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VCL/ICAM-1 pathway is associated with lung inflammatory damage in SARS-CoV-2 Omicron infection

Xue et al., Nature Communications, doi:10.1038/s41467-025-59145-y, Apr 2025
https://c19early.org/xue2.html
Multi-omics and rat model study identifying the VCL/ICAM-1 pathway as a key driver of lung inflammatory damage in SARS-CoV-2 Omicron infection. Authors compared unvaccinated participants infected with Omicron BA.2.76 or ancestral variants to healthy controls, using proteomic and metabolomic analyses of plasma samples. They identified vinculin (VCL) as a critical protein in blood-gas barrier damage and inflammatory exudation, with elevated N-glycosylation in infected participants. Metabolomic analysis revealed disruptions in energy pathways, including altered tricarboxylic acid cycle activity. Validation in male rat models of lung injury demonstrated that anti-VCL intervention reduced plasma VCL levels, mitigated alveolar edema, and restored alveolar-capillary barrier integrity. Compared to ancestral variant, Omicron infections showed a distinctive VCL/ICAM-1 pathway activation pattern, maintaining TCA cycle activity while showing relatively normal anaerobic glycolysis.
Xue et al., 23 Apr 2025, peer-reviewed, 28 authors. Contact: sunbaoqing@vip.163.com.
VCL/ICAM-1 pathway is associated with lung inflammatory damage in SARS-CoV-2 Omicron infection
Mingshan Xue, Zhiwei Lin, Youli Wen, Shaohui Fan, Youxia Li, Hui-Qi Qu, Qiurong Hu, Qian Guo, Lijun Su, Qianyue Yang, Jiahong Chen, Chuci Jiang, Huimin Huang, Peiyan Zheng, Ning Li, Quan Yuan, Meixia Zhang, Xin Zhao, Qunhua Wu, Fengyu Hu, Lu Li, Xiaowen Wang, Peixin Liu, Hakon Hakonarson, Zhiping Deng, Hongman Wang, Xiaoping Tang, Baoqing Sun
Nature Communications, doi:10.1038/s41467-025-59145-y
precisely capturing the comprehensive pathological landscape of SARS-CoV-2 5 . The damage mechanism of SARS-CoV-2 is primarily attributed to the host immune system dysfunction resulting in uncontrolled inflammation, rather than the direct toxicity of the virus. However, viral load is directly correlated with the severity clinical outcomes 6 . Once immune dysfunction takes place within the lungs, uncontrolled inflammatory chemotaxis leads to the secretion of numerous cytokines, causing damage to alveolar epithelium and vascular endothelium. The damage can even progress to the development of deep vein micro thrombosis or bleeding, disruption of the gas-blood barrier, and potential complications like multiple organ failure 7, 8 . The likelihood of severe cases with the Omicron variant is lower, and these cases are characterized by mild inflammation. Research has found that changes in the condition of mild to moderate symptoms do not necessarily parallel changes in infection indicators such as C-reactive protein (CRP), procalcitonin (PCT), and inflammatory cells. These indicators may even remain at clinically normal levels 9, 10 . According to the most recent research, although Omicron exhibits lower infection indicators and decreased risk when contrasted with the ancestral and Delta variants, it should not be classified as a "mild" variant of Coronavirus Disease 2019 (COVID-19) 4, 11 . Previous studies by our team have identified that coagulation-related pathways play a critical role in symptomatic Omicron infections, though the key pathways and proteins involved remain unknown 12 . At the same time, compared with original variant, what unique symptoms, disease progression, and diagnostic indicators Omicron has remained to be explored. Understanding the unique impacts of the Omicron variant on the human body is crucial for shaping public health strategies and therapeutic approaches that address not only the current but also emerging viral variants, thereby enhancing our capacity to manage COVID-19 effectively. Compared to the ancestral variant, the Omicron variant has approximately twice the affinity for ACE2, making it more transmissible. In terms of respiratory symptoms, Omicron is almost indistinguishable from earlier variants and generally causes milder symptoms 4 . However, Omicron infections exhibit highly heterogeneous characteristics, with symptoms ranging from asymptomatic to severe pneumonia, respiratory distress, organ dysfunction, and even death in participants across all age groups 13 . This diversity in infection outcomes highlights the importance of further research into Omicron's pathogenic mechanisms. A study has shown that the damaging effect on the blood-gas barrier during persistent lung functional impairment during and posthospitalization is the main cause of refractory hypoxemia 14 , but the mechanism remains unclear. Furthermore, the ambiguous disease characteristics in low-risk populations pose challenges for..
Data availability The proteomics and glycoproteomics data have been deposited in ProteomeXchange (Submission reference: PXD054443) and The Metabolomics data have been deposited in MetaboLights (Submission reference: MTBLS12231). Supporting source data used in the generation of figures and results are provided with this paper. Source data are provided with this paper. Author contributions These authors contributed equally to this work: M.X., Z.L., Y.W. Conception and design of the research: B.S., X.T., H.W., and Z.D. Drafting the manuscript: M.X. and Z.L. Manuscript Editing: H.Q., H.Ha. Article structure design: M.X. and Z.L. Statistical analysis: Z.L., Q.H., S.F. and Y.L. Samples collection and detection: Y.L., F.H., L.L., H.Hu., P.Z., N.L., and Q.Yu. Experimental management: J.C., C.J., P.L., M.Z., X.Z., X.W., and Q.W. Acquisition of data: Q.G., L.S., X.Z., S.F. and Y.L. Data Interpretation: M.X., Z.L., Q.Ya., J.C., H.Q., H.Ha. All authors read and approved the final version of the manuscript. Competing interests The authors declare no competing interests.
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