Potential utility of melatonin in deadly infectious diseases related to the overreaction of innate immune response and destructive inflammation: focus on COVID-19

Melatonin in deadly virus infection

  • Dunxian X Tan S.T. Bio-Life, San Antonio, TX, USA
  • Ruegiger Hardeland Johann Friedrich Blumenbach Institute of Zoology and Anthropology, University of Göttingen, Germany
Keywords: melatonin, virus, innate immunity, inflammation, COVID-19, SARS, MERS, Avian flu, cytokines

Abstract


The high mortality of deadly virus infectious diseases including SARS, MERS, COVID-19, and avian flu is often caused by the uncontrolled innate immune response and destructive inflammation. The majority of viral diseases are self-limiting under the help of the activated adaptive immune system. This activity is cell proliferation dependent and thus, it requires several weeks to develop. Patients are vulnerable and mortality usually occurs during this window period. To control the innate immune response and reduce the inflammation during this period will increase the tolerance of patients and lowers the mortality in the deadly virus infection. Melatonin is a molecule that displays respective properties, since it downregulates the overreaction of the innate immune response and overshooting inflammation, but also promotes the adaptive immune activity. Many studies have reported the beneficial effects of melatonin on deadly virus infections in different animal models and its therapeutic efficacy in septic shock patients. Furthermore, melatonin has a great safety margin without serious adverse effects. We suggest the use of melatonin as an adjunctive or even regular therapy for deadly viral diseases, especially if no efficient direct anti-viral treatment is available.

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Published
2020-03-23
How to Cite
[1]
Tan, D.X. and Hardeland, R. 2020. Potential utility of melatonin in deadly infectious diseases related to the overreaction of innate immune response and destructive inflammation: focus on COVID-19. Melatonin Research. 3, 1 (Mar. 2020), 120-143. DOI:https://doi.org/https://doi.org/10.32794/mr11250052.