In a new study, researchers have found that Epigallocatechin Gallate (EGCG), a component found in Green Tea, is able to block SARS-CoV-2 including the variants of concern (VOC) from binding to human ACE2 receptors and can help prevent infection of human lung cells.
Green tea is known as one of the most consumed beverages in the world, especially in Asia. It has been attributed to have high anti-inflammatory and anti-oxidative properties that could help fight against the risk of developing severe COVID-19 symptoms.
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The team created several pseudoviruses that contained S proteins with a single mutation (K417N, E484K, N501Y, D614G) or with full-set mutations of the newly emerged variants (B.1.1.7, B.1.351, and B.1.429). They transfected the pseudoviruses into HEK293T-hACE2 cells. The wild-type S or D614G S was able to cause infection as observed by increased luciferase activity. Although, convalescent plasma of COVID-19 patients was successful in blocking both of these pseudoviruses.
The transfected cells showed little cytotoxicity to green tea beverages, indicating it was safe to use.
Green tea effectively prevented infection from the wild-type SARS-CoV-2 or D614G and the COVID-19 variants B.1.429 found in California and B.1.351 found in South Africa — in a dose-dependent manner. Researchers also found green tea beverages prevented other coronaviruses’ infection as observed when tested against HCoV OC43 in HCT-8 cells.
The researchers next looked to see what was in green tea that was causing these antiviral effects. Catechins — EGCG, EGC, ECG, and EC — were studied because they are green tea’s active ingredients.
The results showed three catechins: EGCG, EGC, and ECG, dose-dependently blocked a pseudovirus infection caused by the wild-type SARS-CoV-2 strain.
Upon closer inspection, the researchers deduced EGCG as the most potent inhibitor for viral infection. EGCG makes up more than 50% of catechins found in green tea beverages.
In addition, exposing EGCG to mutated strains such as D614G, K417N, E484K, and N501Y suppressed its ability to cause infection.
The researchers also found EGCG inhibited viral infection of cells containing variants of concern, including B.1.17, B.1.351, and B.1.429.
EGCG was tested on infected human lung epithelial cells, where they discovered it could suppress SARS-CoV-2 before and after infection. Although, the inhibitory activity was greater when cells were pretreated with EGCG before SARS-CoV-2 infection.
Catechin’s antiviral activity was also effective in preventing infection from other related coronaviruses. EGCG was the most effective in suppressing HCoV OC43, while EC was the least effective.
EGCG was most effective in stopping the viral entry of SARS-CoV-2 in human cells before infection — although it was also somewhat effective during infection.
The researchers found it blocked viral entry by preventing the S1 subunit — which has the highest binding affinity — to ACE2. EGCG also decreased binding of the S2 subunit, although it already had a little binding affinity to ACE2.
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The study is available as a preprint on the bioRxiv, while the article undergoes peer review.