Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, has become a major threat to the global public health and economy [1, 2]. While the majorities of SARS-CoV-2 infected individuals only suffer mild or moderate symptoms, unfortunately, some patients develop severe chronic respiratory diseases (CRDs) and have to be admitted to intensive care units [3, 4]. When the lungs of CRDs patients were analyzed histologically, many of them possess multinucleate pneumocytes. Two independent studies from the Mauro Giacca group and the Qiang Sun group, which were just published in Nature and Cell Death and Differentiation, provided critical insights into the causes and consequences of syncytia during SARS-CoV-2 infections [5, 6].

Syncytia are evolutionarily conserved cellular structures form by the multiple cell fusions of uninuclear cells. In mammals, the best example of physiological syncytia is muscle fibers, which contain thousands of fused muscle cells to allows their rapid coordinated contraction [7]. It is also important in the decidualization process during embryo implantation [8]. Syncytia can also be induced by certain types of infections by viruses, such as human immunodeficiency virus, respiratory syncytial virus, and herpes simplex virus [9]. It could be envisioned that virus-induced cell fusion facilitates the transfer of viral genomes to the neighboring cells. However, the viral and cellular mechanisms regulating the formation of syncytia during SARS-CoV-2 infection remains largely elusive.

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