在核外围不同空间结构域的单等位基因var转录，原本相同的var基因上的差异组蛋白标记以及端粒异染色质介导的var沉默。此外，还讨论了抗原变异中围绕var遗传元件的争论。