Abstract:
The world was brought to a standstill by the rapid spread
of Severe Acute Respiratory Syndrome Coronavirus 2
(SARS-CoV-2), responsible for COVID-19. Initially
recognized in Wuhan, China, in December 2019, it was
announced to be a pandemic. It is known to spread from
person to person via respiratory droplets such as saliva,
cough and sneeze. The infection can be established by the
real-time reverse transcription-polymerase chain reaction
(rRT-PCR) test on the mucosal swabs and by testing the IgG
and IgM on the blood samples. Patients experiencing severe
symptoms are advised to undergo computed tomography
(CT) scans to rule out extensive lung involvement.1
The pathophysiology of respiratory distress in SARS-CoV-
2 is explained by the enveloped nature of the non-segmented
positive-sense RNA virus that mainly expresses various
proteins, primarily the S-protein. The S-protein interacts
with ACE-2 receptors present in the alveolar cells of the
lungs, nasal epithelium, intestinal lining, etc. 2,3 This
interaction causes suppression of ACE-2 receptors, resulting
in potential complications like pulmonary hypertension,
acute lung injury, and lung fibrosis. While many are
asymptomatic from the infection, a large spectrum of the
patient population presents with fever, lethargy, headache,
muscle pains, and diarrhoea. The respiratory viral infection
even manifested as silent hypoxemia, respiratory distress,
and multi-organ failure.3