SARS-CoV-2 Entry Factors ACE2, TMPRSS2 and FURIN in Salivary Glands From Primary Sjögren's Disease

Abstract

Background

Salivary glands are the reservoir for severe acute respiratory syndrome Coronavirus 2 virus (SARS-CoV-2). It is known that SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2), transmembrane serine protease 2 (TMPRSS2) and FURIN to infect cells. Salivary glands express these entry factors, and it is unclear if these molecules are expressed in salivary glands from primary Sjögren's disease (pSjD). This study assessed ACE2, TMPRSS2, and FURIN gene expression by RT-qPCR in pSjD compared to normal salivary gland and pleomorphic adenoma.

Methods

An integrated study of ACE2, TMPRSS2, and FURIN gene expression across pSjD, pleomorphic adenoma, and normal salivary gland by RT-pPCR was performed. The association between gene expression and clinicopathological data was also examined.

Results

pSjD showed ACE2 upregulation compared with normal salivary gland and pleomorphic adenoma (p < 0.05). TMPRSS2 and FURIN mRNA levels are also higher in pSjD compared to pleomorphic adenoma (p < 0.05). ACE2 expression levels were associated with anti-SSA/SSB positivity (p < 0.05). A strong correlation was observed between TMPRSS2 and FURIN in pSjD (r = 0.768; p = 0.001).

Conclusion

Our analysis revealed a high expression of ACE2 in pSjD. ACE2, TMPRSS2, and FURIN mRNA levels are increased in pSjD in comparison to pleomorphic adenomas. Neither ACE2, TMPRSS2, nor furin was consistently associated with SARS-CoV-2 positivity in pSjD. These findings may guide future investigations on the effects of SARS-CoV-2 in a subset of salivary gland diseases.