Chomkatekaew Chalita, Boonklang Phumrapee, Sangphukieo Apiwat, Chewapreecha Claire
Mahidol-Oxford Tropical Medicine Research Unit (MORU), Bangkok, Thailand.
Bioinformatics and Systems Biology Program, School of Bioresource and Technology, King Mongkut's University of Technology Thonburi, Bangkok, Thailand.
Front Microbiol. 2021 Jan 21;11:612568. doi: 10.3389/fmicb.2020.612568. eCollection 2020.
A better understanding of co-evolution between pathogens and hosts holds promise for better prevention and control strategies. This review will explore the interactions between , an environmental and opportunistic pathogen, and the human host immune system. causes "Melioidosis," a rapidly fatal tropical infectious disease predicted to affect 165,000 cases annually worldwide, of which 89,000 are fatal. Genetic heterogeneities were reported in both and human host population, some of which may, at least in part, contribute to inter-individual differences in disease susceptibility. Here, we review (i) a multi-host-pathogen characteristic of the interaction; (ii) selection pressures acting on and human genomes with the former being driven by bacterial adaptation across ranges of ecological niches while the latter are driven by human encounter of broad ranges of pathogens; (iii) the mechanisms that generate genetic diversity in bacterial and host population particularly in sequences encoding proteins functioning in host-pathogen interaction; (iv) reported genetic and structural variations of proteins or molecules observed in -human host interactions and their implications in infection outcomes. Together, these predict bacterial and host evolutionary trajectory which continues to generate genetic diversity in bacterium and operates host immune selection at the molecular level.
更好地理解病原体与宿主之间的共同进化,有望带来更好的预防和控制策略。本综述将探讨一种环境性机会致病菌与人类宿主免疫系统之间的相互作用。该病菌会引发“类鼻疽病”,这是一种迅速致命的热带传染病,预计全球每年有16.5万例感染病例,其中8.9万例死亡。病菌和人类宿主群体中均存在遗传异质性,其中一些至少在一定程度上可能导致个体对疾病易感性的差异。在此,我们综述:(i)这种相互作用的多宿主-病原体特征;(ii)作用于病菌和人类基因组的选择压力,前者由细菌在不同生态位的适应所驱动,而后者由人类接触广泛的病原体所驱动;(iii)在细菌和宿主群体中产生遗传多样性的机制,特别是在编码参与宿主-病原体相互作用的蛋白质的序列中;(iv)在病菌与人类宿主相互作用中观察到的蛋白质或分子的遗传和结构变异及其对感染结果的影响。这些共同预测了细菌和宿主的进化轨迹,该轨迹继续在细菌中产生遗传多样性,并在分子水平上进行宿主免疫选择。