Researchers provide ultrastructural details of SARS-CoV-2-infected respiratory epithelial cells
A team of scientists from the United Kingdom recently investigated the ultrastructural details of the attachment, entry, and budding processes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the human airway epithelium. They have used a highly differentiated air-liquid interface cultures of airway epithelium to thoroughly investigate the viral infection cycle. The study is currently available on the
Background
SARS-CoV-2, the causative pathogen of coronavirus disease 2019 (COVID-19), is an enveloped RNA virus belonging to the Coronaviridae family. The virus primarily attacks human airway epithelial cells to initiate infection. Mechanistically, the receptor-binding domain (RBD) of the S1 subunit of the viral spike glycoprotein binds to angiotensin-converting enzyme 2 (ACE2), which is ubiquitously expressed at the apical surface of host airway epithelial cells. This is followed by proteolytic cleavage of the spike S1/S2 subunit by a serine protease TMPRSS2 present within airway epithelial cells. This leads to dissociation of the S1 subunit and a conformational alteration in the S2 subunit to generate a post-fusion state of the spike protein, which in turn is necessary for the fusion of the viral envelope to the epithelial cell plasma membrane. Upon fusion, the viral components are released from the viral lumen into the host cell cytoplasm to initiate viral replication.