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Source: COVID-19 Research  Jun 08, 2020  3 years, 10 months, 2 weeks, 4 days, 19 hours, 37 minutes ago

European COVID-19 Research Indicates That Individuals With Blood Group Type A Might Be More Vulnerable To Respiratory Failure

European COVID-19 Research Indicates That Individuals With Blood Group Type A Might Be More Vulnerable To Respiratory Failure
Source: COVID-19 Research  Jun 08, 2020  3 years, 10 months, 2 weeks, 4 days, 19 hours, 37 minutes ago
COVID-19 Research: A European study involving more than 52 research centers, universities, medical schools and hospitals and more than a hundred researchers from a variety of countries has performed the first genome-wide association study to reveal host genetic factors that may contribute to respiratory failure in cases of COVID-19 disease including blood group types. It was found that those from blood group A were more at risk whereas those from blood group O were more or less protected from respiratory failure.


The medical researchers say that the genetic variants they have identified could help guide further research into the pathophysiology of COVID-19 and aid the clinical risk profiling of patients.
 
The study findings were released as a pre-print that is currently being reviewed for publication into a leading medical journal. https://www.medrxiv.org/content/10.1101/2020.05.31.20114991v1
 
Most individuals infected with the SARS-CoV-2 coronavirus, the causative agent of COVID-19, only experience mild or even no symptoms.
 
Mortality rates are mainly driven by patients who are more susceptible to respiratory failure after becoming ill with pneumonia or respiratory distress syndrome. However, for reasons that are not properly understood, this is only the case for less than 10 percent of individuals who become infected with SARS-CoV-2.
 
So far, the development of severe disease has also been associated with the presence of comorbidities such as cardiovascular disease, obesity, diabetes, and hypertension. However, the role these health problems play in determining the severity of disease risk is unclear.
 
Certain past studies and observations of endothelitis and vascular complications have suggested that the disease is systemic and mainly involves the vascular endothelium. Still, these insights into the pathology of severe COVID-19 are only hypothetical.
 
To further investigate, Professor Dr Tom Karlsen from Oslo University Hospital Rikshospitalet-Norway and colleagues in Spain, Italy, and Germany, recruited 1,980 COVID-19 patients with respiratory failure from five cities in Spain and Italy.
The team conducted a genome-wide association analysis with the aim of identifying any host genetic susceptibility factors that contribute to the development of respiratory failure.
 
Dr Karrlsen said, “Utilizing a pragmatic approach with simplified inclusion criteria and a complementary team of clinicians at the European Covid-19 epicenters in Italy and Spain and available German and Norwegian scientists, we were able to perform a complete GWAS for Covid-19 respiratory failure in about two months.”
 
Upon considering quality control and potential outliers, the final study population included 835 patients and 1,255 controls from Italy and 775 patients and 950 controls from Spain.
 
In all a total of 8,582,968 single-nucleotide polymorphisms (SNPs) were analyzed, and a meta-analysis of the Italian and Spanish cohorts was conducted.
 
The study detected a cross-replicating association between SNPs on chromosome 3 and chromosome 9 that reached genome-wide significance. A cluster of genes that could be relevant to the development of severe COVID-19 was identified on chromosome 3p21. One of these genes: SLC6A20 encodes a transporter protein that interacts with angiotensin-converting enzyme 2 (ACE2), the host cell receptor that SARS-CoV-2 uses to gain viral entry.
 
It was found that in the lungs, this protein, which is called Sodium/Imino-acid Transporter 1 (SIT1), is mainly expressed in pneumocytes, and the authors think these cells should be investigated for any involvement that SIT1 may have in viral entry.
 
Significantly a lead SNP was also identified on chromosome 9 at the ABO blood group locus, and further analysis showed that A-positive participants were at a 45% increased for respiratory failure, while individuals with blood group O were at a 35% decreased risk for respiratory failure.
 
The researchers say that early clinical reports have suggested the ABO blood group system is involved in determining susceptibility to COVID-19 and has also been implicated in susceptibility to SARS-CoV-1.

Dr Karlsen said, “Our data thus aligns with the suggestions that blood group O is associated with lower risk compared with non-O blood groups whereas blood group A is associated with higher risk of acquiring Covid-19 compared with non-A blood groups.”
 
He further added, “We herein report the first robust genetic susceptibility loci for the development of respiratory failure in Covid-19. Identified variants may help guide targeted exploration of severe Covid19 pathophysiology. Further exploration of current findings, both as to their utility in clinical risk profiling of Covid-19 patients and mechanistic understanding of the underlying pathophysiology, is now warranted.”
 
Interestingly enough, this is one of the many emerging research studies linking blood group types with severity outcomes of COVID-19 disease. In March this year, a similar study with similar outcome by conducted by researchers from China. https://www.thailandmedical.news/news/breaking-coronavirus-research-reveals-that-people-with-blood-type-a-have-higher-risk-of-contracting-covid-19-compared-to-blood-type-o-which-has-a-low
 
However many non-credible fact-checkers employed by Facebook were quick to dismiss the studies as being fake initially.
 
For more COVID-19 research, keep on logging to Thailand Medical News
 
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