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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Parasite-intrinsic factors can explain ordered progression of trypanosome antigenic variation
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Parasite-intrinsic factors can explain ordered progression of trypanosome antigenic variation

机译：寄生虫内在因素可以解释锥虫抗原变异的有序进展

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摘要

Pathogens often persist during infection because of antigenic variation in which they evade immunity by switching between distinct surface antigen variants. A central question is how ordered appearance of variants, an important determinant of chronicity, is achieved. Theories suggest that it results directly from a complex pattern of transition connectivity between variants or indirectly from effects such as immune cross-reactivity or differential variant growth rates. Using a mathematical model based only on known infection variables, we show that order in trypanosome infections can be explained more parsimoniously by a simpler combination of two key parasite-intrinsic factors: differential activation rates of parasite variant surface glycoprotein (VSG) genes and density-dependent parasite differentiation. The model outcomes concur with empirical evidence that several variants are expressed simultaneously and that parasitaemia peaks correlate with VSG genes within distinct activation probability groups. Our findings provide a possible explanation for the enormity of the recently sequenced VSG silent archive and have important implications for field transmission.
机译：由于抗原变异，病原体通常在感染过程中持续存在，因为它们通过在不同的表面抗原变异体之间切换来逃避免疫。一个中心问题是如何实现变异的有序出现，这是慢性病的重要决定因素。理论表明，它直接源自变体之间过渡连接的复杂模式，或间接源自免疫交叉反应或差异变体生长速率等效应。使用仅基于已知感染变量的数学模型，我们表明，可以通过以下两种简单的寄生虫内在因素的更简单组合来更简洁地解释锥虫感染的顺序：寄生虫变异表面糖蛋白（VSG）基因的差异激活率和密度-依赖寄生虫分化。该模型的结果与经验证据一致，该证据同时表达了几种变体，并且寄生虫血症峰与不同激活概率组内的VSG基因相关。我们的发现为最近已排序的VSG静默档案的庞大性提供了可能的解释，并且对现场传输具有重要意义。

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