The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing COVID-19 is associated with excessive inflammation, as a main reason for severe condition and death. Increased inflammatory cytokines and humoral response to SARS-CoV-2 correlate with COVID-19 immunity and pathogenesis. Importantly, the levels of pro-inflammatory cytokines that increase profoundly in systemic circulation appear as part of the clinical pictures of two overlapping conditions, sepsis and the hemophagocytic syndromes. Both conditions can develop lethal inflammatory responses that lead to tissue damage, however, in many patients hemophagocytic lymphohistiocytosis (HLH) can be differentiated from sepsis. This is a key issue because the life-saving aggressive immunosuppressive treatment, required in the HLH therapy, is absent in sepsis guidelines. This paper aims to describe the pathophysiology and clinical relevance of these distinct entities in the course of COVID-19 that resemble sepsis and further highlights two effector arms of the humoral immune response (inflammatory cytokine and immunoglobulin production) during COVID-19 infection.

引起 COVID-19 的严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 与过度炎症有关，这是导致病情严重和死亡的主要原因。增加的炎症细胞因子和对 SARS-CoV-2 的体液反应与 COVID-19 免疫和发病机制相关。重要的是，在全身循环中显着增加的促炎细胞因子水平似乎是脓毒症和噬血细胞综合征这两种重叠病症的临床表现的一部分。这两种情况都可以发展导致组织损伤的致死性炎症反应，但是，在许多患者中，噬血细胞性淋巴组织细胞增多症 (HLH) 可以与脓毒症区分开来。这是一个关键问题，因为 HLH 治疗所需的挽救生命的积极免疫抑制治疗在脓毒症指南中是不存在的。