Are patients with chronic rhinosinusitis with nasal polyps at a decreased risk of COVID‐19 infection?

Abstract

To the Editor: Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) uses the SARS-CoV receptor angiotensinconverting enzyme 2 (ACE2) for entry to the cell and the transmembrane serine protease 2 (TMPRSS2) for S protein priming. 1,2 Higher ACE2 expression was recently reported in nasal compared to throat tissue. 3 In fact, higher SARS-CoV-2 viral load was detected in nasal compared to throat swabs obtained from COVID-19-infected patients. This was attributed to the difference in ACE2 expression between both tissues. 4 Recently, we have also shown that the upper airway expresses more SARS-CoV-2 entry genes, ACE2 and TMPRSS2, compared to the lower airway. 5 Moreover, Hou et al. 6 have recently established that multiciliated cells are the main cell types expressing ACE2 in nasal tissue and infected with SARS-CoV-2. Moreover, Sungnak et al., 7 by analyzing data of single-cell RNA-sequencing from healthy human nasal epithelial cells, showed that ACE2 and TMPRSS2 are co-expressed in nasal epithelium with genes involved in host innate immunity, referring to the potential role of these cells in initiating SARS-CoV-2 infection. Therefore, the level of SARS-CoV-2 receptors in nasal tissue may determine the level of viral infectivity because these receptors are not upregulated following infection. 1 With that in mind, we decided to investigate potential factors that may affect the expression of SARS-CoV-2 receptors and hence the risk of infectivity with COVID-19 in various phenotypes of sinonasal inflammation. To achieve this, gene-expression data sets were used to determine the expression pattern of SARS-CoV-2 cell entry genes, ACE2 and TMPRSS2, in the inflamed uncinate process from patients with chronic rhinosinusitis without nasal polyps (CRSsNPs) and nasal polyps from patients with CRS with nasal polyps (CRSwNP) (see Supplementary

Distinct expression of SARS‐CoV‐2 receptor ACE2 correlates with endotypes of chronic rhinosinusitis with nasal polyps

“…Our findings demonstrated that patients with nonECRSwNP have increased expression of ACE2 in nasal tissues compared to ECRSwNP patients and control subjects, indicating that this might lead to increased susceptibility to SARS‐CoV‐2 infection in nonECRSwNP patients. Analysis with published gene expression data sets also confirmed the up‐regulated expression of ACE2 in nasal tissues of nonECRSwNP compared to ECRSwNP 35 …”

Evaluation of effects of chronic nasal steroid use on rhinological symptoms of COVID-19 with SNOT-22 questionnaire

“…The successful outcomes of systemic and topical steroid treatment for post-viral olfactory dysfunction (PVOD) are reported in the literature, but the level of evidence is low [ 11 ]. Sharif-Askari et al reported downregulating ACE2 expression in the nasal tissues of patients with chronic rhinosinüsitis (CRS) after prolonged use of steroids [ 10 ]. The authors suggested the possible protective effect of steroids during these infections [ 10 ].…”

“…Sharif-Askari et al reported downregulating ACE2 expression in the nasal tissues of patients with chronic rhinosinüsitis (CRS) after prolonged use of steroids [ 10 ]. The authors suggested the possible protective effect of steroids during these infections [ 10 ]. Nasal steroids are frequently used for the treatment of nasal inflammatory diseases such as allergic rhinitis or CRS [ 5 , 15 ].…”

“…SARS-CoV-2 uses the SARS-CoV receptor ACE2 for adhesion and entry to the host cell. Recent studies revealed that ACE2 expression is higher at the nasal mucosa [ 9 , 10 ]. The ACE2 expression in human nasal epithelial cells is significantly suppressed with Dexamethasone, in vitro [ 10 ].…”

“…Recent studies revealed that ACE2 expression is higher at the nasal mucosa [ 9 , 10 ]. The ACE2 expression in human nasal epithelial cells is significantly suppressed with Dexamethasone, in vitro [ 10 ]. Post-viral olfactory dysfunction is a sensorineural disorder and the use of oral or intranasal steroids is a C-level recommendation for the treatment [ 11 ].…”