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Alzheimer's Blood

Alzheimer’s blood test in your doctor’s office closer to reality, studies say – CNN

(CNN)A simple blood test to diagnose Alzheimer’s disease — on the wish list of many doctors, researchers and patients — may be closer to becoming a reality, according to the results of studies presented virtually this week during the Alzheimer’s Association International Conference 2020.

In a study presented Tuesday at the conference and published in JAMA, a blood test to detect the tau protein, one of the hallmark signs of Alzheimer’s, was as accurate as a spinal tap or a positron emission tomography (PET) scan, which are the current gold standards of diagnosis while a person is living.
The test could also differentiate between different types of cognitive dementia and even flag early signs of Alzheimer’s. While more research is required and such a test is likely still years away from being available, experts say the results are encouraging.
“This research represents an exciting step towards developing a blood test that could help identify Alzheimer’s disease by focusing on specific sub-types of tau, one of the key proteins that becomes abnormal as part of the Alzheimer’s disease changes in the brain,” said Clive Ballard, professor of age-related disease at the University of Exeter Medical School, in the UK, who was not involved in the study.
“A reliable blood test for Alzheimer’s disease would be a huge boost for dementia research, allowing scientists to test treatments at a much earlier stage which in turn could lead to a breakthrough for those living with dementia,” said Dr. Rosa Sancho, head of research at Alzheimer’s Research UK, who was also not involved in the study.

Looking for a mutant protein

In a three-part study, researchers from the United States and Sweden measured an abnormal version of the tau protein called p-tau217 and found more of that modified tau in the blood of people with Alzheimer’s disease than in healthy participants.
How does tau get into blood? It appears to cross the blood-brain barrier.
“Tau protein is modified and clumps abnormally in the brains of people with Alzheimer’s disease and some frontotemporal dementias, and some of this tau protein leaks out of the brain into the blood,” said Tara Spires-Jones, the deputy director of the Centre for Discovery Brain Sciences at the University of Edinburgh, who was not involved in the study.
The researchers report the blood test can distinguish Alzheimer’s disease from other types of dementia and Parkinson’s with a high degree of accuracy — 89% to 98%.
Additionally, measuring p-tau217 levels may also be able to detect brain changes 20 years before dementia symptoms occur.
“This test, once verified and confirmed, opens the possibility of early diagnosis of Alzheimer’s before the dementia stage, which is very important for clinical trials evaluating novel therapies that might stop or slow down the disease process,” the researchers, led by Dr. Oskar Hansson from Lund University in Sweden, wrote.
Another study, published Tuesday in the Journal of Experimental Medicine, also verified that p-tau217 was more closely related to amyloid buildup in the brain than other chemicals that have been investigated.
“These two papers add to increasing evidence that modified tau proteins in the blood can accurately reflect Alzheimer’s disease in processes occurring in the brain,” said Amanda Heslegrave, a senior research fellow at the UK Dementia Research Institute at University College London, who was not involved in the study.

In your doctor’s office

The formation of brain proteins, amyloid and tau, into clumps of amyloid plaques and tau tangles are defining physical features of Alzheimer’s disease, but they are hard to detect without expensive PET scans or invasive spinal taps, neither of which is routinely covered by insurance.
Doctors are left with verbal and written tests of memory and cognitive impairment, combined with interviews with patients’ family members and caregivers about their behavior. That approach makes it tough to accurately diagnosis Alzheimer’s as distinct from other types of cognitive impairment.
In addition, brain scans and spinal taps can only identify beta amyloid plaques, not the tau protein. A test for tau is important, experts say — beta amyloid alone isn’t enough to diagnose Alzheimer’s because some people with high levels don’t develop the neurological disease.
The new blood test is able to detect both amyloid plaques and tau tangles and is very specific to Alzheimer’s, experts said.
A third abstract presented at the Alzheimer’s conference found the test could differentiate between less common frontotemporal dementia, which affects younger people and leads to changes in behavior and personality rather than memory loss, and Alzheimer’s, illustrating the test’s diagnostic abilities. These include changes in personality, behavior and difficulties with language.
“These studies (and others) show that blood based tau is a marker of amyloid pathology. Very interesting and not what would have been predicted 5 years ago,” said John Hardy, the chair of Molecular Biology of Neurological Disease at University College London.
These advances mean a day may come in the next few years when your health care provider can do a blood test for Alzheimer’s while you are at the doctor’s office, experts say.
“It is very exciting, because we all know that blood tests are really important and they’re necessary as a first pass in the clinic, in your general practitioner’s office,” said Maria Carrillo, chief medical officer of the Alzheimer’s Association.
And unlike current detection methods, blood tests could more easily be scaled up to test many people at much lower cost.
Early detection and treatment before significant damage from Alzheimer’s disease occurs to the brain would be a game changer for individuals, experts said. The test could also help to identify the right people for clinical drug trials.
“We know that brain changes in Alzheimer’s disease can occur decades before symptoms start to show and the early stages of disease are likely to be the time when future drugs are most effective,” Sancho said.
Carrillo and other experts caution that while promising, the blood test still needs to be tested among asymptomatic people and larger populations.
“Now we need longer and larger studies to validate these results and find out if this test could accelerate our ability to develop new treatments for Alzheimer’s disease in the future.” said Fiona Carragher, director of policy and research at Alzheimer’s Society in the UK.
Ballard agrees: “Although this research looks extremely promising, further validation in people from more routine clinical settings are still needed, and a lot of work will be needed to achieve standardisation of the test across laboratories.
“So it could still be at least five years before we see an accurate blood biomarker test for dementia it in the clinic.”

