Role of Hypoxia Signalling Pathway in COVID-19 Infection

Abstract

The outbreak of COVID-19 caused by SARS-CoV-2 (severe acute respiratory syndrome) has caused a severe pandemic globally. In 2020 the virus-infected around 56 million people, and 1.5 million people already died due to this fatal atypical pneumonia caused by COVID-19. The respiratory system is mainly affected by COVID-19, although several other organs such as the lung, heart, kidney, and gastrointestinal tract can be affected by SARS-CoV2. Severe illness with COVID-19 infection is common in patients with a history of preexisting chronic diseases such as diabetes, hypertension, or chronic obstructive pulmonary disease (COPD). For example, lung cancer patients are highly vulnerable to COVID-19 infection. This novel SARS- CoV2 virus shares sequence similarities with the previously identified SARS-CoV virus that caused the SARS pandemic in 2002. The genome of SARS-CoV2 shares 79.2% sequence identity to SARS-CoV and approximately 96% identity to the bat coronavirus BatCoV. The COVID-19 infected patients show different types of symptoms ranging from mild to severe acute respiratory distress syndrome (ARDS) and result in pneumonia in the lung, which in severe cases can lead to the death of the patients. ARDS is characterized as an inflammatory response caused by the accumulation of immune cells in the lung. Besides, ARDS COVID-19 mainly impair oxygen supply in the lung and creates local hypoxia. A clear link exists between hypoxia and inflammatory response, and activation hypoxia signalling can induce the expression of several hundred genes known to facilitate the proliferation of inflammatory cells. Therefore, we hypothesized that hypoxia-inducible factor (HIF) might have a potential role in COVID19 infection, and manipulation of components of HIF signalling may offer a potential therapeutic opportunity for the treatment of COVID-19 infection.