Abstract

To date, there have been rapidly spreading new SARS-CoV-2 “variants of concern”. They all contain multiple mutations in the ACE2 receptor recognition site of the spike protein, compared to the original Wuhan sequence, which is of great concern, because of their potential for immune escape. Here we report on the efficacy of common dandelion (Taraxacum officinale) to block protein–protein interaction of SARS-COV-2 spike to the human ACE2 receptor. This could be shown for the wild type and mutant forms (D614G, N501Y, and a mix of K417N, E484K, and N501Y) in human HEK293-hACE2 kidney and A549-hACE2-TMPRSS2 lung cells. High-molecular-weight compounds in the water-based extract account for this effect. Infection of the lung cells using SARS-CoV-2 spike D614 and spike Delta (B.1.617.2) variant pseudotyped lentivirus particles was efficiently prevented by the extract and so was virus-triggered pro-inflammatory interleukin 6 secretion. Modern herbal monographs consider the usage of this medicinal plant as safe. Thus, the in vitro results reported here should encourage further research on the clinical relevance and applicability of the extract as prevention strategy for SARS-CoV-2 infection in terms of a non-invasive, oral post-exposure prophylaxis.

Highlights

  • In late 2019, the disease known as Corona Virus Disease 2019 or COVID-19 was first reported [1]

  • The aim of this study was to investigate whether T. officinale aqueous leaf extracts and its high molecular weight components block the interaction of

  • Metabolomics-based fingerprinting of T. officinale and Cichorium intybus L., leaf extract was performed by untargeted Ultra-Performance Liquid Chromatography (UPLC)-TOF-MS analysis (Figure 1) and putative metabolite identification was done by database search of accurate mass and MSe fragmentation patterns

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Summary

Introduction

In late 2019, the disease known as Corona Virus Disease 2019 or COVID-19 was first reported [1]. It is induced by the severe acute respiratory syndrome coronavirus 2. The S2 subunit plays a key role in mediating virus–cell fusion and in concert with the host transmembrane protease serine subtype 2 (TMPRSS2), promotes cellular entry [3]. This interaction between the virus and host cell at entry site is crucial for disease onset and progression

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