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Blood Hands

‘Blood on his hands’: In scathing obituary, woman blames governor for her father’s covid-19 death – The Washington Post

When her father died of covid-19 last month, Kristin Urquiza minced no words assigning blame.

Mark Urquiza, 65, should still be alive, his daughter wrote in a scathing obituary, published Wednesday in the Arizona Republic.

“His death is due to the carelessness of the politicians who continue to jeopardize the health of brown bodies through a clear lack of leadership, refusal to acknowledge the severity of this crisis, and inability and unwillingness to give clear and decisive direction on how to minimize risk,” she wrote.

The searing tribute encapsulates the fury of critics who say governments at multiple levels are failing at their most basic duty: keeping citizens safe. The obituary also nods at the outbreak’s disproportionate impact on black and Hispanic communities, which have experienced higher rates of coronavirus-related hospitalization and death.

Among the leaders whom Kristin Urquiza feels failed her father, a Mexican American resident of Phoenix who worked in manufacturing, are Arizona Gov. Doug Ducey (R) and the Trump administration. Ducey, she said, “has blood on his hands” for beginning to reopen the state in early May, roughly three weeks before new infections started to rise quickly.

Patrick Ptak, a spokesman for Ducey, said in a statement: “Our hearts go out to the family and loved ones of Mark Anthony Urquiza. We know nothing can fully alleviate the pain associated with his loss, and every loss from this virus is tragic.”

A spokesperson for Trump did not immediately respond to a request for comment.

Mark Urquiza rarely left the house while Arizona’s stay-at-home order was in place except to do his job, which was deemed essential, his daughter said. He started to go out with friends after Ducey and Trump said people could safely resume their normal lives, even as his daughter begged him to stay home.

Kristin Urquiza remembers that as the state continued to reopen, her father told her the governor was encouraging residents to go out in public again. Mark Urquiza asked his daughter: Why would he do that if it was still dangerous?

“Despite all of the effort that I had made to try to keep my parents safe, I couldn’t compete with the governor’s office and I couldn’t compete with the Trump administration,” Kristin Urquiza said.

Inspired by the famous AIDS quilt meant to humanize victims, Kristin Urquiza wrote to Ducey, asking him to attend her father’s funeral to see a result of what she called his “inaction and active denial” of the pandemic’s effects. Ducey’s office, she said, did not reply.

Ptak declined to say whether the governor received the request and whether anyone from his office responded.

About three weeks after Arizona’s stay-at-home order expired, Mark Urquiza developed a cough and a high fever, according to his daughter. His family arranged for him to take a coronavirus test the next day, but Kristin Urquiza said he never received the result.

By June 16, Mark Urquiza felt sick enough that he asked to go to a hospital. There, his daughter said, he tested positive for the virus.

Kristin Urquiza said she struggled to get news about her father’s condition from his doctors and nurses, who were stretched thin by a surge of patients. Sometimes, she said, her family spent hours on the phone with hospital employees, trying desperately to get information.

Mark Urquiza died on June 30, four days after entering the intensive care unit. His family never determined how he became infected. A GoFundMe page raised money for his funeral.

