September 27th, 2021
23 and Me has been working hard behind the scenes to obtain some solid scientific genetic evidence behind COVID risk.
In two studies published in MedRxIV over the past year, we see evidence based on over 1,000,000 gene analysis that blood type, ethnicity and metabolic risk factors are associated with a worse outcome. Blood group O is protective while A, as discussed in other studies, may be deleterious for health. The mechanism behind this effect is still up for debate.
Being of a minority group, especially African American, carries a higher disease severity burden above the increased risk based on socioeconomic risks and antecedent metabolic disease burden compared to caucasian and hispanic populations. Further research needs to look at these data sets to identify cause and effect. Finally, they reaffirmed that metabolic diseases obesity and diabetes confer significant risk increases. The take home from this data set is that identified risk factors for severe disease should be discussed with the at risk groups to further encourage vaccination and lifestyle alterations.
Study number two looked at the genetic loci for smell and taste changes. "We ran a trans-ethnic genome-wide association study (GWAS) comparing loss of smell or taste (n=47,298) with no loss of smell or taste (n=22,543) among those with a positive SARS-CoV-2 test result. We identified an association (rs7688383) in the vicinity of the UGT2A1 and UGT2A2 genes, which have been linked to olfactory function. These results may shed light on the biological mechanisms underlying COVID-19 related anosmia."
The mechanism hypothesis is below for those interested.
The take home is that over time genetic analysis can shed light on risk and help to target populations at risk for certain undesirable outcomes from a particular disease. 23 and Me is a private company with a 10,000,000 person genome database that is ripe for data mining based on risk. The future is here.
Consider becoming an active member of the platform for genomic understanding. (Full disclosure - I own the stock because I believe in the technology)
Dr. M
Shelton MedRxIV
Shelton MedRxIV
"While many mechanistic explanations have been proposed for the COVID-19-related loss of smell, experimental studies suggest that the loss of smell is related to damage to the cilia and olfactory epithelium, but not infection of the olfactory neurons. For example, in an experiment where hamsters were nasally infected with SARS-CoV-2, the olfactory epithelium and cilia became very damaged, which can completely inhibit the ability to smell, but no infection was observed in the olfactory neurons. Recent evidence suggests that SARS-CoV-2 enters and accumulates in olfactory support cells, specifically, sustentacular cells, which abundantly express the viral entry proteins ACE2 and TMPRSS2 unlike olfactory neurons. These support cells are metabolically and functionally associated with olfactory neurons and with odorant signal transduction (processing odorants by endocytosing the odorant-binding protein complex, detoxifying, maintaining the cilia of mature olfactory receptor neurons, and maintaining epithelial integrity). It has been proposed that olfactory sensation is impaired when these essential functions are disrupted, causing cilial impairment. We have identified a genetic locus containing two genes (UGT2A1 and UGT2A2) expected to have a relationship with olfactory function. Given their localization and essential function in the metabolization and detoxification of such compounds, these genes may play a role in the physiology of infected cells and the resulting functional impairment that contributes to loss of ability to smell. We hope that the identification of this genetic association with COVID-19 related anosmia may serve as a clue as to how the virus affects cells in the nasal pathway." (Shelton et. al. 2021)
