Abstract

Morbidity and mortality of coronavirus disease 2019 (COVID-19) are due in large part to severe cytokine storm and hypercoagulable state brought on by dysregulated host-inflammatory immune response, ultimately leading to multi-organ failure. Exacerbated oxidative stress caused by increased levels of interleukin (IL)-6 and tumor necrosis factor α (TNF-α) along with decreased levels of interferon α and interferon β (IFN-α, IFN-β) are mainly believed to drive the disease process. Based on the evidence attesting to the ability of glutathione (GSH) to inhibit viral replication and decrease levels of IL-6 in human immunodeficiency virus (HIV) and tuberculosis (TB) patients, as well as beneficial effects of GSH on other pulmonary diseases processes, we believe the use of liposomal GSH could be beneficial in COVID-19 patients. This review discusses the epidemiology, transmission, and clinical presentation of COVID-19 with a focus on its pathogenesis and the possible use of liposomal GSH as an adjunctive treatment to the current treatment modalities in COVID-19 patients.

Highlights

  • With approximately 11 million confirmed cases and over 525,000 deaths documented, the novel strain of coronavirus, which initially emerged at the end of 2019 in Hubei Province of the People’sRepublic of China, has been found to precipitate clinical acute respiratory distress syndrome (ARDS) [1].Coronaviridae are a large family of enveloped RNA viruses with virulent capacity observed across many species

  • Cytokine profiles of SARS-CoV-2 positive individuals show an elevation in IL-6, IL- 2, IL- 7, ILphase reactants such as IL-6 and tumor necrosis factor α (TNF-α)

  • Evaluation of viruses in the family Coronaviridae reveals that considerable release of proinflammatory cytokines, including IL-2, IL-6, IL-7, IL-10, and TNF-α (Figures 1 and 2), plays a crucial role in the pathogenesis of SARS-CoV-1 and MERS-CoV infections [16]

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Summary

Introduction

With approximately 11 million confirmed cases and over 525,000 deaths documented, the novel strain of coronavirus, which initially emerged at the end of 2019 in Hubei Province of the People’s. Republic of China, has been found to precipitate clinical acute respiratory distress syndrome (ARDS) [1]. Coronaviridae are a large family of enveloped RNA viruses with virulent capacity observed across many species Investigation of this novel emergent strain is ongoing and its pathological features have yet to be fully revealed. The role of cytokine dysregulation in COVID-19 pathophysiology has been documented in multiple studies. This provides the scientific community with the foundation to propose possible mechanisms of pathogenesis and develop treatment modalities to limit morbidity and mortality

SARS-CoV-2 Microbiology
Transmission
COVID-19 Epidemiology
Clinical Presentation and Diagnosis
Pathogenesis of COVID-19
Severe
Phase I
SARS-CoV-2
Resolution
Severe Illness
Interleukin-6 and ARDS
Septic Shock and Hypercoagulability in COVID-19
10. Glutathione and Tuberculosis
11. Glutathione and Viral Infections
12. GSH and Pulmonary Disease
13. The Role of GSH in Ferroptosis
14. GSH and SARS-CoV-2
15. Conclusions
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