Empirical Treatment and Prevention of COVID-19

Abstract

The rapid spread of severe acute respiratory coronavirus syndrome 2 (SARS-CoV-2) in the population and throughout the cells within our body has been developing. Another major cycle of coronavirus disease 2019 (COVID-19), which is expected in the coming fall, could be even more severe than the current one. Therefore, effective countermeasures should be developed based on the already obtained clinical and research information about SARS-CoV-2. The aim of this review was to summarize the data on the empirical treatment of COVID-19 acquired during this SARS-CoV-2 infection cycle; this would aid the establishment of an appropriate healthcare policy to meet the challenges in the future. The infectious disease caused by SARS-CoV-2 is characterized by common cold along with hypersensitivity reaction. Thus, in addition to treating common cold, it is essential to minimize the exposure of cells to the virus and to mitigate the uncontrolled immune response. A proper combination of antiviral agents, immune modulators such as prednisolone, and anticoagulants such as heparin and anti-C5a antagonists could be employed to minimize lung damage and prevent systemic involvements. Finally, strategies to achieve population immunity against SARS-CoV-2 should be developed through understanding of the interaction between the immune system and the virus.

Can Non-steroidal Anti-inflammatory Drugs Affect the Interaction Between Receptor Binding Domain of SARS-COV-2 Spike and the Human ACE2 Receptor? A Computational Biophysical Study

“…The present study provides information about of the possibility of a new mechanistic route of action anti COVID-19 for Ibuprofen by affect the biomacromolecular docking between RBD and ACE2 which is known as relevant for the proliferation of this virus. However, this statement, although it contributes to the described use of NSAIDs for the empirical treatment and prevention of COVID-19 [93], requires its experimental demonstration because our predictions cannot guarantee a pharmacologically and clinically relevant interaction. Therefore, more studies are needed, especially given the real controversy that exists regarding the use of these drugs against COVID-19 [19][20][21][22][23][24][25][26][27].…”

“…Results that show Ibuprofen as one of the few NSAIDs, which, under the conditions described in this research, may have the highest probability of generating an alteration in the stability of the RBD-ACE2 complex and affecting its formation. A result that contributes to the use that has been given to NSAIDs against COVID-19 [93].…”

Binding of raloxifene to human complement fragment 5a (hC5a): a perspective on cytokine storm and COVID19

“…In a recent control study, both coagulation and complement cascade have been targeted together, by recruiting a combination of ruxolitinib, a JAK1/2 inhibitor alongside eculizumab (Giudice et al, 2020 ), an anti-C5 antibody as an alternative therapy to manage the outcome of COVID19. In similar lines, some even hypothesize that a combination of heparin and h C5a antagonist (Shin, 2020 ) can be potentially successful in alleviating the symptoms related to COVID19. Thus, controlling undesired assault of complement is very important and h C5a, which has established itself, both as a chemoattractant and anaphylatoxin can be the perfect candidate.…”

The roles and potential therapeutic implications of C5a in the pathogenesis of COVID-19-associated coagulopathy

“…Moreover, clinical outcomes in eculizumab (an anti-C5a complement mAb)-treated COVID-19 patients showed significant improvements in respiratory symptoms and radiographic pulmonary lesions and a decrease in circulating d -dimer levels [ 65 ]. Currently, clinical trial outcomes also suggest that C5a antagonists, as anticoagulants, could be employed to minimize lung damage and prevent systemic involvement in COVID-19 patients [ 71 ]. Zilucoplan is a small compound composed of a 15-amino acid macrocyclic peptide that binds to C5 with high affinity and specificity [ 72 ].…”