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Chloroquine Is a Potent Inhibitor of SARS Coronavirus Infection and Spread (Also Inhibits SARS-COV-2 COVID-19)

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Chloroquine Is a Potent Inhibitor of SARS Coronavirus Infection and Spread

Conclusion: Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.

Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding

When the protein sequence of the SARS-CoV-2 receptor binding site was analyzed, an interesting result was found. While SARS-CoV-2 is overall more similar to bat coronaviruses, the receptor binding site was more similar to SARS-CoV.

2019-nCoV is sufficiently divergent from SARS-CoV to be considered a new human-infecting betacoronavirus. Although our phylogenetic analysis suggests that bats might be the original host of this virus, an animal sold at the seafood market in Wuhan might represent an intermediate host facilitating the emergence of the virus in humans. Importantly, structural analysis suggests that 2019-nCoV might be able to bind to the angiotensin-converting enzyme 2 receptor in humans. The future evolution, adaptation, and spread of this virus warrant urgent investigation.

PROOF – Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein

Both SARS-CoV-2 and SARS-CoV use the same host cell receptor. It also found that, for both viruses, the viral proteins used for host cell entry bind to the receptor with the same tightness (affinity).
Knowledge is power.

SARS-CoV-2 Recognizes hACE2 with Comparable Affinity to SARS-CoV

The binding affinity of SARS-CoV for hACE2 correlates with the overall rate of viral replication in distinct species as well as with transmissibility and disease severity (Guan et al., 2003, Li et al., 2004, Li et al., 2005c, Wan et al., 2020). Indeed, specific SB mutations enabled efficient binding to hACE2 of SARS-CoV isolates from the three phases of the 2002–2003 epidemic, which were associated with marked disease severity (Consortium, 2004, Kan et al., 2005, Li et al., 2005c, Sui et al., 2004). In contrast, SARS-CoV isolates detected during the brief 2003–2004 re-emergence interacted more weakly with hACE2 and had low pathogenicity and transmissibility (Consortium, 2004, Kan et al., 2005, Li et al., 2005c).

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