Adding to its long list of health benefits, new research finds antiviral activity from green tea. In a new study, one of its constituents, epigallocatechin gallate (EGCG), inhibited acute respiratory coronavirus 2 (SARS-CoV-2) syndrome from binding to human angiotensin-converting enzyme 2 (ACE2) receptors and it can prevent human infection. lung cells. This activity was also observed in the SARS-CoV-2 (VOC) anxiety variables.
Green tea is one of the worst drinks in many countries across Asia. It has high anti-inflammatory and anti-oxidative properties that may help reduce the risk of developing severe COVID-19 symptoms.
The researchers wrote:
Taken together, our data as well as the findings are just reported by others[48-50] indicate the potential consumption of green tea or the active ingredient EGCG beneficial for preventing or reducing the transmission and infection of SARS-CoV-2… Due to its low toxicity, antiinflammation, antioxidant, and anti-inflammatory properties -SARS-CoV-2, use of GTB or EGCG tends to reduce SARS-CoV-2 transmission, mitigation symptoms and disease depth. ”
The study “Epigallocatechin Gallate from Green Tea Effectively Blocks Infection of SARS-CoV-2 and New Variants by blocking spike binding to ACE2 receptor” is available as a preview of the bioRxiv* server, while the article is under peer review.
Design of the research study
The team created several pseudoviruses containing S mutations with a single mutation (K417N, E484K, N501Y, D614G) or with mutations of a complete set of the newly emerged variants (B.1.1.7, B.1.351, and B.1.429). They translocated the pseudoviruses into HEK293T-hACE2 cells. The wild-type S or D614G S was able to cause infection as seen with increased luciferase activity. Although, convalescent plasma of COVID-19 patients was successful in inhibiting both of these pseudoviruses.
The transplanted cells did not show much cytotoxicity to green tea drinks, indicating that it was safe to use.
Viral inhibition caused by green tea drink
Green tea effectively prevented infection from the wild-type SARS-CoV-2 or D614G and the COVID-19 B.1.429 strains found in California and B.1.351 found in Africa South – in a dose-dependent manner. Researchers also found that green tea drinks prevented other coronaviruses infection as seen when tested against HCoV OC43 in HCT-8 cells.
The researchers then looked to see what green tea was causing these antiviral effects. Catechins – EGCG, EGC, ECG, and EC – have been studied because they are green tea active ingredients.
The results showed three catechins: EGCG, EGC, and ECG, a dose-dependent pseudovirus infection caused by the wild-type SARS-CoV-2.
After closer inspection, the researchers identified EGCG as the most powerful protector for viral infection. EGCG makes up over 50% of catechins found in green tea drinks.
Furthermore, exposure to EGCG to trivalent rays such as D614G, K417N, E484K, and N501Y undermined its ability to cause infection.
The researchers also found that EGCG inhibited viral infection of cells that contained changes of concern, including B.1.17, B.1.351, and B.1.429.
EGCG was tested on human lung epithelial cells, where they found that it could suppress SARS-CoV-2 before and after infection. Although, the inhibitory activity was greater when cells were predicted by EGCG prior to SARS-CoV-2 infection.
Catechin’s antiviral activity was also effective in preventing infection from other associated coronaviruses. EGCG was the most effective in the elimination of HCoV OC43, and EC was the lowest effective.
EGCG inhibits inhibition by ACE2 receptor binding binding to SARS-CoV-2
EGCG was most effective in inhibiting the viral entry of SARS-CoV-2 into human cells prior to infection – although it was also somewhat effective at the time of infection.
The researchers found that it inhibited viral entry by blocking the S1 subunit – which has the highest binding affinity – to ACE2. EGCG also reduced S2’s underground binding, although it already had some binding to ACE2.
The researchers concluded:
We found that the recombinant RBD could bind to ACE2 with an EC50 of 4.08 ng / mL, while EGCG significantly reduced the RBD binding affinity (4.7-fold) with EC50 of 19.19 ng / mL. In addition, EGCG reduced the full-length binding affinity of S to ACE2 by 2.5-fold (EC50: 43.48 to 107.6 ng / mL). The inhibitory effect of EGCG on RBD or full-length S was associated with ACE2-dependent doses. ”
* Important message
bioRxiv publish preliminary scientific reports that are not peer-reviewed and, therefore, should not be seen as final, guiding health-related clinical practice / behavior, or be treated as information established.