Cancer vs. SARS-CoV-2 induced inflammation, overlapping functions, and pharmacological targeting

Abstract

Inflammation is an intrinsic defence mechanism triggered by the immune system against infection or injury. Chronic inflammation allows the host to recover or adapt through cellular and humoral responses, whereas acute inflammation leads to cytokine storms resulting in tissue damage. In this review, we present the overlapping outcomes of cancer inflammation with virus-induced inflammation. The study emphasises how anti-inflammatory drugs that work against cancer inflammation may work against the inflammation caused by the viral infection. It is established that the cytokine storm induced in response to SARS-CoV-2 infection contributes to disease-associated mortality. While cancer remains the second among the diseases associated with mortality worldwide, cancer patients' mortality rates are often observed upon extended periods after illness, usually ranging from months to years. However, the mortality rates associated with COVID-19 disease are robust. The cytokine storm induced by SARS-CoV-2 infection appeared to be responsible for the multi-organ failure and increased mortality rates. Since both cancer and COVID-19 disease share overlapping inflammatory mechanisms, repurposing some anticancer and anti-inflammatory drugs for COVID-19 may lower mortality rates. Here, we review some of these inflammatory mechanisms and propose some potential chemotherapeutic agents to intervene in them. We also discuss the repercussions of anti-inflammatory drugs such as glucocorticoids and hydroxychloroquine with zinc or antiviral drugs such as ivermectin and remdesivir against SARS-CoV-2 induced cytokine storm. In this review, we emphasise on various possibilities to reduce SARS-CoV-2 induced cytokine storm.