Abstract
Due to the rapid spread of the SARS-CoV-2 virus, many health systems worldwide are overwhelmed, leading to the triggering of the scarcity of medical resources. The identification of indicators that require hospital admission help in the efficient allocation of medical resources. Olfactory impairment is also one of the indicators of COVID-19 infection. Many studies have analyzed olfactory dysfunction in COVID-19 with a variable prevalence rate but underreporting of this problem is very much likely as the problem is considered benign. Many scientific societies have stated that olfactory dysfunction is a frequent symptom of COVID-19 and have published recommendations for it.
Highlights
The COVID-19 is an ongoing viral pandemic that started in December 2019 from Wuhan, Hubei province, China, and quickly spread to the rest of the world.[1]
This review summarizes various studies' findings on olfactory dysfunction during the COVID-19 pandemic, its pathophysiology, and strategies to cope with this problem
Chemosensitive disorders like loss of olfaction is a frequent symptom of COVID-19 patients
Summary
The COVID-19 is an ongoing viral pandemic that started in December 2019 from Wuhan, Hubei province, China, and quickly spread to the rest of the world.[1]. In 2006, Hwang et al described a case of anosmia that persisted for two years post-SARS infection.[25] In 2001, Schwob et al and Youngentob et al, on examining the olfactory bulb of SARS-CoV patients, found an abnormal predominance of immature neurons, indicating accelerated turnover of cells.[26,27] This reduction in neurons' lifespan is due to the loss of trophic support supplied by the olfactory bulb to the sensory neurons.[26,27] In 2008, Netland et al hypothesized that neuronal death in SARS-CoV infection occurs due to the production of interleukin-6 (IL-6) under the stimulation of viral N-spike protein.[28] various COVID-19 case series report a high recovery rate of olfactory function within two weeks of infection.[18,29,30] In addition to this, the frequency of central nervous system symptoms is much lower than SARS-CoV infection This suggests that the target of the COVID-19 virus may not be neurons but other supporting cells that express ACE-2 receptors like sustentacular cells, microvillar cells, Bowman's gland cells, horizontal basal cells, and olfactory bulb pericytes.[31]. SARS-CoV virus showed transneuronal penetration through the olfactory bulb in mouse models resulting in the rapid intracranial spread.[32]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
