UVB Radiation Alone May Not Explain Sunlight Inactivation of SARS-CoV-2

Abstract: a consensus on sampling, methodologies for clinical measurement, and cutoff values to guide the treatment of severe COVID-19 patients with endothelialstabilizing agents, such as statins, glucocorticoids, and anticoagulants. Moreover, endothelial function measurement is a possible alternative method for the early detection of cardiovascular sequelae. Notes Ming Tong,1,2 Fang Chen,2 Qing Zheng,3 and Yimin Zhu2 1 Department of Infectious Diseases, The First-affiliated Hospital of Hunan Normal University (Hunan Provincial People’s Hospital), Changsha, Hunan, China, 2Institute of Emergency Medicine, Hunan Provincial Key Laboratory of Emergency and Critical Care Metabonomics, The Firstaffiliated Hospital of Hunan Normal University (Hunan Provincial People’s Hospital), Changsha, Hunan, China, 3 Department of Geriatrics, The First-affiliated Hospital of Hunan Normal University (Hunan Provincial People’s Hospital), Changsha, Hunan, China References 1. Bauer W, Ulke J, Galtung N, et al. Role of cell adhesion molecules for disease development of patients with and without COVID-19 in the emergency department. J Infect Dis 2021; 223:1497–9. 2. Page AV, Liles WC. Biomarkers of endothelial activation/dysfunction in infectious diseases. Virulence 2013; 4:507–16. 3. Pons S, Fodil S, Azoulay E, Zafrani L. The vascular endothelium: the cornerstone of organ dysfunction in severe SARS-CoV-2 infection. Crit Care 2020; 24:353. 4. Tong M, Jiang Y, Xia D, et al. Elevated expression of serum endothelial cell adhesion molecules in COVID-19 patients. J Infect Dis 2020; 222:894–8. 5. Kong Y, Han J, Wu X, Zeng H, Liu J, Zhang H. VEGF-D: a novel biomarker Received 28 December 2020; editorial decision 20 January 2021; accepted 28 January 2021; published online January 30, 2021. Correspondence: Yimin Zhu, MD, PhD, Institute of Emergency Medicine, Hunan Provincial Key Laboratory of Emergency and Critical Care Metabonomics, The FirstAffiliated Hospital of Hunan Normal University (Hunan Provincial People’s Hospital), Changsha, Hunan 410005, P. R. China (cszhuyimin@163.com). 2021;223:1499–500 The Journal of Infectious Diseases® © The Author(s) 2021. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com. DOI: 10.1093/infdis/jiab041 UVB Radiation Alone May Not Explain Sunlight Inactivation of SARS-CoV-2 To the Editor—Recently, RatnesarShumate et al [1] reported rapid 1500 • jid 2021:223 (15 April) • CORRESPONDENCE sunlight inactivation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in simulated saliva and in complete growth medium (gMEM). Independently and essentially simultaneously, Sagripanti and Lytle [2] introduced a theory for sunlight inactivation of SARS-CoV-2, building on their earlier work with similar viruses [3]. To the best of our knowledge, these data and theory had not been compared. When establishing this comparison, the experimentally reported sunlight inactivation in Ratnesar-Shumate et al [1] is several times faster than predicted by theory, suggesting that additional experiments and hypotheses may be needed to fully elucidate the mechanism of SARS-CoV-2 sunlight inactivation. Briefly, the theory of Sagripanti and Lytle [2, 3] considers direct photochemical damage to viral RNA, which is maximal for UVC (wavelengths between 200 and 280 nm). The effectiveness of UVC is expressed as the exposure that produces one e-fold reduction..