Systemic diseases and disorders

Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia

“…A possible association between olfactory dysfunction and CoV-2 is consistent with a case report describing a patient with SARS with long term anosmia after recovery from respiratory distress 14 , with the observation that olfactory function is commonly altered after infection with endemic coronaviruses 7,[15][16][17] , and with data demonstrating that intentional experimental infection of humans with hCoV-299E raises the thresholds at which odors can be detected 18 . Although definitive reports of pervasive CoV-2-associated anosmia have not yet been published in the literature (but see 19 ), these collective findings raise the question of how CoV-2 might influence odor processing mechanisms to change smell perception in COVID-19 patients.…”

“…Many possible mechanisms have been proposed through which viruses can alter olfactory function, including inflammation-related deficits in odor conduction and primary damage to the olfactory epithelium 15,16 . Viral injury has been extensively modeled in rodents, which has revealed substantial diversity among viruses (and even within different types of coronaviruses) in the nature and extent of damage to the OE 16,[58][59][60][61] . Intriguingly, infection of the rat with the SDAV coronavirus appears to cause denuding of ciliary cells in the RE, reduction in the number of goblet cells in the RE, and focal infection of subsets of sustentacular cells in the OE.…”

“…However, viral-induced deficits in olfactory function may also be caused by central dysfunction in higher-order olfactory structures. Many viruses, including coronaviruses, have been shown to propagate from the nasal epithelium past the cribriform plate to infect the olfactory bulb and downstream areas like piriform cortex; this form of central infection has been suggested to mediate olfactory deficits, even in the absence of lasting OE damage 16,40,59,61,[67][68][69] . Coronoviral RNA has been identified in the brains of patients, suggesting this possibility as a pathophysiological mechanism in the case of COVID-19 67,70 .…”

Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia

“…Two anosmic patients with COVID-19 have presented with functional magnetic resonance imaging-identified hyperintensity in both OBs that reverted to normal after resolution of the anosmia (58,59), consistent with central involvement in at least some cases. Many viruses, including coronaviruses, have been shown to propagate from the nasal epithelium past the cribriform plate to infect the OB; this form of central infection has been suggested to mediate olfactory deficits, even in the absence of lasting OE damage (60)(61)(62)(63)(64)(65). The rodent coronavirus MHV (mouse hepatitis virus) passes from the nose to the bulb, although rodent OSNs do not express Ceacam1, the main MHV receptor (figs.…”

Olfactory dysfunction from acute upper respiratory infections: relationship to season of onset

“…Olfactory loss can be devastating to patients, significantly altering the flavor of foods and beverages, their nutrition, and their safety. Although loss of smell function can arise from head trauma, 1 exposures to toxic agents, 2 and a number of diseases, 3 including Alzheimer's and Parkinson's, 4 acute viral upper respiratory infections that damage the olfactory neuroepithelium are the major cause of chronic olfactory dysfunction, a condition termed postviral olfactory disorder (PVOD) 5‐7 . Importantly, a number of viruses have the propensity to invade the brain via the olfactory fila 8,9 …”