Category: Covid-19

How has COVID-19 affected extreme income poverty across the world? We may never know the full answer. Poverty data is typically drawn from household surveys, and for obvious reasons it is nigh impossible to conduct proper surveys under current conditions in many countries. But we do know that the strongest driver of poverty is economic growth and for this indicator, the International Monetary Fund has just produced new estimates for 2020 and beyond from which inferences can be made as to the impact on poverty. Interested readers can access poverty estimates for every country in the world on the World Poverty Clock, a tool with which I am associated.

The results are sobering. Table 1 shows topline figures, built up from an analysis of 183 countries for which data is reported.

The first row of Table 1 shows a baseline of poverty estimates made in late 2019. A total of 650 million people were thought to be in extreme poverty in 2019 and, given likely growth trajectories, poverty was on a path of a steady reduction in most countries, as well as in the aggregate.

Today, the pattern is quite different. Some small data updates affect the historical record2019 may have been a better year than previously believed, with slightly fewer poor people in the world. But in 2020, the impact of collapsing growth will be substantial.

Compared to 2019, poverty in 2020 could rise by 120 million people. Compared to the baseline path for poverty, the 2020 figure is 144 million people higher. Some of this will be offset as economies start to recover in 2021, but the longer-term scenario suggests that half of the rise in poverty could be permanent. By 2030, the poverty numbers could still be higher than the baseline by 60 million people.

Figure 1 shows the top 10 countries where extreme poverty is likely to rise the most. Far and away the biggest impact is likely to be felt in India. India is a particular case in having a large number of highly vulnerable people, only recently escaped from poverty, coupled with a very significant expected fall in economic growth. Indias per capita growth rate for 2020 has been revised downwards to about -11 percent this year, one of the deepest recessions in the world. This has sharply altered its poverty trajectory that had been trending downwards. India recently gave up its title as the country with the largest number of extreme poor to Nigeria but will reclaim its title this year, adding 85 million people to its poverty rolls in 2020.

COVID-19 is widely viewed as a temporary shock to economic growth, and indeed the experience of China, which has had a sharp V-shaped recession and recovery, shows this could be the case. For the majority of countries, however, the economic damage could be more long-lasting, and this is the real risk to families that have been pushed below the poverty line. The experience of living with poverty for short periods of time is harsh, but some families have coping mechanismsassets they can sell, assistance from governments, relatives, and neighbors. But over longer periods of time, poverty leaves permanent scarsmalnutrition, susceptibility to disease, missed schooling. For this reason, it is useful to look at the longer-term impact of COVID-19 on poverty, despite all the caveats associated with any decadelong economic forecasts.

Figure 2 provides an estimate of the countries that could have the deepest, long-lasting impact of COVID-19 on poverty. With the exception of Venezuela, they are all in Africa. The Asian countries that appear in Figure 1Bangladesh, India, and the Philippinesdisappear from Figure 2 because trend growth rates in Asia are higher, so the impact of recession on poverty is quickly reversed. By contrast, in the African countries that are listed in Figure 2, trend economic growth is slow, so the impact of COVID-19 could set back development for several years. Indeed, for some of the countries with high levels of poverty, like Nigeria and the Democratic Republic of Congo, poverty numbers in 2030 could exceed those in 2020.

The countries listed in Figure 2 are those where the largest effort is needed to offset COVID-19s impact on the poorest families, by international and domestic, official, and philanthropic actors.

While the trajectories summarized above look grim, they are not set in stone. An important lesson from the response to COVID-19 is that cash transfers to poor households can be quickly and effectively deployed. Several countries now have digitized rolls of families eligible for social assistance, along with a capability of making cash payments directly into bank accounts or into mobile wallets from which cash can be extracted at registered dealers. For example, Pakistan introduced the Ehsaas Emergency Relief program in April 2020, designed to provide 12 million families with a cash equivalent of $75. Thanks to a national registration scheme, families could simply send an SMS message to a designated number with their ID number to find out if they were eligible to receive support or not. Simple criteria such as foreign travel, vehicle registration, and monthly phone bill were cross-checked against broader socioeconomic data to determine eligibility. Once eligibility was confirmed, a family member could use a previously issued biometric ID card to receive cash at any one of 18,000+ branches of two local banks.

