Abstract
Viral infections have already been implicated with otitis media and sudden sensorineural hearing loss. However, the pathophysiology of COVID-19 as it relates to otologic disorders is not well-defined. With the spread of SARS-CoV-2, it is important to evaluate its colonization of middle ear mucosa. Middle ear and nasal tissue samples for quantitative RT-PCR and histologic evaluations were obtained from post-mortem COVID-19 patients and non-diseased control patients. Here we present evidence that SARS-CoV-2 colonizes the middle ear epithelium and co-localizes with the primary viral receptor, angiotensin-converting enzyme 2 (ACE2). Both middle ear and nasal epithelial cells show relatively high expression of ACE2, required for SARS-CoV-2 entry. The epithelial cell adhesion molecule (EpCAM) was use as a biomarker of epithelia. Furthermore, we found that the viral load in the middle ear is lower than that present in the nasal cavity.
Highlights
COVID-19 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been linked to acute otitis media (OM) [1], as well as longer term otologic sequelae including hearing loss and tinnitus [2]
SARS-CoV-2 RNA expression in the middle ear (ME) and the nasal cavity are overall increased in COVID-19 subjects compared to non-infected patients control tissue, with higher expression in the nasal cavity compared to the ME (Fig. 1)
Histological evaluations of tissue from patients P4, P5 and P6 all showed that expression of SARS-CoV-2 was found in both the ME and nasal septum which co-localized with angiotensin-converting enzyme 2 (ACE2) expression (Fig. 2)
Summary
COVID-19 caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been linked to acute otitis media (OM) [1], as well as longer term otologic sequelae including hearing loss and tinnitus [2]. Other respiratory viruses are known to cause OM through increased susceptibility to bacterial OM or, less commonly, direct viral infection of the middle ear (ME) [4, 5]. The nasal cavity is a known viral entry site, there is little data as to whether the mucosal epithelium lining the ME is infected and if so, the resulting clinical implications. More information is needed regarding ME colonization, viral distribution, the potential ME effects of COVID-19 and its relationship to viral infection in the nasal cavity
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