Dengue virus (DENV) infection is a disease that is endemic to many parts of the world, and its increasing prevalence ranks it among the diseases considered to be a significant threat to public health. The clinical manifestations of DENV infection range from mild dengue fever (DF) to more severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Increased proinflammatory cytokines and vascular permeability, both of which cause organ injury, are the hallmarks of severe dengue disease. Signs of liver injury were observed in studies using hepatic cell lines, mouse models, and autopsy specimens from DENV-infected patients, and these signs substantiated the effects of inflammatory responses and hepatic cell apoptosis. Mitogen-activated protein kinases (MAPK) are involved in inflammatory responses and cellular stress during viral infections. The roles of MAPK signaling in DENV infection were reviewed, and published data indicate MAPK signaling to be involved in inflammatory responses and hepatic cell apoptosis in both in vitro cultures and in vivo models. Modulation of MAPK signaling ameliorates the inflammatory responses and hepatic cell apoptosis in DENV infection. This accumulation of published data relative to the role of MAPK signaling in inflammatory responses and cell apoptosis in DENV infection is elucidatory, and may help to accelerate the development of novel or repositioned therapies to treat this unpredictable and often debilitating disease.

登革热病毒（DENV）感染是世界许多地方流行的疾病，其流行率不断上升，使其被认为是对公共卫生的重大威胁。DENV感染的临床表现范围从轻度登革热（DF）到更严重的登革热出血热（DHF）和登革热休克综合征（DSS）。引起器官损伤的促炎细胞因子和血管通透性增加，是严重登革热疾病的标志。在使用DENV感染患者的肝细胞系，小鼠模型和尸检标本进行的研究中观察到了肝损伤的迹象，这些迹象证实了炎症反应和肝细胞凋亡的作用。丝裂原激活的蛋白激酶（MAPK）参与病毒感染过程中的炎症反应和细胞应激。体外培养和体内模型。MAPK信号的调节可改善DENV感染中的炎症反应和肝细胞凋亡。与MAPK信号传导在DENV感染中的炎症反应和细胞凋亡中的作用有关的已发表数据的这种积累是阐明性的，并且可能有助于加速新颖或重新定位的疗法的发展，以治疗这种无法预测且常常使人衰弱的疾病。