Molecular Pathology Group, Cell Biology & Histology, Faculty of Medicine and Health Sciences and.
Laboratory of Medical Microbiology, Vaccine & Infectious Disease Institute, University of Antwerp, Antwerp, Belgium.
J Clin Invest. 2023 Mar 15;133(6):e166032. doi: 10.1172/JCI166032.
BackgroundThe role of host immunity in emergence of evasive SARS-CoV-2 Spike mutations under therapeutic monoclonal antibody (mAb) pressure remains to be explored.MethodsIn a prospective, observational, monocentric ORCHESTRA cohort study, conducted between March 2021 and November 2022, mild-to-moderately ill COVID-19 patients (n = 204) receiving bamlanivimab, bamlanivimab/etesevimab, casirivimab/imdevimab, or sotrovimab were longitudinally studied over 28 days for viral loads, de novo Spike mutations, mAb kinetics, seroneutralization against infecting variants of concern, and T cell immunity. Additionally, a machine learning-based circulating immune-related biomarker (CIB) profile predictive of evasive Spike mutations was constructed and confirmed in an independent data set (n = 19) that included patients receiving sotrovimab or tixagevimab/cilgavimab.ResultsPatients treated with various mAbs developed evasive Spike mutations with remarkable speed and high specificity to the targeted mAb-binding sites. Immunocompromised patients receiving mAb therapy not only continued to display significantly higher viral loads, but also showed higher likelihood of developing de novo Spike mutations. Development of escape mutants also strongly correlated with neutralizing capacity of the therapeutic mAbs and T cell immunity, suggesting immune pressure as an important driver of escape mutations. Lastly, we showed that an antiinflammatory and healing-promoting host milieu facilitates Spike mutations, where 4 CIBs identified patients at high risk of developing escape mutations against therapeutic mAbs with high accuracy.ConclusionsOur data demonstrate that host-driven immune and nonimmune responses are essential for development of mutant SARS-CoV-2. These data also support point-of-care decision making in reducing the risk of mAb treatment failure and improving mitigation strategies for possible dissemination of escape SARS-CoV-2 mutants.FundingThe ORCHESTRA project/European Union's Horizon 2020 research and innovation program.
在治疗性单克隆抗体(mAb)压力下,宿主免疫在逃避 SARS-CoV-2 刺突突变的出现中的作用仍有待探索。
在 2021 年 3 月至 2022 年 11 月期间进行的一项前瞻性、观察性、单中心 ORCHESTRA 队列研究中,对 204 例接受巴姆单抗、巴姆单抗/etesevimab、casirivimab/imdevimab 或 sotrovimab 的轻至中度 COVID-19 患者进行了为期 28 天的病毒载量、新出现的 Spike 突变、mAb 动力学、针对感染关注变体的血清中和作用以及 T 细胞免疫的纵向研究。此外,构建了一种基于机器学习的循环免疫相关生物标志物(CIB)特征,用于预测逃避 Spike 突变,并在包括接受 sotrovimab 或 tixagevimab/cilgavimab 的患者的独立数据集(n=19)中进行了验证。
接受各种 mAb 治疗的患者以显著的速度和针对靶向 mAb 结合位点的高特异性产生了逃避 Spike 突变。接受 mAb 治疗的免疫功能低下患者不仅继续显示出显著更高的病毒载量,而且出现新出现的 Spike 突变的可能性也更高。逃逸突变的发展也与治疗性 mAb 的中和能力和 T 细胞免疫密切相关,表明免疫压力是逃逸突变的重要驱动因素。最后,我们表明,抗炎和促进愈合的宿主环境促进 Spike 突变,其中 4 个 CIB 可准确识别出具有高风险发生针对治疗性 mAb 的逃逸突变的患者。
我们的数据表明,宿主驱动的免疫和非免疫反应对于突变 SARS-CoV-2 的发展至关重要。这些数据还支持在减少 mAb 治疗失败风险和改进可能传播逃逸 SARS-CoV-2 突变体的缓解策略方面进行即时决策。
ORCHESTRA 项目/欧盟地平线 2020 研究和创新计划。