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Excerpts:
LIVESCIENCE
Your risk of severe COVID-19 may be affected by blood type, new genetic analysis suggests
By Mindy Weisberger – Senior Writer
People with blood type O may have a reduced risk of developing severe symptoms
Genes associated with certain blood types may increase the risk of severe COVID-19 infections, leading to respiratory failure and death, a new study suggests.
The study authors found that people with blood type A were 50% more likely than people with other blood types to experience severe COVID-19 symptoms and respiratory failure. By comparison, people with blood type O had a 50% reduced risk of developing severe symptoms of COVID-19 — the disease caused by the novel coronavirus — or those severe enough to require oxygen or a ventilator.
Scientists uncovered the connection between blood type and COVID-19 outcome using a genome-wide association study. By looking at the single-letter changes in many genes across a large population, researchers can pinpoint gene variants that may be tied to disease risk, according to the National Human Genome Research Institute.
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In the new study, researchers identified two regions in the genome where genetic variants were linked to severe cases of COVID-19 and a higher risk of death; in one of these regions was a gene that determines blood type. They published their findings online June 17 in the New England Journal of Medicine.
The researchers sampled the genomes of 1,610 COVID-19 patients and more than 1,300 healthy blood donors from Italy and Spain, and analyzed more than 8 million single-letter changes in the DNA code, called single nucleotide polymorphisms, or SNPs (pronounce “snips”). There are millions of SNPs sprinkled throughout a person’s genome, and they can be used as markers for locating genes associated with disease, according to the U.S. National Library of Medicine.
The study authors pinpointed regions of the genome that were linked to respiratory failure from COVID-19 — symptoms severe enough to require supplemental oxygen or the use of a mechanical ventilator. One signal originated in a region that included genes linked to immune response in the lungs. The other signal came from a region that also codes for blood type, enabling the researchers to confirm “a potential involvement of the ABO blood-group system in COVID-19,” they wrote in the study. This link suggests that blood type may be connected to the severity of respiratory symptoms.
The other region they identified contained six genes, some of which interact with the ACE2 receptor that SARs-CoV-2 targets, while others are tied to chemicals that interact with immune cells in the lung. It’s not clear which of these genes play a role in disease susceptibility.
“A genetic test and a person’s blood type might provide useful tools for identifying those who may be at greater risk of serious illness,” Francis Collins, director of the National Institutes of Health, said in a statement about the new study.
“The hope is that these and other findings yet to come will point the way to a more thorough understanding of the biology of COVID-19,” Collins said.
However, many other factors also determine how dramatically an individual is affected by the illness.
Underlying health conditions such as heart disease, chronic lung disease and diabetes greatly increase the chances of getting very sick or dying from COVID-19. Indeed, while older people are generally considered to be more vulnerable to severe cases of COVID-19, that could be explained by the chronic medical conditions that often accompany aging, Live Science previously reported.
https://www.livescience.com/covid-19-blood-type.html
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Excerpts:
The danger of blaming Covid-19 deaths on our genes
Opinion by Kent Sepkowitz
Updated 1820 GMT (0220 HKT) June 6, 2020
Kent Sepkowitz is a CNN medical analyst and a physician and infection control expert at Memorial Sloan Kettering Cancer Center in New York. The views expressed in this commentary are his own. View more opinion at CNN.
(CNN)A profound and unexpected disparity in Covid-19 death rates has emerged among different countries. In South Korea, Norway and Australia, for example, less than 3% of confirmed cases die, while in Belgium, Italy and the United Kingdom, the case fatality rate is as high as 14%.
The reasons for this disparity remain unclear. Theories have included differences in the quality of healthcare and its accessibility, population testing rates or age, differences in mutations of the virus, rates of concurrent conditions such as heart or lung disease and, for some countries, concerns about the inconsistent reporting of deaths.
As clinicians and epidemiologists continue to analyze the data, a new group of scientific experts with a different set of tools has begun to look into genes and whether genetic differences might protect some or endanger others.
Last week, a group of American and British researchers with a primary interest in Alzheimer’s disease published a paper suggesting a genetic basis for the differences in mortality among Covid-19 patients. Their work utilizes genetic information from about 400,000 people in the United Kingdom, all with European ancestry, to identify whether certain genes are associated with certain diseases.
The researchers noticed that dementia was an underlying condition among many patients who died from Covid-19 and decided to explore whether the same gene that made people predisposed to Alzheimer’s disease might also be associated with severe Covid-19 outcomes.
