Center for Biodiscovery and Molecular Development of Therapeutics, James Cook University, Cairns, Australia.
J Allergy Clin Immunol. 2012 Jul;130(1):13-21. doi: 10.1016/j.jaci.2012.05.029.
Hookworms produce a vast repertoire of structurally and functionally diverse molecules that mediate their long-term survival and pathogenesis within a human host. Many of these molecules are secreted by the parasite, after which they interact with critical components of host biology, including processes that are key to host survival. The most important of these interactions is the hookworm's interruption of nutrient acquisition by the host through its ingestion and digestion of host blood. This results in iron deficiency and eventually the microcytic hypochromic anemia or iron deficiency anemia that is the clinical hallmark of hookworm infection. Other molecular mechanisms of hookworm infection cause a systematic suppression of the host immune response to both the parasite and to bystander antigens (eg, vaccines or allergens). This is achieved by a series of molecules that assist the parasite in the stealthy evasion of the host immune response. This review will summarize the current knowledge of the molecular mechanisms used by hookworms to survive for extended periods in the human host (up to 7 years or longer) and examine the pivotal contributions of these molecular mechanisms to chronic hookworm parasitism and host clinical outcomes.
钩虫产生了大量结构和功能多样化的分子，这些分子介导其在人体宿主中的长期生存和发病机制。这些分子中的许多是寄生虫分泌的，然后它们与宿主生物学的关键成分相互作用，包括对宿主生存至关重要的过程。这些相互作用中最重要的是钩虫通过摄取和消化宿主血液来中断宿主对营养物质的获取。这导致缺铁，最终导致小细胞低色素性贫血或缺铁性贫血，这是钩虫感染的临床特征。钩虫感染的其他分子机制导致宿主对寄生虫和旁观者抗原（例如疫苗或过敏原）的免疫反应受到系统性抑制。这是通过一系列分子来实现的，这些分子帮助寄生虫在宿主免疫反应中偷偷地逃避。这篇综述将总结钩虫在人体宿主中长时间（长达 7 年或更长时间）生存所使用的分子机制的现有知识，并研究这些分子机制对慢性钩虫寄生和宿主临床结局的关键贡献。
