Like severe acute respiratory syndrome coronavirus (SARS-CoV), human coronavirus (HCoV)- NL63 employs angiotensin-converting enzyme 2 (ACE2) as a receptor for cellular entry. SARSCoV infection causes robust downregulation of cellular ACE2 expression levels and it has been suggested that the SARS-CoV effect on ACE2 is involved in the severity of disease. We investigated whether cellular ACE2 downregulation occurs at optimal replication conditions of HCoV-NL63 infection. The expression of the homologue of ACE2, the ACE protein not used as a receptor by HCoV-NL63, was measured as a control. A specific decrease for ACE2 protein level was observed when HCoV-NL63 was cultured at 34 6C. Culturing the virus at the suboptimal temperature of 37 6C resulted in low replication of the virus and the effect on ACE2 expression was lost. We conclude that the decline of ACE2 expression is dependent on the efficiency of HCoV-NL63 replication, and that HCoV-NL63 and SARS-CoV both affect cellular ACE2 expression during infection. © 2012 SGM.
download 🔖 [BibTeX]