Not all countries have such systems in place. But they could. The largest digital ID system in the world is Indias Aadhar unique identification, with over 1.2 billion people registered. A similar approach could be used for a digital moonshot that would register all Africans within a decade at modest cost.

If such systems could be put in place, extreme poverty could be eradicated at a global cost of around $100 billion. This is the size of the poverty gap, post-COVID-19. Figure 3 shows that the number had already stabilized at around $90 billion before COVID-19, and has now been pushed higher.

The poverty gap can be filled by a combination of domestic and international resources. It can be compared to official aid of $105 billion in 2018 (net disbursements to developing countries). It is less than the $130 billion in debt service owed by developing countries in 2020, of which about half will go to private lenders. It is well under 1 percent of the $11 trillion being spent by advanced economies to protect their own citizens and businesses from the impact of COVID-19. It is a fraction of the $2.5 trillion that the IMF has indicated that developing countries should spend to respond appropriately to COVID-19.

There is no technological or financial reason to accept the reversals in global poverty being wrought by COVID-19. The damage is due to a lack of political will and international leadership on the issue.

Read more from the original source:

The impact of COVID-19 on global extreme poverty - Brookings Institution

This week, Grand Forks County tallied a record number of infections. Grand Forks Public Health Director Debbie Swanson said no longer are the county's COVID-19 numbers driven by individual outbreaks as they were early in the pandemic. Instead, she said the county is watching numbers rise due to uncontrolled spread throughout the community.

On Thursday, Oct. 22, 25 staff members and five residents have COVID-19 at Valley Senior Living on Columbia, the highest number of confirmed active cases at any Grand Forks senior living facility. Woodside Village has 11 staff members who have tested positive for COVID-19, Edgewood Parkwood Place has four positive staff members and three positive residents, and Wheatland Terrace has four positive staff members. There are no active cases of COVID-19 in Maple View Memory Care, St. Ann's Guest House or Tufte Manor, according to NDDOH.

Sally Grosgebauer, a spokesperson for Valley Senior Living, which operates multiple homes in Grand Forks, said nine residents are being treated at the organization's shared Covid Care Area at Valley Senior Living on Columbia. Of those, two are hospitalized. The number of patients in the Covid Care Area is down from last week, when there were 23 patients.

On Thursday, there were 609 active positive cases in Grand Forks County, including 59 new active positives reported Thursday morning. Forty-five people were reported to have newly recovered on Thursday.

Altru Health System Director of Quality and Safety Kari Jensen reported that, as cases have risen in Grand Forks, the hospital also has recorded an uptick in inpatients with COVID-19 over the past few weeks.

Though COVID-19 has stretched hospital resources thin throughout the state in recent weeks, Jensen said capacity at Altru changes constantly throughout the day. On Thursday, she reported there were 14 inpatients being treated for COVID-19, down from 21 the day before.

Data reported to NDDOH by Altru indicate that on Thursday, there were 16 available non-ICU beds at Altru, and one available ICU bed.

According to Jensen, there are beds available in the hospital's COVID-19 units, but an Altru spokesperson did not provide the exact number of available beds in COVID-19 versus non-COVID-19 units.

Visit link:

COVID-19 numbers remain high in Grand Forks nursing homes amid 'uncontrolled community spread' - Grand Forks Herald

Every player tested neg.

The text message seemed full of relief as much as hope.

It was sent Oct. 13 by Ernesto Lerma, a 78-year-old assistant coach for the Palmview High School football team in the Rio Grande Valley, where the southern tip of Texas forms the toe of a cowboy boot along the border with Mexico.

A day later, Lerma sent an ominous update.

Big left tackle tested positive.

This was what everyone had feared as the fall sports season approached.

The coronavirus pandemic had ravaged the valley in summer. In July, ambulances lined up in a grim parade, waiting to drop patients at emergency rooms. Some funeral homes ordered refrigerated trucks to store bodies.

During such a crisis, Palmview High Schools fragile effort to hold a football season might seem inconsequential. But the game is perhaps more urgent and galvanizing in Texas than anywhere else. As towns along or near the Rio Grande like La Joya, Palmview, Mission, Progreso, Weslaco, Rio Hondo have shut off their Friday night lights, or left them flickering in uncertainty, there has been a sense of cultural casualty.

