Host-pathogen interaction of human coronaviruses - MAPK signaling

This pathway describes the activation of the human MAPK signaling system during human coronavirus infection, per Fung and Liu, Figure 7 [10.1146/annurev-micro-020518-115759]. The MAPK signaling system regulates response to different environmental stimuli, e.g. inflammation due to infection. Its downstream effects include regulation of cell cycle, apoptosis, differentiation and immune response. During coronavirus infection, three MAPK signaling pathways were studied and described. The p38 pathway (MAPK11 - MAPK14) leads to stimulation of apoptosis via CHOP (DDIT3) while the ERK pathway (MAPK1 and MAPK3) counteracts apoptosis stimulation and supports cell survival by stimulating ATF2 and FOS. The JNK pathway (MAPK 8 - MAPK10) inhibits cell survival protein BCL2, thus stimulating apoptosis but also stimulating the AP1 complex that leads to the production of effectors to fight the infection. The interplay of apoptosis stimulation and cell survival is not yet fully understood in SARS-CoV-2 infection.

本路径图详述了人类在新型冠状病毒感染过程中，MAPK信号传导系统的激活情况，依据Fung和Liu的研究，如图7[10.1146/annurev-micro-020518-115759]。MAPK信号传导系统调控对各种环境刺激的反应，例如感染引起的炎症。其下游效应包括细胞周期、凋亡、分化和免疫反应的调节。在新型冠状病毒感染期间，研究了三条MAPK信号传导路径并进行了描述。p38通路（MAPK11 - MAPK14）通过CHOP（DDIT3）的介导，促进凋亡；而ERK通路（MAPK1和MAPK3）则通过刺激ATF2和FOS，对抗凋亡刺激并支持细胞存活；JNK通路（MAPK 8 - MAPK10）抑制细胞存活蛋白BCL2，从而促进凋亡，并刺激AP1复合物，导致效应子的产生以抵御感染。在SARS-CoV-2感染中，凋亡刺激与细胞存活之间的相互作用尚未得到充分理解。