Authors : Syeda Hajra Fatima, Syeda Hajra Fatima, Uzma Viquar, Uzma Viquar, Tasleem Ahmed, Tasleem Ahmed, Munawwar Hussian Kazmi, Munawwar Hussian Kazmi
DOI : 10.18231/j.ijpo.2020.105
Volume : 7
Issue : 4
Year : 2020
Page No : 519-526
A highly infectious outbreak of Coronavirus disease (COVID-19) caused by a new coronavirus - Severe
Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) was first officially reported in December 2019
inWuhan, China which spread rapidly worldwide infecting millions of people in many countries. Although
most of infected patients are asymptomatic or develop mild symptoms that usually recover with good
prognosis, 10-20% of infected people especially old age and those with underlying medical co-morbidity
conditions, develops severe disease with multiple organ failure, primarily respiratory failure and death.
SARS-CoV-2 infection shares similar genetics, pathogenic, epidemiological and clinical features with
two other viruses belonging to same coronavirus family that have caused serious infections over the
last two decades i.e SARS-CoV (Severe Acute Respiratory Syndrome Coronavirus) and MERS-CoV
(Middle East Respiratory Syndrome Coronavirus) and pathogenesis and immune changes observed in
these infections can be applied to this new pandemic in order to learn the imperative role of the immune
system during the course of coronavirus infections and possible use of immunomodulatory intervention
and immunosuppressive drugs in management of severe patients. As the immunopathogenesis of SARSCoV-
2 infection is still not clear and understanding this underlying mechanism which leads to severe form
of disease is important for identifying effective treatment for critically ill patients, this article reviews the
immunopathogenic changes observed in SARS-CoV-2 infection and identify the possible mechanisms by
which it induces immune changes including cytokine storm, in order to provide a reference for the early
clinical identification and management of severe form of COVID-19 infection.
Keywords: COVID-19, SARS-CoV-2, Pathogenesis, Cytokine storm.