PMC:7309518 / 9864-11656 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7309518","sourcedb":"PMC","sourceid":"7309518","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7309518","text":"l and patient relatives, as in the Wuhan case.7 The series also highlights that GBS peaks 5–10 days after the first COVID-19 symptoms, which in intensive care unit (ICU) settings helps to distinguish GBS from critical illness neuropathy that usually appears later in the course of very sick ICU patients.\n\nSignificance of anosmia/ageusia and other cranial nerve palsies\nThe early manifestation of anosmia and ageusia not only in the present GBS series that often occurred in conjunction with other cranial neuropathies but also in large worldwide cohorts reporting sudden loss of smell and taste early in the infection in up to 60% of COVID-19 carriers5,6,12 is highly informative about COVID-19 neurovirulence or even possible viral entry into the brain. In contrast to commonly reversible anosmia when the non-neural olfactory epithelial cells are virally infected, the often persistent anosmia/ageusia after COVID-19 suggests neurotropism targeting olfactory neurons. SARS-CoV and MERS-CoV, the 2 coronaviruses similar to COVID-19, are neurovirulent and can enter the brain via olfactory nerves.13 In mice, after oronasal infection with SARS-CoV, the virus not only infects epithelial cells of the respiratory tract but also the olfactory receptor neurons in the neuroepithelium gaining access to the olfactory bulb and brainstem.13 These viruses can also enter the CNS via retrograde axonal transport through other cranial nerves, such as trigeminal, which possesses nociceptive neuronal receptors in the nasal cavity, the sensory fibers of the glossopharyngeal, and via peripheral nerves.13 The present GBS series, where oculomotor, trigeminal, and MRI-enhanced facial and nerves roots were concurrently affected, strengthens (but not prove) this notion. Accordingly, it will not be 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