In late August, the school district that includes Palmview High, La Joya High and Juarez-Lincoln High decided to cancel fall sports. But some parents and athletes protested, and in late September officials reconsidered. In the end, though, only Palmview decided to proceed with football and only with severe limitations and precautions.

Margarito Requnez, 44, the head coach, insisted that every player and coach be screened weekly for the virus. If anyone was infected, the season would be shut down to keep the spread from getting out of hand.

I dont want that on my conscience, he said.

Accommodations were made for Lerma, who as a septuagenarian would be especially vulnerable to effects of the virus. He coached the offensive line from the bleachers as Palmview opened practice, wearing a mask and gloves and spraying his whistle with disinfectant. For games, he planned to coach from the running track surrounding the field.

We have to be very cautious, Lerma said. This is a deadly disease.

Palmview hoped to play an abbreviated season, beginning Oct. 30. But 16 days before kickoff, a starting tackle had tested positive and was awaiting the results of a retest. So was one other player. Palmviews four scheduled games seemed in jeopardy.

Meeting today, Lerma texted on Oct. 14. Decision?

The valleys fields are rich with cotton and grapefruit and oranges, but its predominantly Latino population is among the poorest in Texas and among the most susceptible to the worst effects of the virus.

As of Wednesday, more than 63,200 coronavirus infections had been reported and more than 3,200 people had died in the four counties that constitute the valley more fatalities than in any of the urban centers of Houston, Dallas and San Antonio.

If this were a season of expectation instead of sickness, every team in the valley would be chasing the elusive accomplishment of Donna High School, which in 1961 became the first and last team in the region to win a state football championship.

The story of that team is legend. Eighteen players. A six-hour bus ride to Austin, the capital, to play the title game on a rainy evening. A stop to eat and perform a parking-lot rehearsal of a trick formation that proved decisive. A trip home in the middle of the night because the school could not afford hotel rooms. An early-morning walk of eight miles along Highway 83, accompanied by dozens of townspeople, to attend a celebratory Mass at the Basilica of Our Lady of San Juan del Valle.

Its community pride, said Luz Pedraza, now 76, the quarterback of that championship team. It shows anything is possible.

Surely, said Progreso High Schools coach, Jos Meza, every member of his Mighty Red Ants team has driven past the water tower in nearby Donna that commemorates the long-ago title. But Progresos season has been canceled. There is no championship to aim for.

Underclassmen are training for next season, flipping tractor tires and fashioning weights from gallons of water. The sounds of fall have gone silent the pompom verve of the cheerleaders, the brassy pep of the band.

It feels empty, said Meza, 45. Even the traffic level feels low. Its an eerie feeling walking the halls and theres nobody there.

At Rio Hondo High School, extracurricular activities will not be permitted until students return to classrooms, said Rocky James, 52, the football coach and athletic director. In-person schooling kept being pushed back, to next Monday or possibly into November. That would have left room for only two football games. So the season was shelved.

James said he might have expected dozens of calls of complaint. He got none.

If theyre too scared to come to school, how is it fair to play football? he said.

Only six offensive linemen were among the interested in playing at La Joya High.

Some parents didnt think it was safe, said Reuben Faras, 54, La Joyas head coach. No vaccine.

Faras understood. Over the summer, when he would normally have been preparing for the season, he instead found himself among the grieving. On July 18, his father, Ruben, died of a heart attack related to Covid-19. He was 83.

Ruben Faras was a longtime coach, teacher, administrator and school board member. After retirement, he still attended all of his sons games.

But he also possessed fragile health diabetes, kidney failure that required dialysis, a heart condition that forced him to wear a pacemaker conditions all too familiar to the valleys close-knit but vulnerable families. More than a third live in poverty. Up to half of the residents lack health insurance, and more than 60 percent are diabetic or prediabetic. Rates of obesity and heart disease, two of the conditions that tend to worsen effects of the virus, are among the nations highest.

While driving his father to a dialysis treatment in the spring, when the pandemic was imminent, Reuben Faras asked if he was prepared to die. The son remembered the answer as philosophical. His father said he had lived a good life. He had wanted to reach 75 and outlive his own mother. He had.

