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Respiratory failure during COVID-19 could be linked to certain genetic variants
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Respiratory failure during COVID-19 could be linked to certain genetic variants

Using data from genome-wide association study, experts speculate that gene variants encoding blood types and a multidisciplinary chromosome 3 could be the reason behind respiratory failure during COVID-19.

Though it’s been several months since its first case, COVID-19 still manages to surprise scientists. In spite of numerous studies, experts are still unable to understand the reason why the virus reacts differently among different people, for example how some people get really sick, while others stay asymptomatic. 

In a report published in the journal MedRx, using data from genome-wide association study (GWAS), scientists find abnormalities, a variant in the gene encoding blood types was noticed in COVID-19 patients suffering from respiratory failure. In addition, a displacement in the multi-gene cluster chromosome 3 was also noticed. 

More on the gene variants:

Analyzing data from GWAS depends on the availability of genome in the bank. This is especially tricky and crucial in a brand new pandemic such as COVID-19. The authors of this study, in a candid statement, mentioned that it was his link with several scientists from Norway and Spain which helped him collect the data that was needed. 

The research team of this study initially collected and analyzed around 775 COVID-19 patients and 950 control patients from Spain and 835, 1255 patients, and control from Italy respectively.  All the collected samples were from patients who tested positive for COVID-19 and suffered moderate to severe respiratory failure. 

The team performed genomic analysis from the COVID-19 positive patient and compared the results with the control. They observed a peculiar result, a variant in the gene locus encoding blood types. Patients with blood type A were observed to be at a higher risk for respiratory failure, while blood group O patients were more immune. Blood group A were almost 1.5 times more prone to respiratory failure compared to blood type O. 

Experts observed another genomic variant on the human chromosome 3 and several other genes. One such gene is SLC6A20. This gene specifically encodes an amino acid transporter that interacts with the ACE2 receptor used by the COVID-19 virus to enter the host cells. 

How can this possibly help in the fight against COVID-19:

From an individual’s point of view, a patient or people with a blood type A may be at a higher risk to contract the virus, but it should be noted that these effect size very small when compared to the effect the age and sex of the person have on the virus.

Experts from the study also mention that there is a higher risk due to the gene cluster chromosome 3 when compared to the gene locus encoding blood types. 

“SLC6A20 association is intriguing because of the interaction with ACE2, but that the findings for both the chromosome 3 and blood group loci need to be replicated to give more insight into”, says Benjamin Fairfax, a geneticist at the University of Oxford, who was not involved in the study.

Though the possibility of higher risk, the results from this study cannot be individually used to determine the severity of COVID-19 cases. Though the information is not enough to develop treatments, it is a place to start looking.

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