Goblet Cells in SARS-CoV-2 Pathogenesis |Biomedgrid

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, a causative agent of coronavirus disease 2019, COVID-19) cellular tropism depends on its receptor-binding specificity. Therefore, the answer for why SARS-CoV-2 is more transmissible than SARS-CoV may find in the expression of the entry receptor angiotensin-converting enzyme II (ACE2) on host cells. SARS-CoV-2 spike protein shows ten times more affinity in binding ACE2 than does SARS-CoV [1]. For successful SARS-CoV-2 entry, spike protein priming is required by a host cell co-factor transmembrane serine protease 2 (TMPRSS2) [2]. Thus, cells with high ACE2 and TMPRSS2 expression are more susceptible to SARS-CoV-2. Previously, RNA-seq based studies suggested that both ACE2 and TMPRSS2 predominately express by the secretory cells in the respiratory system [3-5]. Recent studies suggest that mucus-secreting goblet cells are permissive to SARS-CoV-2 infection [6-8].