Kristin Urquiza said that since her father’s death, she has felt like a storm is forming inside her body, preparing to bear down on the desert of her home state. She started an ofrenda, a traditional Mexican display to honor the dead, for her father outside the state capitol. When it was time to write his obituary, Kristin Urquiza said, “there was no question in my mind that I wouldn’t just say the truth.”

She has also channeled her rage into a social media campaign called “Marked by Covid,” which uses a play on her father’s name to spread information about covid-19 in hopes of sparing other families similar suffering. She said the Trump administration should create an enforceable federal mask requirement and stop minimizing the advice of its health experts.

The nation’s leaders, Kristin Urquiza said, have failed to lead.

“This entire tragedy is the fault of a terrible policy,” she said, “and on top of that, inconsistent and embarrassing leadership.”

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affect Blood

How blood type may affect your coronavirus risk – NBC News

Recent studies have suggested that people’s blood types may affect their risk of contracting the COVID-19 virus or developing a serious case of the disease. Overall, the findings indicate that people with Type O blood seem to be more protected and that those with Type A appear more vulnerable.

So does that mean some people can slack off on preventive measures while others need to ratchet them up?

Not so fast, say doctors who point out that the findings show associations, not causation — and don’t indicate that any particular blood type guarantees protection.

While the findings may catch the public’s attention at a time when people fatigued by the pandemic are looking for signs of hope, doctors say the results are more relevant to researchers trying to better understand the virus.

“I think something like this has much more sex appeal than it does real practical value,” said Dr. Aaron Glatt, chair of medicine and chief of infectious diseases at Mount Sinai South Nassau in New York.

Everybody should practice exactly the same way, whatever your blood type is, in terms of appropriate masking and social distancing.

Any possible influence of blood type on COVID-19 appears small compared with the substantial impact of known risk factors, such as older age and underlying health conditions, said Glatt, who is a spokesperson for the Infectious Diseases Society of America. “In any individual patient, if they have risk factors or they don’t have risk factors, that is far, far more important,” he said.

People shouldn’t jump to conclusions that they are safer or not because of their blood types, he said.

“They certainly shouldn’t walk around high-fiving and saying, ‘I can do whatever I want, I don’t have to mask, I don’t have to worry about anything because I have O,'” Glatt said. “And they shouldn’t crawl into a corner of the world and not let anyone near them because they have A. Everybody should practice exactly the same way, whatever your blood type is, in terms of appropriate masking and social distancing.”

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Full coverage of the coronavirus outbreak

Dr. Lewis Kaplan, a professor of surgery at the University of Pennsylvania who is president of the Society of Critical Care Medicine, agreed.

Even if some people have reduced risks based on blood type — and the risks vary by study — they don’t have zero risk, Kaplan said. “It might mean they have less risk, but if you engage in risky behavior, we don’t know just how much risk you need to incur to overwhelm whatever potential protection you might have,” he said. “We have no clue.”

A European study published last month in the New England Journal of Medicine found that people with Type A blood were 45 percent more likely to develop severe COVID-19 requiring oxygen supplementation or a ventilator than people with other blood types and that those with Type O blood were 35 percent less likely. The study involved 1,610 patients with severe COVID-19 and 2,205 control subjects.

But people with Type O can still get very sick.

“They have a decreased risk to get infected and to develop severe disease,” study author Andre Franke, a professor of molecular medicine at the University of Kiel in Germany, said in an email. “However, this is only a relative risk reduction, i.e. there is no full protection. Among our patients who died there were also many with blood group O.”

A couple of related papers have been released on the preprint server medRxiv without the peer review scrutiny that published papers typically receive. Studies in China and New York both found that people with Type A blood had a greater risk of coronavirus infection than those with other blood types, while those with Type O had a lower risk.

And the gene testing company 23andMe wrote a blog post about preliminary unpublished data suggesting that people with Type O blood were less likely to test positive for the coronavirus than others.

Dr. Roy Silverstein, a professor and chair of medicine at the Medical College of Wisconsin who is senior investigator at Versiti Blood Center of Wisconsin, cautioned against putting too much weight on findings that haven’t been peer-reviewed and said more research is needed.

“We have to be careful about overreacting,” Silverstein said.

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Blood types O and A are most common, so the studies were able to draw stronger statistical conclusions about those types than B and AB, he said.