If I die today, Ruben Faras told his son, Im ready to go.

Elva Faras, 77, Rubens wife and Reubens mother, tested positive for the virus on July 17. Her husband felt fatigued that night and labored to breathe the next morning. He was admitted to a hospital, which determined he had pneumonia and the coronavirus, his son said. That afternoon, Ruben Faras had one heart attack, then another, and could not be resuscitated.

It was out of the question to hold the funeral immediately. Stricken with Covid-19, the family matriarch would not be able to attend. Reuben Faras moved in with his mother, leaving his own family and putting himself at risk of getting the virus, but he could not bear to leave her by herself at such a time.

Both of them developed symptoms of Covid-19 fever, fatigue, a cough, congestion. But Elva declined to go to a hospital, telling her son, Id rather die here at the house instead of alone at the hospital.

Eventually, they began to recover. After three weeks in isolation, they said, they tested negative for the virus and finally turned their attention to burying the family patriarch. Twenty-four days after he died, Ruben Faras was laid to rest.

Even in death, the coronavirus was disruptive. Drive-by funerals became part of the pandemic lexicon. Ruben Farass funeral procession stopped at Our Lady of Guadalupe Catholic Church in Mission, Texas, and a priest came outside to bless the coffin with incense and holy water. At the Rio Grande Valley State Veterans Cemetery, mourners remained in their cars. The priest approached Elva Faras, who lowered her window in her mask and face shield, and read from the Scriptures, standing close in his own mask so she could hear.

It was hard, everything we went through, Elva Faras said. I wouldnt wish this on anybody.

Two weeks after the funeral, when football was abandoned at Juarez-Lincoln High, Isabel Rocha, 42, felt a sense of relief. Her son, ngel Portillo, 17, was to be a senior cornerback. Rocha felt bad he would miss his final season, but said she had not wanted him to play. Her father and an uncle had died of Covid-19. She feared that her son might catch the coronavirus and spread it to their extended family. Portillo said he understood and would not have played.

I didnt want to be the one to hurt my family just to play football, he said. Safety over sport. Family over anything.

At Palmview, the safety concerns remained worrying into mid-October: The two Palmview players who had tested positive were being screened again. Practices for last Thursday and Friday were called off.

With our poor kids, it was a matter of time, Requnez, the coach, said. If colleges and pro teams are having trouble containing it, what makes us think a high school team that doesnt have the resources could?

On Friday, Palmview received good news. The initial tests turned out to be false positives. The retests were negative. Another weekly screening for the entire team took place on Monday. The results for 45 of the schools 60 or so players had been returned by Wednesday, all negative. Practice resumed after a week for those who were cleared.

I dont know how other school districts are doing it, Requnez said, referring to teams that have continued after players tested positive. I dont know how they can put peoples lives in jeopardy.

When one of your athletes gets sick, all you do is next man up, send him home and monitor the rest, he added. Were not going to do that. Were going to make sure we protect everybody.

But things continued to grow complicated at Palmview. A volunteer helping out the team tested positive early last week, Requnez said on Wednesday, so Lerma, the 78-year-old assistant, went into quarantine as a precaution. The season wont start now until Nov. 6.

Palmviews principal and the school districts athletic director suggested that football continue, Requnez said, to give the team every opportunity to play at least one game. He and his assistants agreed, as long as testing continued weekly, he said, and with the understanding that if there is a positive test once the season starts, Thats it, were done.

Were going to give it one more shot, Requnez said. If it happens, it happens. If it doesnt, it doesnt. But at least we tried.

Read more:

Covid-19 Dims the Friday Night Lights of Texas Football - The New York Times

Find all of the most important pandemic education news on Educating N.J., a special resource guide created for parents, students and educators.

The number of New Jersey schools where health investigations determined students or teachers transmitted COVID-19 in school or during extracurricular activities rose to 25 this week, according to the state's covid19.nj.gov website.

Since the start of the school year, at least 111 New Jersey students and educators have either contracted COVID-19 or passed it on to someone else while in the classroom, walking around their schools or participating in extracurricular activities, state officials said Thursday.

