Research that shows Interaction of SARS-Cov-2 Spike Protein to CD147 in COVID-19 Associated Lymphopenia











Dr. Mohamed Helal and his team at the Drug Design lab, in collaboration with Dr. Nagwa El-Badri and her team at the Center of Excellence for Stem Cells and Regenerative Medicine (CESC) have published a paper entitled ''Molecular Basis of the Potential Interaction of SARS-Cov-2 Spike Protein to CD147 in COVID-19 Associated Lymphopenia' in the Journal of Biomolecular Structure and Dynamics.  

Lymphopenia is considered one of the most characteristic clinical features of the coronavirus disease 2019 (COVID-19). Angiotensin-converting enzyme 2, ACE-2 receptor, has been proved to be the entry point of SARS-CoV-2 into the lungs and other types of human cells. However, T lymphocytes are rarely expressing this receptor. Therefore, a novel receptor might be involved in the entry of SARS-CoV-2 into T cells. Several recent studies have suggested that CD147 is a probable route for SARS-CoV-2 invasion into certain host cells. CD147 (also known as Basigin) is a transmembrane glycoprotein that was originally identified in 1992 as a T lymphocyte activation-associated antigen. We employed docking and MD simulation to investigate this possibility. Our model shows interaction of CD147 C-terminal domain within a groove in the SARS-CoV-2 spike external subdomain, followed by membrane fusion and viral entry. This model provides an appreciation for targeting CD147 for adjuvant drug therapy strategies, to improve the prognosis of COVID-19 patients. Our data is supported by the results of using Meplazumab, an anti-CD147 humanized antibody, for viral clearance and lymphocyte count normalization. The mechanisms proposed in our study encourage research on CD147 involvement in SARS-CoV-2 in direct invasion to T lymphocytes and associated lymphopenia.