SARS-CoV-2 virus causes upper and lower respiratory diseases including pneumonia, and in some cases, leads to lethal pulmonary failure. Angiotensin converting enzyme-2 (ACE2), the receptor for cellular entry of SARS-CoV-2 virus, has been shown to protect against severe acute lung failure. Here, we provide evidence that SARS-CoV-2 spike protein S1 reduced the mRNA expression of ACE2 and type I interferons in primary cells of lung bronchoalveolar lavage (BAL) from naïve rhesus macaques. The expression levels of ACE2 and type I interferons were also found to be correlated with each other, consistent with the recent finding that ACE2 is an interferon-inducible gene. Furthermore, induction of ACE2 and type I interferons by poly I:C, an interferon inducer, was suppressed by S1 protein in primary cells of BAL. These observations suggest that the downregulation of ACE2 and type I interferons induced by S1 protein may directly contribute to SARS-CoV-2-associated lung diseases.
【저자키워드】 SARS-CoV-2, ACE2, type I interferon, Spike protein, lung bronchoalveolar lavage, 【초록키워드】 Pneumonia, interferon, lung, SARS-CoV-2 virus, BAL, SARS-CoV-2 spike protein, Lung diseases, Respiratory disease, cellular entry, receptor, rhesus macaques, Evidence, Bronchoalveolar lavage, angiotensin, primary cell, observation, pulmonary failure, expression level, naïve, downregulation, S1 protein, mRNA expression, inducer, lung failure, PROTECT, shown, reduced, contribute, correlated, cause, suppressed, 【제목키워드】 spike, macaque, lavage, Type,