PMC:7214327 / 1499-4004 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7214327","sourcedb":"PMC","sourceid":"7214327","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7214327","text":"One of these drugs is remdesivir (RDV), which shows a broad spectrum of anti-viral activity against many viruses like Ebola (4,5), Nipah (6, 7, 8), respiratory syncytial virus (RSV) family (8) and a diverse category of coronaviruses including SARS CoV and MERS CoV (9). Remdesivir is a nucleotide analogue (4), and the triphosphate form of RDV, i.e., RDV-TP is being used as a substrate for many viral RNA-dependent RNA polymerase (RdRp) complexes and it has been reported to inhibit the viral RNA synthesis by a specific mechanism of delayed chain termination for all three coronaviruses (MERS-CoV, SARS-CoV and SARS-CoV-2) RdRp (10). It has been observed that RDV-TP resembles specifically Adenosine triphosphate (ATP) molecule and competes with the nucleotide during the viral RNA synthesis (Figure 1 ). It has been reported that 3′ hydroxyl group of RDV-TP forms a phosphodiester bond with the next nucleotide but it terminates the formation of viral RNA synthesis at 3 nucleotides downstream, precisely at i + 3 position, whereas the RDV-TP is the i-th position. Moreover, it has also been fascinating to note that the underlying mechanism of chain termination is more or less common in many viruses including all the recent coronaviruses, namely MERS-CoV, SARS-CoV and SARS-CoV-2, though the precise molecular mechanism remains elusive. Additionally, it has been reported very recently that the main reason of chain termination at i + 4 position is due to a steric clash between 1′-CN substituent of the incorporated RDV-TP and a specific residue S861 (10). It is consistent with the chain termination at i + 3 position due to the imposed inability of RdRp to translocate a single position downstream, so eventually it terminates the nascent viral RNA synthesis. Moreover, it has also been imperative to note that this serine residue is conserved in all coronaviruses. Though, the actual molecular mechanism is still not very clear but this could be a plausible explanation of termination viral RNA synthesis. Recently, scientists also expressed RdRp of different viruses and measure kinetic parameters to infer its interaction with RDV-TP and also determined a score of 0.77 mmol half maximal concentration against SARS-CoV-2 (11).\nFigure 1 Probable molecular mechanism of Remdisivir against SARS-CoV- 2. (A) Thematic diagram shows the SARS-CoV-2 viral entry and its RNA synthesis which can be block by Remdisivir. (B) Detail molecular mechanism of Remdisivir to inhibit the synthesis of viral 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