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PRINT ISSN : 2319-7692
Online ISSN : 2319-7706 Issues : 12 per year Publisher : Excellent Publishers Email : editorijcmas@gmail.com / submit@ijcmas.com Editor-in-chief: Dr.M.Prakash Index Copernicus ICV 2018: 95.39 NAAS RATING 2020: 5.38 |
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is enveloped, single-stranded, positive- sense RNA virus which is responsible for coronavirus disease 2019 (COVID-19) characterized by pulmonary infection in humans. Effective prophylactic and therapeutic management for COVID-19 are urgently required to control this pandemic. Angiotensin-converting enzyme 2 (ACE2) is the receptor for SARS-CoV-2 in host cell. Spike protein of virus bindswith the peptidase domain of ACE2 receptor. After binding with the receptor the next step of virus is to gain entry to the host cell cytosol which is accomplished by the proteolyti cleavage of S protein in acidic pH. The proteolytic cleavage is followed by fusion of SARS-CoV-2 and its host cell membrane leading to release of the viral genomeinto the cytoplasm. The anti-malarialdrug chloroquine and its analog hydroxy-chloroquine are known to restrict viral replication by increasing endosomal pH which inhibits viral-cell fusion. After uncoating, viral RNA genome is translated to form structural viral protein with the help of RNA-dependent RNA polymerase (RdRp), which is the target for adenosine analogue remdesivir. The combination therapy including Remdesivir and chloroquine are exceptionally successful in the control of 2019-nCoV disease in vitro. Fundamental preliminaries of Remdesivir and chloroquine repurposing in the treatment of COVID-19 have been empowering, prompting a few new trials. In this review, pathogenesis of the SARS-CoV-2 and the potential mechanism of two potent inhibitors remdesivir and chloroquine as effective therapeutic agents against COVID-19 are described.