Abstract
After several months of rapid pandemic expansion, it is now apparent that the SARS-CoV-2 coronavirus interferes with smell and taste sensation in a substantial proportion of COVID-19 patients. Recent epidemiological data documented intriguing differences in prevalence of chemosensory dysfunctions between different world regions. Viral genetic factors as well as host genetic factors appear to be relevant; however, it is not yet known which mutations or polymorphisms actually contribute to such phenotypic differences between populations. Here, we discuss recent genetic and epidemiological data on the D614G spike protein variant and assess whether current evidence is consistent with the notion that this single nucleotide polymorphism augments chemosensory impairments in COVID-19 patients. We hypothesize that this spike variant is an important viral genetic factor that facilitates infection of chemosensory epithelia, possibly acting together with yet to be identified host factors, and thereby increases smell and taste impairment. We suggest that the prevalence of chemosensory deficits may reflect the pandemic potential for transmissibility and spread which differs between populations.
Highlights
The rapid spread of the novel human SARS-CoV-2 coronavirus across the globe is associated with an unexpectedly high incidence of chemosensory deficits in infected patients
No direct evidence has been shown so far, and results of genetic analysis of expression quantitative trait loci indicated that ACE2 tends to have higher expression levels in East Asian populations than in Caucasians, but these data were from lung tissue, not from the nasal olfactory epithelium.[3]
We propose that variants of the spike protein with higher RBD affinity to human ACE2 receptor (hACE2) and/or higher RBD exposure on the virion surface are strong candidates that may enhance SARS-CoV-2 infection in the olfactory epithelium and thereby increase the probability of chemosensory deficits (Figure 1)
Summary
The rapid spread of the novel human SARS-CoV-2 coronavirus across the globe is associated with an unexpectedly high incidence of chemosensory deficits in infected patients. It has been shown that the switch to the G614 variant does not increase the severity of the disease.[5] the chemosensory deficits correlate with the mild rather than severe COVID-19 form.[1] It is established, by using molecular modeling and “wet” experiments, that the D614 to G614 switch increases viral infectivity in vitro and likely increases disease transmissibility.[5,11,15] It should be emphasized that currently no other mutation in the SARS-CoV-2 spike protein with similar functional characteristics and distribution frequency is known, despite the fact that many others were detected and examined.[15] a suspected increase in SARS-CoV-2 infectivity and a faster interindividual spread outside of East Asia appears to be associated with an increase in the incidence of chemosensory dysfunction during the pandemic’s progression.[2] recent studies show that both the G614 variant and a more frequent occurrence of chemosensory deficits correlate with a higher viral load in the upper respiratory tract.[5,16] the above correlations require further experimental confirmation, they do support the scenario that the switch from D614 to G614 in the SARSCoV-2 spike protein may contribute to the increase in prevalence of chemosensory dysfunctions in the COVID-19 pandemic. The usage of appropriate animal models is another strategy to obtain insights about the role of the D614G variant in the incidence of chemosensory dysfunction
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