Abstract：
Pathogens exploit multiple cellular and molecular pathways in the host organisms for their entry, survival and dissemination. The cell surface receptors such as G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) constitute the targets of many pathogens. This is due to the ubiquitous expression of these two receptor families in the organism and their pivotal role in various cellular and physiological processes. At the molecular level, receptor hijacking implies either direct or indirect interactions between pathogens\' effectors or toxins with GPCRs and RTKs at the cell surface thereby interfering with their activation and their downstream signaling pathways inside the host cells. As a result, the pathogens manipulate and redirect GPCR/RTK-mediated signaling pathways and different aspects of cell function for their benefit. The review presents a compilation of the major examples of pathogen infections where GPCRs and RTKs and their related intracellular signaling pathways are targeted. This provides a molecular basis for pathogens hijacking cell signaling and their virulence. Our understanding of such complex host-pathogen interactions at the molecular level will open new opportunities to develop new prophylactic and therapeutic approaches against infections. In this context, the pharmacological targeting of GPCRs and RTKs may be a promising approach.
摘要：
病原体利用宿主生物中的多种细胞和分子途径进入，生存和传播。细胞表面受体如G蛋白偶联受体(GPCRs)和受体酪氨酸激酶(RTKs)构成许多病原体的靶标。这是由于这两个受体家族在生物体中的普遍表达及其在各种细胞和生理过程中的关键作用。在分子水平上,受体劫持意味着病原体效应子或毒素与细胞表面的GPCRs和RTKs之间直接或间接相互作用,从而干扰宿主细胞内的激活及其下游信号通路.因此,病原体操纵和重定向GPCR/RTK介导的信号传导途径和细胞功能的不同方面以获得益处。这篇综述提供了病原体感染的主要例子的汇编，其中GPCRs和RTK及其相关的细胞内信号通路是靶向的。这为病原体劫持细胞信号及其毒力提供了分子基础。我们在分子水平上对这种复杂的宿主-病原体相互作用的理解将为开发新的预防和治疗感染的方法开辟新的机会。在这种情况下，GPCRs和RTKs的药理学靶向可能是一种有前途的方法。
