Pulsed Ultraviolet C as a Potential Treatment for COVID-19

Abstract

Currently, low dose radiotherapy (LDRT) is being tested for treating life-threatening pneumonia in COVID-19 patients. Despite the debates over the clinical use of LDRT, some clinical trials have been completed, and most are still ongoing. Ultraviolet C (UVC) irradiation has been proven to be highly efficient in inactivating the coronaviruses, yet is considerably safer than LDRT. This makes UVC an excellent candidate for treating COVID-19 infection, especially in case of severe pneumonia as well as the post COVID-19 pulmonary fibrosis. However, the major challenge in using UVC is its delivery to the lungs, the target organ of COVID-19, due to its low penetrability through biological tissues. We propose to overcome this challenge (i) by using pulsed UVC technologies which dramatically increase the penetrability of UVC through matter, and (ii) by integrating the pulsed UVC technologies into a laser bronchoscope, thus allowing UVC irradiation to reach deeper into the lungs. Although the exact characteristics of such a treatment should yet to be experimentally defined, this approach might be much safer and not less efficient than LDRT.

Repair and regeneration of the alveolar epithelium in lung injury

“…Reactive oxygen species (ROS) continuously generated by cell metabolism stimulate lipid peroxidation, cause cell membrane damage, and induce alveolar epithelial cell apoptosis 34 . Besides, oxidative stress also causes mitochondrial structural damage by damaging cellular DNA, such as DNA point mutations, DNA breaks, etc 34–36 . Ke et al.…”

“…34 Besides, oxidative stress also causes mitochondrial structural damage by damaging cellular DNA, such as DNA point mutations, DNA breaks, etc. [34][35][36] Ke et al studied the damage of particulate matter 2.5 (PM2.5) to rat AT2 cells and found that excessive ROS levels led to a significant increase in malondialdehyde (MDA) and a decrease in antioxidant enzyme superoxide dismutase (SOD) and antioxidant glutathione (GSH), indicating that oxidative stress is induced by PM2.5 exposure. At the same time, lactate dehydrogenase (LDH) levels increase, mitochondrial membrane potential decreases, and caspase-3/9 expression increases, ultimately leading to AT2 cells apoptosis and indicating the relationship between oxidative stress and apoptosis.…”