Patients with COVID-19 have been reported to develop olfactory dysfunction – reduced ability to smell – which can be severe and long-lasting. The cause remains uncertain. A team of experts from HKUMed studied the impact of SARS-CoV-2 infection on the olfactory epithelium (OE) – tissue inside the nasal cavity – in golden Syrian hamsters. This study contributed to the understanding of olfactory dysfunction in COVID-19. Study results were published in Clinical Infectious Diseases, a leading journal.
Key takeaways from the study:
- SARS-CoV-2 readily infected OE of the Syrian hamster when the virus was introduced through the nose. Cell damage was detected 12 hours after infection.
- SARS-CoV-2 infected different types of cells of the OE. The virus protein was detected in the mature and immature olfactory sensory neurons (OSNs), and sustentacular cells – cells that provide energy and physical support to the OSNs.
- SARS-CoV-2 caused cell death in mature OSNs at 2–4 days after infection. Mature OSNs relay smell information from the nasal cavity to the olfactory bulb; hence, damaging these cells may contribute to olfactory dysfunction.
- The basal layer, ie, the innermost layer of the OE involved in replenishing lost skin, appeared to be infected by the virus, indicating that SARS-CoV-2 prevented the olfactory cells from recovering.
- An increased inflammatory response was detected in the OE 2–4 days after infection. Most damage to the OE was observed at 4 days after infection.
- The olfactory bulb, the part that transmits smell information from the nose to the brain, was not infected by SARS-CoV-2.
This study demonstrated that inflammation of the OE, and infection of the OSNs and sustentacular cells by SARS-CoV-2 may explain the olfactory dysfunction that patients with COVID-19 experience.
To read the original article published in Clinical Infectious Diseases, click here.