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The influx of geneticists studying Covid-19 is good news; brilliant minds that examine a problem from different perspectives is our most likely way forward.But it also highlights a new set of concerns. Finding a gene is one thing; whether that gene determines an incontrovertible cause for Covid-19 mortality is something else. A genetic predisposition can easily be mistaken as a death sentence, but in many cases, luck, exercise, and a good diet can still play a role in reducing the risk of disease.
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We welcome the expertise of the newest scientists on the block with their swirls of DNA and brilliantly sideways views of how things happen. But even if they do find a genetic basis to explain the different rates of mortality, we must not lose sight of the fact that the government’s indifference, missteps and political calculations are responsible for the tragic deaths of more than 109,000 people in the US.
https://edition.cnn.com/2020/06/06/opinions/genetics-covid19-case-fatality-rates-sepkowitz/index.html
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medRxiv
Study shows COVID-19 vulnerability is highly dependent on host genetic architecture
By Dr. Tomislav Meštrović, MD, Ph.D.
May 10 2020
A new US study available on the preprint server medRxiv* reveals certain genetic variations that are associated with infection susceptibility and diverse clinical presentation of coronavirus disease (COVID-19) – including asymptomatic cases and severe forms of the disease in younger patients.
The ongoing pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) brought to the attention the pressing public health demand to adequately understand human genetic variation in response to the viral challenge.
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In this new study, the researchers utilized the data from the UK Biobank population-based cohort in order to evaluate the relationship between host genetics and its viral response. They have analyzed the data of 7,924 participants in total (predominantly of European ancestry).
The goal was to appraise 28 antigens for 16 viruses that have been linked to neurodegenerative diseases and malignancies but also to put the emphasis on the SARS-CoV-2 test in a separate subset of UK Biobank participants.
Accordingly, they have conducted integrative genome-wide and transcriptome-wide analyses of antibody response and positivity to viral antigens. Pleiotropic associations between lead variants affecting antibody levels and several chronic diseases with viral risk factors were explored in depth.
Study findings confirm that human leukocyte antigen (HLA) class II and III genes are pivotal host genetic factors implicated in regulating the immune response to diverse viral antigens, with potential implications for complex diseases.
Furthermore, the researchers have also discovered that specific HLA alleles linked to multiple common infections are associated with SARS-CoV-2 positive tests. More specifically, based on 1028 subjects tested for SARS-CoV-2, they have identified seven class II HLA susceptibility alleles (five associated with other viruses).
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Research implications
“Understanding the interplay between host genetic factors and immune response has implications for public health and may facilitate the discovery of novel therapeutics including vaccines,” said study authors.
“Upon further elucidation of the risk of infection and COVID-19 severity, our results suggest that HLA typing may be a feasible tool in the SARS-CoV-2 response for identifying at-risk populations and, prioritizing vaccine distribution”, they conclude.
Naturally, further research is needed in order to understand the viability of this approach in diverse populations, whereas therapeutic research on ACE2 inhibitors will elucidate what is happening behind the downregulation of SARS-CoV-2 receptors after infection.
*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.
https://www.news-medical.net/news/20200510/Study-shows-COVID-19-vulnerability-is-highly-dependent-on-host-genetic-architecture.aspx
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Excerpts:
Scientific American
Do Your Genes Predispose You to COVID-19?
Individual differences in genetic makeup may explain our susceptibility to the new coronavirus and the severity of the disease it causes
By Loïc Mangin
April 30, 2020
Since the start of the COVID-19 pandemic several months ago, scientists have been puzzling over the different ways the disease manifests itself. They range from cases with no symptoms at all to severe ones that involve acute respiratory distress syndrome, which can be fatal. What accounts for this variability? Might the answer lie in our genes?
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Attention has now shifted to SARS-CoV-2, the new coronavirus that causes COVID-19. And TLRs have once again drawn researchers’ interest—this time to help explain the excess number of men who suffer from severe infections.
Men made up 73 percent of severe cases of COVID-19 in intensive care in France, according to a national survey published April 23. Behavioral and hormonal differences may be partially responsible. But genes may also factor into the mix. Unlike men, women have two X chromosomes and so carry double the copies of the gene TLR7, a key detector of viral activity that helps boost immunity.
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Several projects are underway to investigate the genetic variants that influence SARS-CoV-2 infection in greater depth. Andrea Ganna of the University of Helsinki has launched the COVID-19 Host Genetics Initiative, which aims to mobilize the international community of geneticists working on this topic. Jean-Laurent Casanova of the Necker Hospital for Sick Children in Paris and the Rockefeller University is coordinating a similar effort to identify genetic variants that promote the development of particularly severe forms of COVID-19 in people under 50 years of age.
We may not all be equal when it comes to SARS-CoV-2. But identifying why these inequalities exist could help reduce them.
This article originally appeared in Pour la Science and was reproduced with permission.
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