Health Management Institute, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China.
Department of Laboratory Medicine, Peking Union Medical College Hospital, Beijing, China.
Front Immunol. 2020 Dec 10;11:596684. doi: 10.3389/fimmu.2020.596684. eCollection 2020.
The current outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses an unprecedented health crisis. The most common chronic illness among patients infected with SARS-CoV-2 is hypertension. Immune dysregulation plays an important role in SARS-CoV-2 infection and in the development of hypertension; however, the dynamic immunological characteristics of COVID-19 patients with hypertension remain largely unclear.
In total, 258 hypertensive patients infected with SARS-CoV-2 were included in this study. CD38HLA-DR and CD38PD-1 CD8 T cells, IFNγCD4 and IFNγCD8 T cells, the titers of IgG, IgM, and IgA against SARS-CoV-2 spike protein, and SARS-CoV-2 throat viral loads were measured weekly over 4 weeks after the onset of symptoms. Clinical outcomes were also monitored.
CD4 T lymphopenia was observed in 100% of the severe and critical cases. Compared with the surviving patients, the patients with fatal outcomes exhibited high and prolonged expression of CD38HLA-DR and CD38PD-1 on CD8 T cells, low expression of SARS-CoV-2-specific IFNγCD4 and IFNγCD8 T cells, low titers of IgG, IgM, and IgA against SARS-CoV-2 spike protein, and high SARS-CoV-2 viral load during the illness. In the surviving patients, the viral load was significantly inversely correlated with SARS-CoV-2-specific IFNγCD8and IFNγCD4 T cells, IgG, IgM, and IgA.
T lymphopenia is common in critical or severe COVID-19 cases with hypertension. Prolonged activation and exhaustion of CD8 T cells were associated with severe disease. The delayed SARS-CoV-2-specific antibody responses may be insufficient for overcoming severe SARS-CoV-2 infection in the absence of SARS-CoV-2-specific cellular responses.
由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的 2019 年冠状病毒病(COVID-19)疫情爆发构成了前所未有的健康危机。感染 SARS-CoV-2 的患者最常见的慢性疾病是高血压。免疫失调在 SARS-CoV-2 感染和高血压发展中起重要作用;然而,COVID-19 合并高血压患者的动态免疫学特征在很大程度上仍不清楚。
本研究共纳入 258 例感染 SARS-CoV-2 的高血压患者。在症状出现后 4 周内每周测量 CD38HLA-DR 和 CD38PD-1 CD8 T 细胞、IFNγCD4 和 IFNγCD8 T 细胞、针对 SARS-CoV-2 刺突蛋白的 IgG、IgM 和 IgA 的滴度以及 SARS-CoV-2 咽喉病毒载量。还监测了临床结局。
100%的重症和危重症患者均出现 CD4 T 淋巴细胞减少。与存活患者相比,死亡患者的 CD8 T 细胞上 CD38HLA-DR 和 CD38PD-1 表达较高且持续时间较长,SARS-CoV-2 特异性 IFNγCD4 和 IFNγCD8 T 细胞表达较低,针对 SARS-CoV-2 刺突蛋白的 IgG、IgM 和 IgA 滴度较低,疾病期间 SARS-CoV-2 病毒载量较高。在存活患者中,病毒载量与 SARS-CoV-2 特异性 IFNγCD8 和 IFNγCD4 T 细胞、IgG、IgM 和 IgA 呈显著负相关。
T 淋巴细胞减少常见于合并高血压的重症或危重症 COVID-19 病例。CD8 T 细胞的持续激活和耗竭与疾病严重程度相关。在缺乏 SARS-CoV-2 特异性细胞反应的情况下,SARS-CoV-2 特异性抗体反应的延迟可能不足以克服严重的 SARS-CoV-2 感染。