The totals include three new outbreaks at schools in Camden, Hudson and Somerset counties with a total of 28 new cases since last week, according to the data.

We knew going in that there would be cases in our schools and our job has been to work fast to put a lid on any outbreaks, Gov. Phil Murphy said at his coronavirus press briefing.

The 111 cases were part of 25 confirmed school outbreaks that local health investigations concluded were the result of students and teachers catching the coronavirus at school not at home, at parties or other gatherings, according to the state COVID-19 dashboard.

The numbers do not include the positive COVID-19 cases reported among New Jersey students and teachers who are suspected to have contracted the virus outside school. The state has not released those numbers, though a database maintained by the National Education Association says more than 220 New Jersey schools have reported at least one coronavirus case.

Though every case is taken seriously, Murphy said state officials believe the school outbreak numbers are still low as classes continue to practice social distancing and follow mask requirements. There have been outbreaks in less than 1% of the states more than 3,000 public and private schools, though not all of them are offering in-person classes.

So far, so good, Murphy said.

Citing privacy reasons, the state has not named the schools where the outbreaks occurred, nor the dates or any of the circumstances that led to the in-school transmission. However, the state has identified the counties where the schools are located.

The 25 outbreaks include:

Atlantic County: 1 school outbreak with 2 cases.

Bergen County: 3 school outbreaks with a total of 9 cases.

Burlington County: 2 school outbreaks with a total of 6 cases

Camden County: 3 school outbreaks with a total of 33 cases.

Cape May County: 3 school outbreaks with a total of 10 cases.

Gloucester County: 2 school outbreaks with a total of 10 cases.

Hudson County: 1 school outbreak with 4 cases.

Hunterdon County: 1 school outbreak with 3 cases.

Ocean County: 3 school outbreaks with a total of 9 cases.

Passaic County: 1 school outbreak with 9 cases.

Salem County: 2 school outbreaks with a total of 10 cases.

Somerset County: 2 school outbreak with a total of 4 cases.

Sussex County: 1 school outbreak with 2 cases.

Eight counties have reported no school outbreaks. They are: Cumberland, Essex, Mercer, Monmouth, Union, Warren, Morris and Middlesex counties.

Under New Jerseys guidelines, schools can shut down and switch to remote learning for two weeks if two or more students test positive for COVID-19 in different classrooms with the possibility they transmitted the virus to each other. Schools are required to inform families when there are COVID-19 cases in their classrooms, but the rest of the community might not be notified unless local health officials think it is necessary.

Most New Jersey school districts are operating under hybrid plans with a mix of in-person and at-home classes. Several school districts, including Paterson and Newark, are offering all-remote classes and plan to keep their school buildings closed until early 2021 due, in part, to the rise in outbreaks.

Thank you for relying on us to provide the journalism you can trust. Please consider supporting NJ.com with a subscription.

Kelly Heyboer may be reached at kheyboer@njadvancemedia.com.

Read more:

More than 100 students and teachers transmitted or caught COVID-19 in school outbreaks, N.J. officials say - NJ.com

The family of seven known human coronaviruses are known for their impact on the respiratory tract, not the heart. However, the most recent coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has marked tropism for the heart and can lead to myocarditis (inflammation of the heart), necrosis of its cells, mimicking of a heart attack, arrhythmias, and acute or protracted heart failure (muscle dysfunction). These complications, which at times are the only features of coronavirus disease 2019 (COVID-19) clinical presentation, have occurred even in cases with mild symptoms and in people who did not experience any symptoms. Recent findings of heart involvement in young athletes, including sudden death, have raised concerns about the current limits of our knowledge and potentially high risk and occult prevalence of COVID-19 heart manifestations.

The four common cold human coronavirusesHCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1have not been associated with heart abnormalities. There were isolated reports of patients with Middle East respiratory syndrome (MERS; caused by MERS-CoV) with myocarditis and a limited number of case series of cardiac disease in patients with SARS (caused by SARS-CoV) (1). Therefore, a distinct feature of SARS-CoV-2 is its more extensive cardiac involvement, which may also be a consequence of the pandemic and the exposure of tens of millions of people to the virus.

