COVID-19 caused by the SARS-CoV-2 virus, accompanies an unprecedented spike in cytokines levels termed cytokines release syndrome (CRS), in critically ill patients. Clinicians claim that the surge demonstrates a deregulated immune defence in host, as infected cell expression analysis depicts a delay in type-I (interferon-I) and type-III IFNs expression, along with a limited Interferon-Stimulated Gene (ISG) response, which later resume and culminates in elicitation of several cytokines including- IL-6, IL-8, IL-12, TNFα, IL-17, MCP-1, IP-10 and IL-10 etc. Although cytokines are messenger molecules of the immune system, but their increased concentration results in inflammation, infiltration of macrophages, neutrophils and lung injury in patients. This inflammatory response results in the precarious pathogenesis of COVID-19; thus, a complete estimation of the immune response against SARS-CoV-2 is vital in designing a harmless and effective vaccine. In pathogenesis analysis, it emerges that a timely forceful type-I IFN production (18–24 hrs post infection) promotes innate and acquired immune responses, while a delay in IFNs production (3–4 days post infection) actually renders both innate and acquired responses ineffective in fighting infection. Further, underlying conditions including hypertension, obesity, cardio-vascular disease etc may increase the chances of putting people in risk groups, which end up having critical form of infection. This review summarizes the events starting from viral entry, its struggle with the immune system and failure of host immunological parameters to obliterate the infections, which finally culminate into massive release of CRS and inflammation in gravely ill patients.

由 SARS-CoV-2 病毒引起的 COVID-19 伴随着重症患者细胞因子水平前所未有的飙升，称为细胞因子释放综合征 (CRS)。临床医生声称激增表明宿主免疫防御失调，因为受感染的细胞表达分析描述了 I 型（干扰素-I）和 III 型 IFN 表达的延迟，以及有限的干扰素刺激基因（ISG）反应，随后恢复并最终引发多种细胞因子，包括 IL-6、IL-8、IL-12、TNFα、IL-17、MCP-1、IP-10 和 IL-10等. 细胞因子虽然是免疫系统的信使分子，但其浓度升高会导致患者发生炎症、巨噬细胞、中性粒细胞浸润和肺损伤。这种炎症反应导致 COVID-19 不稳定的发病机制；因此，全面评估针对 SARS-CoV-2 的免疫反应对于设计无害且有效的疫苗至关重要。在发病机制分析中，及时有效的 I 型 IFN 产生（感染后 18-24 小时）会促进先天性和获得性免疫反应，而 IFN 产生的延迟（感染后 3-4 天）实际上会导致先天性和获得性免疫反应对抗感染的反应无效。此外，基础疾病包括高血压、肥胖、心血管疾病等可能会增加将人们置于危险人群中的机会，最终导致严重的感染形式。这篇综述总结了从病毒进入开始的事件，它与免疫系统的斗争以及宿主免疫学参数未能消除感染，最终导致重病患者大量释放 CRS 和炎症。