Pathophysiology of SARS-CoV-2 (COVID 19) viral infection

Abstract

The city of Wuhan located in Hubei province of central China was burdened with a series of cases presenting with atypical acute respiratory infections in December 2019. Little did people know at that point in time, that a novel virus known as SARS-CoV-2 (COVID-19) or simply corona virus, was responsible for these peculiar presentations. COVID-19 had begun spreading at an alarming rate worldwide, eventually gaining official status as a global pandemic, as affirmed by the World Health Organisation (WHO) on 11 March 2020. By 6 July 2020, globally, there were 1.5 million cases and around 536 893 deaths. As the pandemic took its toll globally, scientists struggled to classify and specify the manifestations of the virus. Medical practitioners, microbiologists and scientists worldwide gradually joined forces to define COVID-19 as an infection characterised by an immense inflammatory reaction or cytokine storm which may cause acute respiratory distress syndrome (ARDS) and multi-organ dysfunction (MODS). During the latter half of 2020, multiple hospitals in India, France, America, Germany and Netherlands reported an increasing incidence of fatal invasive fungal infections in recovered SARS-CoV-2 patients. Increased severity of infections as well as mortality was observed in immunocompromised patients and those with co existing medical illnesses such as diabetes and hypertension. Furthermore, even though many patients recovered from SARS-CoV-2 infection, it was noted that their immunity post recovery was significantly diminished, and it was during this period they were more susceptible to fatal bacterial and fungal co-infections. This review article explores the pathophysiology of COVID 19 infection and difference in response to the infection in adult and paediatric populations.