What appears to structurally differentiate SARS-CoV-2 from SARS is a furin polybasic site that, when cleaved, broadens the types of cells (tropism) that the virus can infect (2). The virus targets the angiotensin-converting enzyme 2 (ACE2) receptor throughout the body, facilitating cell entry by way of its spike protein, along with the cooperation of the cellular serine protease transmembrane protease serine 2 (TMPRSS2), heparan sulfate, and other proteases (3). The heart is one of the many organs with high expression of ACE2. Moreover, the affinity of SARS-CoV-2 to ACE2 is significantly greater than that of SARS (4). The tropism to other organs beyond the lungs has been studied from autopsy specimens: SARS-CoV-2 genomic RNA was highest in the lungs, but the heart, kidney, and liver also showed substantial amounts, and copies of the virus were detected in the heart from 16 of 22 patients who died (5). In an autopsy series of 39 patients dying from COVID-19, the virus was not detectable in the myocardium in 38% of patients, whereas 31% had a high viral load above 1000 copies in the heart (6).

Accordingly, SARS-CoV-2 infection can damage the heart both directly and indirectly (see the figure). SARS-CoV-2 exhibited a striking ability to infect cardiomyocytes derived from induced pluripotent stem cells (iPSCs) in vitro, leading to a distinctive pattern of heart muscle cell fragmentation, with complete dissolution of the contractile machinery (7). Some of these findings were verified from patient autopsy specimens. In another iPSC study, SARS-CoV-2 infection led to apoptosis and cessation of beating within 72 hours of exposure (8). Besides directly infecting heart muscle cells, viral entry has been documented in the endothelial cells that line the blood vessels to the heart and multiple vascular beds. A secondary immune response to the infected heart and endothelial cells (endothelitis) is just one dimension of many potential indirect effects. These include dysregulation of the renin-angiotensin-aldosterone system that modulates blood pressure, and activation of a proinflammatory response involving platelets, neutrophils, macrophages, and lymphocytes, with release of cytokines and a prothrombotic state. A propensity for clotting, both in the microvasculature and large vessels, has been reported in multiple autopsy series and in young COVID-19 patients with strokes.

There is a diverse spectrum of cardiovascular manifestations, ranging from limited necrosis of heart cells (causing injury), to myocarditis, to cardiogenic shock (an often fatal inability to pump sufficient blood). Cardiac injury, as reflected by concentrations of troponin (a cardiac musclespecific enzyme) in the blood, is common with COVID-19, occurring in at least one in five hospitalized patients and more than half of those with preexisting heart conditions. Such myocardial injury is a risk factor for in-hospital mortality, and troponin concentration correlates with risk of mortality. Furthermore, patients with higher troponin amounts have markers of increased inflammation [including C-reactive protein, interleukin-6 (IL-6), ferritin, lactate dehydrogenase (LDH), and high neutrophil count] and heart dysfunction (amino-terminal pro-Btype natriuretic peptide) (9).

More worrisome than the pattern of limited injury is myocarditis: diffuse inflammation of the heart, usually representing a variable admixture of injury and the inflammatory response to the injury that can extend throughout the three layers of the human heart to the pericardium (which surrounds the heart). Unlike SARS-associated myocarditis, which did not exhibit lymphocyte infiltration, this immune and inflammatory response is a typical finding at autopsy after SARS-CoV-2 infections. Involvement of myocytes, which orchestrate electrical conduction, can result in conduction block and malignant ventricular arrhythmias, both of which can lead to cardiac arrest.

Along with such in-hospital arrythmias, there have been reports of increased out-of-hospital cardiac arrest and sudden death in multiple geographic regions of high COVID-19 spread, such as the 77% increase in Lombardy, Italy, compared with the prior year (10). There have been many reports of myocarditis simulating a heart attack, owing to the cluster of chest pain symptoms, an abnormal electrocardiogram, and increased cardiac-specific enzymes in the blood, even in patients as young as a 16-year-old boy. When there is extensive and diffuse heart muscle damage, heart failure, acute cor pulmonale (right heart failure and possible pulmonary emboli), and cardiogenic shock can occur.

