Can sunlight affect COVID-19 outcomes? What is the available evidence?

Article information

Clin Exp Emerg Med. 2021;8(3):249-250

Publication date (electronic) : 2021 September 30

doi : https://doi.org/10.15441/ceem.21.045

Mohammad Reza Khazdair^,1, Andy Goren²

¹Cardiovascular Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran

²Applied Biology Inc., Irvine, CA, USA

Correspondence to: Mohammad Reza Khazdair Cardiovascular Diseases Research Center, Birjand University of Medical Sciences, Ghafari Street, Birjand, South Khorasan 9717853111, Iran E-mail: khazdairMR@Bums.ac.ir

Received 2021 March 15; Revised 2021 April 13; Accepted 2021 April 20.

Dear Editor,

Coronavirus disease 2019 (COVID-19) has rapidly spread into a global pandemic that challenges the economic, medical, and public health stability of nations worldwide [1]. Severe acute respiratory syndrome coronavirus (SARS-CoV)-2, first identified in China in December 2019 as the “novel coronavirus,” causes COVID-19 by utilizing angiotensin-converting enzyme 2 receptors and transmembrane protease, serine 2 (TMPRSS2, located on host cell surfaces) for entry and infection. Thus, TMPRSS2 is required for SARS-CoV-2 infectivity [1].

Interestingly, total prostate-specific antigen levels vary by season. The prolonged daylight hours of spring and summer are associated with reduced androgen sensitivity, which lowers TMPRSS2 expression and subsequently reduces SARS-CoV-2 infectivity. Conversely, the shortened daylight hours of autumn and winter are associated with increased SARS-CoV-2 infectivity [2].

Dopico et al. [3] demonstrated that the cellular composition of blood also varies by season: soluble interleukin (IL)-6 receptor and C-reactive protein concentrations increase during winter and estradiol receptor gene expression increases during summer. This is pertinent because SARS-CoV-2 infections cause cytokine storms and systemic inflammatory responses that are mediated by the release of large amounts of pro-inflammatory cytokines and chemokines (e.g., IL-1b, IL-6, and interferon-α) from immune effector cells [1].

Sunlight exposure mediates the conversion of previtamin D3 (precholecalciferol) into vitamin D3 (cholecalciferol) by liver enzymes. Vitamin D receptors are highly expressed by monocytes and by B and T lymphocytes, which modulate immune cell function. Thus, vitamin D deficiency is primarily associated with increased susceptibility to, and severity of, many infectious diseases. More specifically, it is associated with low concentrations of the pro-inflammatory cytokine IL-6, which plays a significant role in COVID-19–induced acute respiratory distress syndrome. In addition, low 25-hydroxyvitamin D concentrations may increase COVID-19 mortality [4]. Taken together, studies indicate that sunlight improves immunity by increasing vitamin D production and thus may be useful for the treatment of COVID-19.

The environmental survival of viruses such as SARS-CoV-1 depends on factors, including sunlight, humidity, and temperature. On the other hand, 90% of SARS-CoV-2 is inactivated every 6.8 minutes in simulated saliva and every 14.3 minutes in culture media exposed to simulated sunlight (representative of summer at 40°N latitude). Indeed, during summer, 11 to 34 minutes of midday sunlight can inactivate ≥90% of SARS-CoV 2 viruses in most locations [5].

In conclusion, sunlight modulates immune system function by inducing vitamin D production. It also reduces androgen sensitivity and lowers TMPRSS2 expression. Considering that SARS-CoV-2 are dependent on TMPRSS2 for infectivity, sunlight may be useful in the fight against SARS-CoV-2.