Proteome profiling of nasopharynx reveals pathophysiological signature of COVID-19 disease severity
Salunke, Rahul Pandurang
Ben Rached, Fathia
Hashem, Anwar M.
Magistretti, Pierre J.
KAUST DepartmentKAUST Smart Health Initiative (KSHI), 4700 King Abdullah University of Science and Technology, Thuwal 23955-6900, Kingdom of Saudi Arabia.
Biological and Environmental Science and Engineering (BESE) Division
Computational Bioscience Research Center (CBRC)
Sanger and Third Generation Sequencing
NGS, qPCR and Single Cell Genomics
Computer, Electrical and Mathematical Science and Engineering (CEMSE) Division
KAUST Smart Health Initiative
Permanent link to this recordhttp://hdl.handle.net/10754/693022
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AbstractAn aberrant innate immune system caused by the beta coronavirus SARS-CoV-2 is a characteristic manifestation of severe coronavirus disease 2019 (COVID-19). Here, we performed proteome profiling of nasopharyngeal (NP) swabs from 273 hospitalized patients with mild and severe COVID-19 symptoms, including non-survivors. We identified depletion in STAT1-mediated type I interferon response, retinol metabolism and NRF2 antioxidant system that are associated with disease severity in our patient demography. We found that the dysregulation of glucocorticoid signaling and renin-angiotensin-aldosterone system (RAAS) contribute to the pathophysiology of COVID-19 fatality. Hyperactivation of host innate immune system was observed in severe patients, marked by elevated proteins involved in neutrophil degranulation and platelet aggregation. Our study using high-throughput proteomics on the nasopharynx of COVID-19 patients provides additional evidence on the SARS-CoV-2-induced pathophysiological signatures of disease severity and fatality.
CitationOoi, A., Esau, L. E., Pugachev, A., Groen, A., Mfarrej, S., Salunke, R. P., Subudhi, A. K., Ben-Rached, F., Alofi, F., Alsomali, A., Alquthami, K., Khogeer, A., Hashem, A. M., Almontashiri, N., Magistretti, P. J., Hala, S., & Pain, A. (2023). Proteome profiling of nasopharynx reveals pathophysiological signature of COVID-19 disease severity. https://doi.org/10.1101/2023.07.09.548285
SponsorsThis work is supported by King Abdullah University of Science and Technology (KAUST) Rapid Research Response Team (R3T) sponsored by the KAUST Vice-President Research (VPR) office, a KAUST Smart Health Initiative grant (REI/1/4943-01-01 SHI), KAUST faculty baseline fund (BAS/1/1020-01-01), King Abdulaziz City for Science & Technology (KACST) grant (5-20-01-002-0008) and Saudi Ministry of Health (MOH) numbers 754 and 341. We sincerely thank all the hospital staff members, including the team from the General 802 Directorate of Health Affairs in the Makkah region for their tremendous help in collecting the nasopharyngeal swab samples and patients’ metadata. We also thank the KAUST Health Safety and Environment (HSE) and Security staff for their support in logistics relating to sample transport during the COVID-19 lockdown in KSA in 2020.
PublisherCold Spring Harbor Laboratory