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SARS CoV-2 aggravates cellular metabolism mediated complications in COVID-19 infection

Singh Y 1 , Gupta G 2 , Kazmi I 3 , Al-Abbasi FA 3 , Negi P 4 , Chellappan DK 5 Show all authors , Dua K 6

Affiliations 

  • 1 Mahatma Gandhi College of Pharmaceutical Sciences, Jaipur, India
  • 2 School of Pharmacy, Suresh Gyan Vihar University, Jaipur, India
  • 3 Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia
  • 4 School of Pharmaceutical Sciences, Shoolini University, Solan, Himachal Pradesh, India
  • 5 Department of Life Sciences, School of Pharmacy, International Medical University, Kuala Lumpur, Malaysia
  • 6 Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney (UTS), Ultimo, New South Wales, Australia
Dermatol Ther, 2020 11;33(6):e13871.
PMID: 32558055 DOI: 10.1111/dth.13871

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the primary causative organism in corona virus disease-19 (COVID-19) infections, is a novel member of the human coronavirus family which was first identified in Wuhan, China, towards the end of 2019. This letter reveals new vital missing links in our current understanding of the mechanisms that lead to cell death triggered by ferroptotic stress in COVID-19 infection. It further reveal the importance of homocysteine mediated trans-sulfuration pathway in COVID-19 infection. Hence, Vitamin B6, folic acid, and Vitamin B12 should be incorporated in the treatment regimen for SARS CoV-2 infections to suppress complications, as the virus mediates altered host cell metabolism.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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