Abstract:
COVID-19-infected patients require an intact immune system to suppress viral replication
and prevent complications. However, the complications of SARS-CoV-2 infection that led to death
were linked to the overproduction of proinflammatory cytokines known as cytokine storm syndrome.
This article reported the various checkpoints targeted to manage the SARS-CoV-2-induced cytokine
storm. The literature search was carried out using PubMed, Embase, MEDLINE, and China National
Knowledge Infrastructure (CNKI) databases. Journal articles that discussed SARS-CoV-2 infection
and cytokine storm were retrieved and appraised. Specific checkpoints identified in managing
SARS-CoV-2 induced cytokine storm include a decrease in the level of Nod-Like Receptor 3 (NLRP3)
inflammasome where drugs such as quercetin and anakinra were effective. Janus kinase-2 and signal transducer and activator of transcription-1 (JAK2/STAT1) signaling pathways were blocked by
medicines such as tocilizumab, baricitinib, and quercetin. In addition, inhibition of interleukin (IL)-6
with dexamethasone, tocilizumab, and sarilumab effectively treats cytokine storm and significantly
reduces mortality caused by COVID-19. Blockade of IL-1 with drugs such as canakinumab and
anakinra, and inhibition of Bruton tyrosine kinase (BTK) with zanubrutinib and ibrutinib was also
beneficial. These agents' overall mechanisms of action involve a decrease in circulating proinflammatory
chemokines and cytokines and or blockade of their receptors. Consequently, the actions
of these drugs significantly improve respiration and raise lymphocyte count and PaO2/FiO2 ratio.
Targeting cytokine storms' pathogenesis genetic and molecular apparatus will substantially enhance
lung function and reduce mortality due to the COVID-19 pandemic.