COVID-19associated heart dysfunction can also be attributed to other pathways, including Takotsubo syndrome (also called stress cardiomyopathy), ischemia from endothelitis and related atherosclerotic plaque rupture with thrombosis, and the multisystem inflammatory syndrome of children (MIS-C). The underlying mechanism of stress cardiomyopathy is poorly understood but has markedly increased during the pandemic. MIS-C is thought to be immune-mediated and manifests with a spectrum of cardiovascular features, including vasculitis, coronary artery aneurysms, and cardiogenic shock. This syndrome is not exclusive to children because the same clinical features have been the subject of case reports in adults, such as in a 45-year-old man (11).

Recent series of COVID-19 patients undergoing magnetic resonance imaging (MRI) or echocardiography of the heart have provided some new insights about cardiac involvement (1214). In a cohort of 100 patients recovered from COVID-19, 78 had cardiac abnormalities, including 12 of 18 patients without any symptoms, and 60 had ongoing myocardial inflammation, which is consistent with myocarditis (12). The majority of more than 1200 patients in a large prospective cohort with COVID-19 had echocardiographic abnormalities (13). This raises concerns about whether there is far more prevalent heart involvement than has been anticipated, especially because at least 30 to 40% of SARS-CoV-2 infections occur without symptoms. Such individuals may have underlying cardiac pathology.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has the potential to directly and indirectly induce cardiac damage.

To date, there have been four small series of asymptomatic individuals with bona fide infections who underwent chest computed tomography (CT) scans to determine whether there were lung abnormalities consistent with COVID-19. Indeed, half of the asymptomatic people showed lung CT features that were seen in patients with symptoms. But so far, there have been minimal cardiac imaging studies in people who test positive for SARS-CoV-2 or are seropositive but without symptoms. Furthermore, the time course of resolution or persistence of any organ abnormalities after SARS-CoV-2 infection has not yet been reported. With a high proportion of silent infections despite concurrent evidence of internal organ damage, there is a fundamental and large hole in our knowledge base.

In contrast to people without symptoms, there is a substantial proportion of people who suffer a long-standing, often debilitating illness, called long-COVID. Typical symptoms include fatigue, difficulty in breathing, chest pain, and abnormal heart rhythm. An immunologic basis is likely but has yet to be determined. Nor have such patients undergone systematic cardiovascular assessment for possible myocarditis or other heart abnormalities, such as fibrosis, which could account for some of the enduring symptoms. It would not be surprising in the future for patients to present with cardiomyopathy of unknown etiology and test positive for SARS-CoV-2 antibodies. However, attributing such cardiomyopathy to the virus may be difficult given the high prevalence of infections, and ultimately a biopsy might be necessary to identify virus particles to support causality.

Cardiac involvement in athletes has further elevated the concerns. A 27-year-old professional basketball player, recovered from COVID-19, experienced sudden death during training. Several college athletes have been found to have myocarditis (14), including 4 of 26 (15%) in a prospective study from Ohio State University (15), along with one of major league baseball's top pitchers. Collectively, these young, healthy individuals had mild COVID-19 but were subsequently found to have unsuspected cardiac pathology. This same demographic groupyoung and healthyare the most common to lack symptoms after SARS-CoV-2 infections, which raises the question of how many athletes have occult cardiac disease? Systematic assessment of athletes who test positive for SARS-CoV-2, irrespective of symptoms, with suitable controls through some form of cardiac imaging and arrhythmia screening seems prudent until more is understood.

The most intriguing question that arises is why do certain individuals have a propensity for heart involvement after SARS-CoV-2 infection? Once recognized a few months into the pandemic, the expectation was that cardiac involvement would chiefly occur in patients with severe COVID-19. Clearly, it is more common than anticipated, but the true incidence is unknown. It is vital to determine what drives this pathogenesis. Whether it represents an individual's inflammatory response, an autoimmune phenomenon, or some other explanation needs to be clarified. Beyond preventing SARS-CoV-2 infections, the goal of averting cardiovascular involvement is paramount. The marked heterogeneity of COVID-19, ranging from lack of symptoms to fatality, is poorly understood. A newly emerged virus, widely circulating throughout the human population, with a panoply of disease manifestations, all too often occult, has made this especially daunting to unravel.

Acknowledgments: E.J.T. is supported by National Institutes of Health grant UL1 TR001114.

