What is it about?
Three main hypothesis can be advanced regarding the dysosmia of infected subjects: • Hypothesis 1: the impairment is caused by the nasal blockage after the pooling of blood in the capacitance vessels upon viral upper respiratory infection. Smell impairment is known to be associated with nasal congestion and the mucosal swelling easily impedes the physical access of odors to the olfactory region. • Hypothesis 2: olfactory receptors in the neuroepithelium are disrupted upon excessive local inflammatory responses. In fact, it was suggested that the olfactory function could be independent of nasal congestion, but subjected to recovery after the viscous phase onset. • Hypothesis 3: dysosmia follows a direct viral insult by the virus because of the peripheral destruction of olfactory receptor cells. If this is the case, it is also probable that the virus can invade the central nervous system through the retrograde axonal transport from the olfactory neuroepithelium and olfactory pathways.
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Why is it important?
Strong evidence supports the notion that respiratory viruses are neurotropic and can access the central nervous system via peripheral nerves, including the olfactory bulb. SARS-CoV-2 shares similar infection pathways compared to its predecessors and therefore the infection mechanisms previously found for other coronaviruses may also be applicable for this new strain. It is urgent to discuss whether SARS-CoV-2 can gain access to the central nervous system through a nasal-nervous pathway or other routes and if the fatal respiratory failure may be associated with a neuronal injury in critical brain areas of the host.
Read the Original
This page is a summary of: Disentangling the Hypothesis of Host Dysosmia and SARS-CoV-2: The Bait Symptom That Hides Neglected Neurophysiological Routes, Frontiers in Physiology, June 2020, Frontiers, DOI: 10.3389/fphys.2020.00671.
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