The spike protein of SARS-CoV-2 is known to enable viral invasion into human cells through direct binding to host receptors including ACE2. An alternate entry receptor for the virus was recently proposed to be basigin/CD147. These early studies have already prompted a clinical trial and multiple published hypotheses of the role of this host receptor in viral infection and pathogenesis. We sought to independently characterize the basigin-spike protein interaction. After conducting several lines of experiments, we report that we are unable to find evidence supporting the role of basigin as a putative spike-binding receptor. Recombinant forms of both the entire ectodomain and S1 domain of the SARS-CoV-2 spike protein that directly bind ACE2 do not interact with basigin expressed on the surface of human cells. Using specialized assays tailored to detect receptor interactions as weak or weaker than the proposed basigin-spike binding, we report no evidence for direct binding of the viral spike to either of the two common isoforms of basigin. Given the pressing need for clarity on which targets of SARS-CoV-2 may lead to promising therapeutics, we present these findings to allow more informed decisions about the translational relevance of this putative mechanism in the race to understand and treat COVID-19.

中文翻译：

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没有证据表明basigin / CD147是直接的SARS-CoV-2尖峰结合受体

已知SARS-CoV-2的突触蛋白可通过直接结合包括ACE2的宿主受体使病毒侵入人细胞。最近提出了该病毒的另一种进入受体是basigin / CD147。这些早期研究已经促进了该宿主受体在病毒感染和发病机理中的作用的临床试验和多种已发表的假设。我们试图独立表征basigin穗蛋白相互作用。在进行了几行实验后，我们报告我们无法找到支持basigin作为假定的刺突结合受体作用的证据。直接结合ACE2的SARS-CoV-2突突蛋白的完整胞外域和S1域的重组形式不与在人细胞表面表达的basigin相互作用。使用专门的检测方法来检测受体相互作用比拟议的basigin-spike结合弱或弱，我们报告没有证据表明病毒刺突直接与basisin的两种常见同工型直接结合。鉴于迫切需要明确SARS-CoV-2的哪些靶标可能导致有希望的治疗方法，我们提出这些发现，以便就这种推定机制在理解和治疗COVID-19竞赛中的翻译相关性做出更明智的决定。