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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Death+Differ 2021 ; 28 (9): 2765-2777 Nephropedia Template TP
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SARS-CoV-2 spike protein dictates syncytium-mediated lymphocyte elimination #MMPMID33879858
Zhang Z; Zheng Y; Niu Z; Zhang B; Wang C; Yao X; Peng H; Franca DN; Wang Y; Zhu Y; Su Y; Tang M; Jiang X; Ren H; He M; Wang Y; Gao L; Zhao P; Shi H; Chen Z; Wang X; Piacentini M; Bian X; Melino G; Liu L; Huang H; Sun Q
Cell Death Differ 2021[Sep]; 28 (9): 2765-2777 PMID33879858show ga
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus is highly contagious and causes lymphocytopenia, but the underlying mechanisms are poorly understood. We demonstrate here that heterotypic cell-in-cell structures with lymphocytes inside multinucleate syncytia are prevalent in the lung tissues of coronavirus disease 2019 (COVID-19) patients. These unique cellular structures are a direct result of SARS-CoV-2 infection, as the expression of the SARS-CoV-2 spike glycoprotein is sufficient to induce a rapid (~45.1 nm/s) membrane fusion to produce syncytium, which could readily internalize multiple lines of lymphocytes to form typical cell-in-cell structures, remarkably leading to the death of internalized cells. This membrane fusion is dictated by a bi-arginine motif within the polybasic S1/S2 cleavage site, which is frequently present in the surface glycoprotein of most highly contagious viruses. Moreover, candidate anti-viral drugs could efficiently inhibit spike glycoprotein processing, membrane fusion, and cell-in-cell formation. Together, we delineate a molecular and cellular rationale for SARS-CoV-2 pathogenesis and identify novel targets for COVID-19 therapy.