An explanation for the findings isn’t known, but there is speculation that blood type may affect clotting or other factors in COVID-19 patients or somehow affect infectivity or immunity. The hope is that the findings can be applied to future research to better understand why the coronavirus affects people differently and to develop treatments.

The results aren’t expected to alter how doctors care for patients now.

“The fact that you have O or A is not going to change one iota how we monitor a patient,” said Glatt, of Mount Sinai South Nassau. “If somebody has O and they’re not doing well, I’m not going to say, ‘Oh, don’t worry about it, you have O.’ I would treat them appropriately. And if they have A and they’re doing very well, I would say, ‘OK, we’re going to continue to watch you.'”

Jacqueline Stenson

NBC News contributor Jacqueline Stenson is a health and fitness journalist who has written for the Los Angeles Times, Reuters, Health, Self and Shape, among others. She also teaches at the UCLA Extension Writers’ Program.

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Blood types

Blood types and COVID-19 risk confirmed – News-Medical.Net

Blood type may play a pivotal role in driving disease severity among coronavirus disease (COVID-19) patients. Genetic analysis of COVID-19 patients has shown that people with blood type O seemed to be protected against severe disease. In contrast, those with blood type A may experience complications tied to the viral infection.

A team of European scientists has found that two genetic variations may show who is more likely to get very sick and even die from the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Further, they found a link to blood type, suggesting that some people are predisposed to COVID-19 severe disease.

The study findings, published in The New England Journal of Medicine, shed light on why some people have a higher risk of being infected with the coronavirus and developing worse symptoms.

In three completely separate studies, researchers from Columbia University, Iran’s Mazandaran University of Medical Sciences, and various Chinese institutions all arrived at similar findings.

Image Credit: TippaPatt / Shutterstock

Image Credit: TippaPatt / Shutterstock

Respiratory failure in COVID-19 patients

The pathogenesis of severe COVID-19 and the associated respiratory failure is still unclear, but the higher mortality is consistently tied to older age and being male. Further, people with underlying health conditions are more likely to develop severe COVID-19, including hypertension, diabetes, being obese, and cardiovascular disease.

The relative role of clinical risk factors in determining the severity of COVID-19 has not been clarified. Now, the new study underscores other predisposing factors that may make some people vulnerable to the infection.

Novel Coronavirus SARS-CoV-2 Colorized scanning electron micrograph of an apoptotic cell (pink) heavily infected with SARS-COV-2 virus particles (green), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Credit: NIAID

Novel Coronavirus SARS-CoV-2 Colorized scanning electron micrograph of an apoptotic cell (pink) heavily infected with SARS-COV-2 virus particles (green), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Credit: NIAID

Genetic analysis

The team studied more than 1,900 severely ill coronavirus patients in Spain and Italy, two of the hardest-hit countries at the peak of the coronavirus pandemic. They compared the patients from seven hospitals to 2,300 people who were not sick. Overall, they analyzed more than 8 million single-nucleotide polymorphisms and conducted a meta-analysis of the two case-control panels.

The team has found that a cluster of variants in genes that are involved with immune responses was more common in people with severe COVID-19. The genes are also associated with a cell-surface protein known as angiotensin-converting enzyme 2 (ACE2), which the coronavirus uses to enter and infect cells in the body.

One of the gene clusters increased the risk of getting severe COVID-19 by 77 percent. The researchers believe that discovering these gene clusters may ramp up the development of new vaccines and therapeutics for the coronavirus disease.

Blood type

The researchers also found that people with blood type A had a 45 percent increased risk of contracting the coronavirus and developing respiratory failure compared to people with other blood types. On the other hand, people with blood type O had a 35 percent lower risk of developing severe COVID-19 illness.

Study: 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. Image Credit: Designua

Study: 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. Image Credit: Designua / Shutterstock

However, it is not clear why blood type might influence susceptibility to severe disease. Dr. Robert Glatter, an emergency medicine doctor at Lenox Hill Hospital in New York City, noted that the genes controlling blood type might play a role in the makeup of cell surfaces. The changes in cell-surface structures might influence the susceptibility of the cell to be infected by the novel coronavirus.

“We also know from previous research that blood type affects clotting risk, and it’s now quite evident that critically ill patients with coronavirus demonstrate significant clotting,” Dr. Glatter explained.

The team emphasized that their findings may need further validation and investigation. This way, more information can be gathered on the link between blood type and coronavirus disease severity.

