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Molecular Mechanism of Black Tea (Camellia sinensis) as SARS-CoV-2 Spike Glycoprotein Inhibitor through Computational Approach
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SARS-CoV-2 infection in humans also causes cytokine storm and can lead to patient death, this condition occurs due to the excessive release of pro-inflammatory cytokines by immune cells. SARS-CoV-2 infects cells in the human respiratory tract. Spike glycoprotein aims to bind to ACE2 in the viral entry process. Several studies have suggested that the SARS-CoV-2 spike is an ideal target for drug design. Camellia sinensis or black tea is a member of the Theaceae family and the genus Camellia. Camellia is a vast genus to East India, the Malay Peninsula, and Southeast Asia, together with Indonesia. In truth, Camellia sinensis is a tropical fruit that has been used as a traditional medicine for hundreds of years globally. This study is to identify the bioactive compounds from Camellia sinensis as an antiviral agent via spike glycoprotein inhibitor mechanisms against the SARS-CoV-2 infection through the in silico approach
Title: Molecular Mechanism of Black Tea (Camellia sinensis) as SARS-CoV-2 Spike Glycoprotein Inhibitor through Computational Approach
Description:
SARS-CoV-2 infection in humans also causes cytokine storm and can lead to patient death, this condition occurs due to the excessive release of pro-inflammatory cytokines by immune cells.
SARS-CoV-2 infects cells in the human respiratory tract.
Spike glycoprotein aims to bind to ACE2 in the viral entry process.
Several studies have suggested that the SARS-CoV-2 spike is an ideal target for drug design.
Camellia sinensis or black tea is a member of the Theaceae family and the genus Camellia.
Camellia is a vast genus to East India, the Malay Peninsula, and Southeast Asia, together with Indonesia.
In truth, Camellia sinensis is a tropical fruit that has been used as a traditional medicine for hundreds of years globally.
This study is to identify the bioactive compounds from Camellia sinensis as an antiviral agent via spike glycoprotein inhibitor mechanisms against the SARS-CoV-2 infection through the in silico approach.
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