Xu Ji-Qian, Zhang Wan-Ying, Fu Jia-Ji, Fang Xiang-Zhi, Gao Cheng-Gang, Li Chang, Yao Lu, Li Qi-Lan, Yang Xiao-Bo, Ren Le-Hao, Shu Hua-Qing, Peng Ke, Wu Ying, Zhang Ding-Yu, Qiu Yang, Zhou Xi, Yao Yong-Ming, Shang You
Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
State Key Laboratory of Virology, Center for Antiviral Research, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 43007, China.
Mil Med Res. 2024 Dec 16;11(1):78. doi: 10.1186/s40779-024-00581-0.
Sepsis, characterized as life-threatening organ dysfunction resulting from dysregulated host responses to infection, remains a significant challenge in clinical practice. Despite advancements in understanding host-bacterial interactions, molecular responses, and therapeutic approaches, the mortality rate associated with sepsis has consistently ranged between 10 and 16%. This elevated mortality highlights critical gaps in our comprehension of sepsis etiology. Traditionally linked to bacterial and fungal pathogens, recent outbreaks of acute viral infections, including Middle East respiratory syndrome coronavirus (MERS-CoV), influenza virus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), among other regional epidemics, have underscored the role of viral pathogenesis in sepsis, particularly when critically ill patients exhibit classic symptoms indicative of sepsis. However, many cases of viral-induced sepsis are frequently underdiagnosed because standard evaluations typically exclude viral panels. Moreover, these viruses not only activate conventional pattern recognition receptors (PRRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) but also initiate primary antiviral pathways such as cyclic guanosine monophosphate adenosine monophosphate (GMP-AMP) synthase (cGAS)-stimulator of interferon genes (STING) signaling and interferon response mechanisms. Such activations lead to cellular stress, metabolic disturbances, and extensive cell damage that exacerbate tissue injury while leading to a spectrum of clinical manifestations. This complexity poses substantial challenges for the clinical management of affected cases. In this review, we elucidate the definition and diagnosis criteria for viral sepsis while synthesizing current knowledge regarding its etiology, epidemiology, and pathophysiology, molecular mechanisms involved therein as well as their impact on immune-mediated organ damage. Additionally, we discuss clinical considerations related to both existing therapies and advanced treatment interventions, aiming to enhance the comprehensive understanding surrounding viral sepsis.
脓毒症的特征是宿主对感染的反应失调导致危及生命的器官功能障碍,在临床实践中仍然是一项重大挑战。尽管在理解宿主与细菌的相互作用、分子反应和治疗方法方面取得了进展,但脓毒症的死亡率一直徘徊在10%至16%之间。这种高死亡率凸显了我们对脓毒症病因理解上的关键差距。传统上脓毒症与细菌和真菌病原体有关,近期爆发的急性病毒感染,包括中东呼吸综合征冠状病毒(MERS-CoV)、流感病毒和严重急性呼吸综合征冠状病毒2(SARS-CoV-2),以及其他地区性流行病,都强调了病毒发病机制在脓毒症中的作用,特别是当重症患者表现出脓毒症的典型症状时。然而,许多病毒引起的脓毒症病例常常被漏诊,因为标准评估通常不包括病毒检测项目。此外,这些病毒不仅激活传统的模式识别受体(PRR)和视黄酸诱导基因-I(RIG-I)样受体(RLR),还启动主要的抗病毒途径,如环磷酸鸟苷-磷酸腺苷(cGAMP)合成酶(cGAS)-干扰素基因刺激因子(STING)信号通路和干扰素反应机制。这种激活导致细胞应激、代谢紊乱和广泛的细胞损伤,加剧组织损伤,同时导致一系列临床表现。这种复杂性给受影响病例的临床管理带来了重大挑战。在这篇综述中,我们阐明了病毒脓毒症的定义和诊断标准,同时综合了关于其病因、流行病学、病理生理学、其中涉及的分子机制以及它们对免疫介导的器官损伤的影响的现有知识。此外,我们讨论了与现有疗法和先进治疗干预措施相关的临床考虑因素,旨在增强对病毒脓毒症的全面理解。