Batista Juan C, DeAntonio Rodrigo, López-Vergès Sandra
Department of Research in Virology and Biotechnology, Gorgas Memorial Institute of Health Studies, Panama City 0816-02593, Panama.
MD-PhD Program on Clinical and Biomedical Research, Faculty of Medicine, Universidad de Panamá, Panama City 0830-00929, Panama.
Cells. 2025 May 22;14(11):763. doi: 10.3390/cells14110763.
The COVID-19 pandemic, caused by SARS-CoV-2, has had a profound impact on global health, with nearly 800 million cases reported in the Americas alone. The clinical presentation of the disease is highly variable, with approximately half of all patients experiencing severe symptoms. This variability confounds the complex interplay between immune responses and disease severity. Severe cases are often characterized by elevated levels of inflammatory cytokines. Over 88% of COVID-19 patients have multiple comorbidities; factors such as age and pre-existing conditions further modulate immune responses and contribute to the severity of the disease. While some studies have reported differences in cytokine profiles between severity groups, larger, well-designed cohorts are needed to clarify these relationships. Natural Killer cells, which are critical for the innate immune response against SARS-CoV-2, are often impaired and contribute to immune exhaustion. In addition, SARS-CoV-2 evades innate immune defenses through accessory proteins that inhibit interferon signaling and exacerbate cytokine storms and inflammation. This integrative review aims to synthesize findings from 2020 onward and provide insights into the innate immune responses induced by SARS-CoV-2 and their contributions to disease pathogenesis. Understanding cytokine dynamics, NK cell behaviors, and viral immune evasion strategies is critical for advancing therapeutic approaches.
由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的2019冠状病毒病疫情对全球健康产生了深远影响,仅在美洲就报告了近8亿例病例。该疾病的临床表现高度可变,约半数患者出现严重症状。这种变异性使免疫反应与疾病严重程度之间复杂的相互作用变得扑朔迷离。重症病例通常以炎症细胞因子水平升高为特征。超过88%的2019冠状病毒病患者有多种合并症;年龄和基础疾病等因素进一步调节免疫反应并加重疾病的严重程度。虽然一些研究报告了不同严重程度组之间细胞因子谱的差异,但需要更大规模、设计良好的队列研究来阐明这些关系。自然杀伤细胞对针对SARS-CoV-2的固有免疫反应至关重要,但往往受损并导致免疫耗竭。此外,SARS-CoV-2通过抑制干扰素信号传导并加剧细胞因子风暴和炎症的辅助蛋白来逃避固有免疫防御。本综述旨在综合2020年以来的研究结果,深入了解SARS-CoV-2诱导的固有免疫反应及其在疾病发病机制中的作用。了解细胞因子动态、自然杀伤细胞行为和病毒免疫逃避策略对于推进治疗方法至关重要。