“Further exploration of current findings, both as to their usefulness in clinical risk profiling of patients with Covid-19 and toward a mechanistic understanding of the underlying pathophysiology, is warranted,” they wrote on the paper.

Global toll

The coronavirus pandemic has ravaged across the globe, actively spreading in many countries. The United States remains the country with the highest number of cases. The country’s case toll has surpassed 2.189 million infections, and its death toll topped 118,000.

Brazil trails behind the U.S., with over staggering 978,000 infections in since April. The death toll in the country has topped 47,000. Russia, India, and the United Kingdom have reported an increasing number of infections, with more than 560,000, 366,000, and 301,000, respectively.

Source:

Journal references:

  • Primary Paper – Ellinghaus, D., Degenhardt, F., Buti, M., Bujanda, L., Invernizzi, P., Milani, C. et al. (2020). Genomewide Association Study of Severe Covid-19 with Respiratory Failure. The New England Journal of Medicine. https://www.nejm.org/doi/full/10.1056/NEJMoa2020283?query=featured_coronavirus#article_references
  • Pre-Print – Karlsen T, et al. 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. medRxiv 2020. doi: https://doi.org/10.1101/2020.05.31.20114991
  • Iranian Study – Pourali, F. et al. (2020). Relationship Between Blood Group and Risk of Infection and Death in COVID-19: a live Meta-Analysis. medRxiv. https://doi.org/10.1101/2020.06.07.20124610.
  • Chinese Study – Relationship between the ABO Blood Group and the COVID-19 Susceptibility, Jiao Zhao, Yan Yang, Hanping Huang, Dong Li, Dongfeng Gu, Xiangfeng Lu, Zheng Zhang, Lei Liu, Ting Liu, Yukun Liu, Yunjiao He, Bin Sun, Meilan Wei, Guangyu Yang, Xinghuan Wang, Li Zhang, Xiaoyang Zhou, Mingzhao Xing, Peng George Wang, medRxiv 2020.03.11.20031096; doi: https://doi.org/10.1101/2020.03.11.20031096
  • Colombia University Study  – Testing the association between blood type and COVID-19 infection, intubation, and death, Michael Zietz, Nicholas P. Tatonetti, medRxiv 2020.04.08.20058073; doi: https://doi.org/10.1101/2020.04.08.20058073

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Blood Group

Blood group type may affect susceptibility to COVID-19 respiratory failure – News-Medical.Net

A group of over 120 researchers from various institutions across Europe has performed the first genome-wide association study to reveal host genetic factors that may contribute to respiratory failure in cases of coronavirus disease 209 (COVID-19).

The authors say 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.

A pre-print version of the paper is available on the server medRxiv*, while the article undergoes peer review.

The rapid spread of the pandemic

Since the COVID-19 outbreak began in Wuhan, China, late last year, it has rapidly become a pandemic health emergency that has now infected more than 6.39 million people worldwide and killed almost 400,000.

In Europe, Italy and Spain have been among the most severely affected countries, with epidemics peaking during the second half of February and more than 60,000 fatal cases being reported by May 28th.

Most people infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) – 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 people who become infected with SARS-CoV-2.

Novel Coronavirus SARS-CoV-2 Colorized scanning electron micrograph of an apoptotic cell (pink) heavily infected with SARS-COV-2 virus particles (green), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Credit: NIAID

Novel Coronavirus SARS-CoV-2 Colorized scanning electron micrograph of an apoptotic cell (pink) heavily infected with SARS-COV-2 virus particles (green), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Credit: NIAID

Potential factors involved in respiratory failure

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.

Some 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.

Performing a genome-wide analysis

To investigate, Tom Karlsen (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.

They conducted a genome-wide association analysis with the aim of identifying any host genetic susceptibility factors that contribute to the development of respiratory failure.

“Using 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,” say the researchers.

After 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.

A total of 8,582,968 single-nucleotide polymorphisms (SNPs) were analyzed, and a meta-analysis of the Italian and Spanish cohorts was conducted.

What did the study find?

The team 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.

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.

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 authors 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.

“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,” the authors conclude.

Study: 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. Image Credit: Designua

Study: 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. Image Credit: Designua / Shutterstock

“Further exploration” of the findings is “now warranted”

“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,” say Karlsen and team.

“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,” they conclude.

*Important Notice

medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

Journal reference:

  • Karlsen T, et al. 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. medRxiv 2020. doi: https://doi.org/10.1101/2020.05.31.20114991

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