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Clinical and epidemiological context of COVID-19
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Viswanthram Palanivel, Akanksha Salkar, Radha Yadav, Renuka Bankar, Om Shrivastav, Arup Acharjee
Some of the antiviral therapies which physicians predominantly use are as follows: Targeting viral entry (fusion inhibitors) Baricitinib, a potent Janus kinase (JAK) inhibitor, binds to AP2-associated protein kinase 1. It inhibits both host inflammatory response and viral entry (Zhang et al. 2020).Camostat mesylate is a TMPRSS2 protease inhibitor that blocks the SARS-CoV-2 infection of lung cells (Hoffmann et al. 2021).Targeting virus replication Reverse transcription inhibitors: Remdesivir is an RNA-dependent RNA polymerase (RdRp) inhibitor and is a broad-spectrum antiviral drug against the significant class of single-stranded RNA (ssRNA) viruses (Amirian and Levy 2020).Nucleotide analogs: Favipiravir is a purine (Guanine) analog. It blocks the RdRp to arrest viral RNA synthesis (Furuta, Komeno, and Nakamura 2017). Ribavirin is a guanine derivative analog. It destabilizes viral RNA by inhibiting RNA capping.Protease inhibitors Lopinavir: Lopinavir inhibits the main protease (MPro) of SARSCoV-2. It is used as a lopinavir–ritonavir combination, which shows high efficiency. Primarily, it is an HIV antiviral drug (Nutho et al. 2020).
COVID-19;-The origin, genetics,and management of the infection of mothers and babies
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hassan Ih El-Sayyad, Yousef Ka Abdalhafid
Remdesivir is a broad-spectrum antiviral drug that was developed by the biopharmaceutical company Gilead Sciences used for the treatment of Ebola and coronaviral infections through inhibiting replication by RNA-dependent RNA polymerase [119]. The mechanism of action comes from the structure of RdRp-Remdesivir complex indicating that the partial double-stranded RNA template is inserted into the central channel of RdRp where Remdesivir is covalently incorporated into the primer strand at the first replicated base pair, thus terminating chain elongation [120]. Once incorporated the inhibitor arrest RNA synthesis at position i3 [121].Timothy et al. [122] observed a potent inhibition in MERS-CoV replication with EC50 of 0.09 mM, with no observable cytotoxicity up to 10 mM in primary human lung epithelial cell cultures.