UNDURTI N DAS
President and CEO UND Life Sciences, Battle Ground, USA

Abstract

COVID-19 caused by SARS-CoV-2 is an inflammatory condition involving mainly lungs, vascular endothelium, liver, heart, and brain with significant disturbances in the innate and adaptive immune responses. SARS-CoV-2 virus enters the cells by binding to ACE2 receptor that is present in many tissues. Despite the availability of effective vaccine(s) against SARS-CoV-2 and its variants current pandemic continues to cause significant morbidity and mortality The emergence of several mutant variants of SARS-CoV-2 is a major concern especially about the efficacy of current vaccines against these variants and other variants that are likely to emerge in the future. In this context, the observation that essential fatty acids (EFAs) such as linoleic acid (LA) and their metabolites can inactivate SARS-CoV-2, regulate inflammatory events and immune responses, and suppress inappropriate excess production of pro-inflammatory interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and bradykinin and thus, restore homeostasis is noteworthy. Of all the EFAs, LA and arachidonic acid (AA) are the most effective to inactivate SARS-CoV-2 and other similar viruses and prevent unwarranted inflammation, enhance wound healing by augmenting the production of anti-inflammatory bioactive lipids and cytokines. Since an imbalance between pro- and anti-inflammatory cytokine(s) and other molecules involved in inflammation and wound healing have a significant role in other serious diseases such as sepsis, ARDS (acute respiratory distress syndrome), ischemia-reperfusion injury and severe pneumonia(s), it remains to be seen whether administration of LA and AA and other fatty acids can prevent and suppress these life-threatening diseases in addition to COVID-19.

INTRODUCTION
COVID-19 caused by SARS-CoV-2 (severe acute respiratory syndrome-coronavirus-2), an enveloped virus, is composed of spike proteins (see Figure 1 for the structure of the virus) on their surface which utilize angiotensin-converting enzyme 2 (ACE2) and the cellular protease transmembrane protease serine 2 (TMPRSS2) to enter target cells and lead to the clinical manifestations of the disease. Despite the availability of effective vaccines, the emergence of mutant strains is worrisome and has led to the continuation of the pandemic though at a low scale. Hence, it is necessary to develop other methods of inactivating the virus. In this context, it is noteworthy that certain polyunsaturated fatty acids (PUFAs) can inactive viruses. Furthermore, PUFAs and their metabolites can inlfuence the production and action of both pro- and anti-inflammatory cytokines that may account for some of the serious complications seen in COVID-19. In this context, understanding the interaction between PUFAs and their metabolites and cytokines may throw new light in the pathophysiology of COVID-19 and developing newer therapeutic strategies.