Post by Admin on Jun 6, 2020 6:43:11 GMT
A new study from European scientists has found that genes may leave some people more vulnerable to severe cases of COVID-19, the illness caused by coronavirus.
The study, which is currently undergoing a peer review, found genetic variations at two spots in the human genome that are associated with a greater risk of respiratory failure in coronavirus patients.
The first spot is a gene that determines blood types. Researchers concluded that patients with Type A blood were 50 percent more likely to need to get oxygen or go on a ventilator.
The second spot, showing a stronger link to COVID-19 than the first, was on Chromosome 3 but the team of scientists are not yet sure which of the six genes on the chromosome has an impact on coronavirus.
RELATED: U.S. Should Have ‘Couple of Hundred Million Doses’ of Coronavirus Vaccine by Early 2021: Fauci
Dr. Andre Franke, one of the study’s co-authors, told The New York Times that no one knows why Type A blood is linked to an increased risk of developing severe coronavirus symptoms, though a previous study from China found the same link.
“That is haunting me, quite honestly,” Franke said.
Previously released risk factors for developing severe COVID-19 include being elderly or immunocompromised. Several studies have also found that obesity may be a risk factor, particularly in young people.
One large study of 4,000 COVID-19 patients at NYU Langone Hospital in New York City found that obesity was the second-highest reason why patients were hospitalized with COVID-19.
Another, separate study from NYU Langone found that patients under 60 years old with a body mass index (BMI) between 30 and 34 were twice as likely to be admitted to the hospital with severe cases of COVID-19, and 1.8 times more likely to need treatment in the intensive care unit.
The ABO blood group locus and a chromosome 3 gene cluster associate with SARS-CoV-2 respiratory failure in an Italian-Spanish genome-wide association analysis
Abstract
Background. Respiratory failure is a key feature of severe Covid-19 and a critical driver of mortality, but for reasons poorly defined affects less than 10% of SARS-CoV-2 infected patients. Methods. We included 1,980 patients with Covid-19 respiratory failure at seven centers in the Italian and Spanish epicenters of the SARS-CoV-2 pandemic in Europe (Milan, Monza, Madrid, San Sebastian and Barcelona) for a genome-wide association analysis. After quality control and exclusion of population outliers, 835 patients and 1,255 population-derived controls from Italy, and 775 patients and 950 controls from Spain were included in the final analysis. In total we analyzed 8,582,968 single-nucleotide polymorphisms (SNPs) and conducted a meta-analysis of both case-control panels. Results. We detected cross-replicating associations with rs11385942 at chromosome 3p21.31 and rs657152 at 9q34, which were genome-wide significant (P<5x10-8) in the meta-analysis of both study panels, odds ratio [OR], 1.77; 95% confidence interval [CI], 1.48 to 2.11; P=1.14x10-10 and OR 1.32 (95% CI, 1.20 to 1.47; P=4.95x10-8), respectively. Among six genes at 3p21.31, SLC6A20 encodes a known interaction partner with angiotensin converting enzyme 2 (ACE2). The association signal at 9q34 was located at the ABO blood group locus and a blood-group-specific analysis showed higher risk for A-positive individuals (OR=1.45, 95% CI, 1.20 to 1.75, P=1.48x10-4) and a protective effect for blood group O (OR=0.65, 95% CI, 0.53 to 0.79, P=1.06x10-5). Conclusions. 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 Covid-19 pathophysiology.
The study, which is currently undergoing a peer review, found genetic variations at two spots in the human genome that are associated with a greater risk of respiratory failure in coronavirus patients.
The first spot is a gene that determines blood types. Researchers concluded that patients with Type A blood were 50 percent more likely to need to get oxygen or go on a ventilator.
The second spot, showing a stronger link to COVID-19 than the first, was on Chromosome 3 but the team of scientists are not yet sure which of the six genes on the chromosome has an impact on coronavirus.
RELATED: U.S. Should Have ‘Couple of Hundred Million Doses’ of Coronavirus Vaccine by Early 2021: Fauci
Dr. Andre Franke, one of the study’s co-authors, told The New York Times that no one knows why Type A blood is linked to an increased risk of developing severe coronavirus symptoms, though a previous study from China found the same link.
“That is haunting me, quite honestly,” Franke said.
Previously released risk factors for developing severe COVID-19 include being elderly or immunocompromised. Several studies have also found that obesity may be a risk factor, particularly in young people.
One large study of 4,000 COVID-19 patients at NYU Langone Hospital in New York City found that obesity was the second-highest reason why patients were hospitalized with COVID-19.
Another, separate study from NYU Langone found that patients under 60 years old with a body mass index (BMI) between 30 and 34 were twice as likely to be admitted to the hospital with severe cases of COVID-19, and 1.8 times more likely to need treatment in the intensive care unit.
The ABO blood group locus and a chromosome 3 gene cluster associate with SARS-CoV-2 respiratory failure in an Italian-Spanish genome-wide association analysis
Abstract
Background. Respiratory failure is a key feature of severe Covid-19 and a critical driver of mortality, but for reasons poorly defined affects less than 10% of SARS-CoV-2 infected patients. Methods. We included 1,980 patients with Covid-19 respiratory failure at seven centers in the Italian and Spanish epicenters of the SARS-CoV-2 pandemic in Europe (Milan, Monza, Madrid, San Sebastian and Barcelona) for a genome-wide association analysis. After quality control and exclusion of population outliers, 835 patients and 1,255 population-derived controls from Italy, and 775 patients and 950 controls from Spain were included in the final analysis. In total we analyzed 8,582,968 single-nucleotide polymorphisms (SNPs) and conducted a meta-analysis of both case-control panels. Results. We detected cross-replicating associations with rs11385942 at chromosome 3p21.31 and rs657152 at 9q34, which were genome-wide significant (P<5x10-8) in the meta-analysis of both study panels, odds ratio [OR], 1.77; 95% confidence interval [CI], 1.48 to 2.11; P=1.14x10-10 and OR 1.32 (95% CI, 1.20 to 1.47; P=4.95x10-8), respectively. Among six genes at 3p21.31, SLC6A20 encodes a known interaction partner with angiotensin converting enzyme 2 (ACE2). The association signal at 9q34 was located at the ABO blood group locus and a blood-group-specific analysis showed higher risk for A-positive individuals (OR=1.45, 95% CI, 1.20 to 1.75, P=1.48x10-4) and a protective effect for blood group O (OR=0.65, 95% CI, 0.53 to 0.79, P=1.06x10-5). Conclusions. 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 Covid-19 pathophysiology.