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Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2
Published on: November 5, 2021
SARS CoV-2 aggravates cellular metabolism mediated complications in COVID-19 infection
Yogendra Singh1, Gaurav Gupta2, Imran Kazmi3
1Mahatma Gandhi College of Pharmaceutical Sciences, Jaipur, India.
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.
Insights
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection alters host cell metabolism, triggering ferroptotic cell death. Supplementing with Vitamin B6, folic acid, and Vitamin B12 may help suppress complications by targeting the homocysteine pathway.
Area of Science:
- Virology
- Cell Biology
- Metabolic Medicine
Background:
- Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes COVID-19, a global health concern.
- The mechanisms of cell death, particularly ferroptosis, in SARS-CoV-2 infection are not fully understood.
- Host cell metabolic alterations are implicated in severe COVID-19 outcomes.
Purpose of the Study:
- To elucidate the mechanisms of ferroptotic cell death in SARS-CoV-2 infection.
- To investigate the role of the homocysteine-mediated trans-sulfuration pathway in COVID-19 pathogenesis.
- To identify potential therapeutic strategies targeting metabolic dysregulation.
Main Methods:
- This study is a letter/commentary, synthesizing current research and proposing new mechanistic links.
- Focuses on the biochemical pathways involved in cellular stress responses.
- Highlights the role of specific metabolites and vitamins in viral infection.
Main Results:
- Identifies critical missing links in understanding ferroptosis induction by SARS-CoV-2.
- Reveals the significant involvement of the homocysteine-mediated trans-sulfuration pathway in COVID-19.
- Demonstrates how SARS-CoV-2 alters host cell metabolism, leading to cellular stress.
Conclusions:
- Ferroptosis is a key mechanism of cell death in SARS-CoV-2 infection.
- The homocysteine pathway plays a crucial role in COVID-19 pathogenesis.
- Vitamin B6, folic acid, and Vitamin B12 supplementation are proposed as a therapeutic strategy to mitigate SARS-CoV-2 complications by correcting metabolic imbalances.
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