Journal
JOURNAL OF PERSONALIZED MEDICINE
Volume 12, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/jpm12091396
Keywords
anosmia; COVID-19; SARS-CoV-2; RGS2; NAMPT; PTGS2; CXCL8; RNA-sequencing; nasopharyngeal epithelial cells
Funding
- Tel Aviv University Center for Combating Pandemics (TCCP)
- Horizon 2020-Research and Innovation Framework Programme, PSY-PGx
- Edmond J. Safra Center for Bioinformatics at Tel Aviv University
- Koret-UC Berkeley-Tel Aviv University Initiative in Computational Biology and Bioinformatics
- QBI/UCSF-Tel Aviv University joint Initiative in Computational Biology and Drug Discovery
- Israeli Ministry of Defense, Office of Assistant Minister of Defense for Chemical, Biological, Radiological and Nuclear (CBRN) Defense
- Foundation Fighting Blindness
- Collaborative clinical Bioinformatics research of the Edmond J. Safra Center for Bioinformatics
- Faculty of Medicine at Tel Aviv University
- Israeli Ministry of Science and Technology, Israeli-Russia
- Kodesz Institute for Technologies in Healthcare
- Tel Aviv University Healthy Longevity Research Center
- Djerassi-Elias Institute of Oncology
- Canada-Montreal Friends of Tel Aviv University
- Tel Aviv University
- Yonsei University
- Tel Aviv University Innovation Laboratories (TILabs)
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Anosmia, a common symptom in COVID-19 patients, may be caused by downregulation of olfactory receptors and upregulation of RGS2, a key regulator of odorant receptors. Increased expression of RGS2 is also associated with inflammation markers, suggesting its role in driving neurological symptoms of COVID-19.
Anosmia is common in COVID-19 patients, lasting for weeks or months following recovery. The biological mechanism underlying olfactory deficiency in COVID-19 does not involve direct damage to nasal olfactory neurons, which do not express the proteins required for SARS-CoV-2 infection. A recent study suggested that anosmia results from downregulation of olfactory receptors. We hypothesized that anosmia in COVID-19 may also reflect SARS-CoV-2 infection-driven elevated expression of regulator of G protein signaling 2 (RGS2), a key regulator of odorant receptors, thereby silencing their signaling. To test our hypothesis, we analyzed gene expression of nasopharyngeal swabs from SARS-CoV-2 positive patients and non-infected controls (two published RNA-sequencing datasets, 580 individuals). Our analysis found upregulated RGS2 expression in SARS-CoV-2 positive patients (FC = 14.5, Padj = 1.69 x 10(-5) and FC = 2.4; Padj = 0.001, per dataset). Additionally, RGS2 expression was strongly correlated with PTGS2, ILIB, CXCL8, NAMPT and other inflammation markers with substantial upregulation in early infection. These observations suggest that upregulated expression of RGS2 may underlie anosmia in COVID-19 patients. As a regulator of numerous Gprotein coupled receptors, RGS2 may drive further neurological symptoms of COVID-19. Studies are required for clarifying the cellular mechanisms by which SARS-CoV-2 infection drives the upregulation of RGS2 and other genes implicated in inflammation. Insights on these pathway(s) may assist in understanding anosmia and additional neurological symptoms reported in COVID-19 patients.
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