Originally posted here:

COVID-19 can affect the heart - Science Magazine

Women over 50 are most likely to share pandemic-related stories on Twitter from websites that share fake news, and Republicans are many times more likely to share questionable material than Democrats, according to a new study by researchers from Northeastern, Harvard, Northwestern, and Rutgers.

The study looked at age and demographics to pinpoint who is sharing false pandemic content via Twittercross referencing shares on the social media platform this year with URLs from five websites identified with fake news.

Photo by Adam Glanzman/Northeastern University

80 to 90 percent of fake news comes from a few tenths of one percent of all accounts, says David Lazer, University Distinguished Professor of political science and computer and information sciences at Northeastern, and one of the researchers who conducted the study.

Researchers defined fake news as information that mirrors legitimate news in form, but lacks the news medias editorial norms and processes for ensuring the accuracy and credibility of information.

The fake news domain with the most shares is Gateway Pundit, the study found. Since March, the website has received an order of magnitude more shares than the second most shared fake news domain, Info Wars.

The popularity of Gateway Pundit is even more striking when compared with all other web domainsincluding mainstream news mediathat share news about the pandemic. In August and September respectively, Gateway Pundit was ranked the 4th and 6th most shared domain for URLs about COVID-19. In August, the only domains with more COVID-19-related shares were the New York Times, the Washington Post and CNN, the study found.

It is notable that, during 2020, registered Republicans and older people are more likely to share URLs from fake news domains. The same demographics were also more likely to do so during the 2016 presidential election, researchers wrote in the study released today.

But researchers note that while older people are more likely to share fake news, younger people are more likely to believe it. In a study released earlier this year, researchers found that minorities and younger people are more susceptible to fake news and misinformation about COVID-19, and younger generations are also more likely to believe false claims they receive on closed messaging platforms such as WhatsApp and Facebook Messenger.

Source: Lazer Lab at the Network Science Institute, covidstates.org

According to that report, 22 percent of participants said they believed the rumor that COVID-19 originated as a weapon in a Chinese lab, and 7 percent trusted the claim that the flu vaccine increases the risk of contracting COVID-19.

This time around, researchers were curious about who was behind the sharing of bad information, not who was believing it. The average age of these so-called super sharers is 59, considerably older than the average Twitter user, Lazer says.

In terms of the data, its disproportionately older women, he says.

In October, Twitter started labelingtweets that contain misleading information about COVID-19, flagging the posts in a way that de-amplifies them in the platforms algorithm, regardless of how viral they go. In some cases, misleading tweets are simply deleted.

Since the global respiratory disease took hold, killing more than 1 million people worldwide so far, there has been a great deal of confusion and misinformation surrounding COVID-19much of it occurring online, in the so-called Infodemic.

To conduct the study, researchers collected COVID-19-related tweets from registered voters in America between January and September 2020, and examined the content posted by a list of accounts matched to demographic information such as age, race, gender and political party affiliation. The number of COVID-19-related tweets was almost 30 million.

The study found that despite older people sharing more misinformation, they are actually more informed, likely because older users are more interested in COVID-19 generally. The seeming paradox warrants further research, Lazer says.

It begs the question that maybe older people [overall] are less misinformed, but older people on Twitter are more misinformed. Alternatively, sharing may not be predicated on believing. We dont know. This is a question that we will address with additional data.

For media inquiries, please contact media@northeastern.edu.

Original post:

30M tweets about COVID-19, and not all of them contain the truth. Who's spreading misinformation? - News@Northeastern

NORTH TEXAS (CBSDFW.COM) Doctors are testing a drug in North Texas, which will help with one of the most dangerous complications induced by COVID-19 called the cytokine storm.

Mortality in COVID-19 patients has been linked to its presence where excessive production of proinflammatory cytokines leads to ARDS aggravation and widespread tissue damage resulting in multi-organ failure and death. This means the body starts to attack its own cells and tissues rather than just fighting off the virus.

Targeting cytokines during the management of COVID-19 patients could improve survival rates and reduce mortality.

Unfortunately with some patients, when they get infected with the virus, its as if their foot is on the gas pedal and it stays on the gas pedal and it keeps pushing hard on the gas pedal, said Dr. Cameron Durrant, CEO of Humanigen. What Lenzilumab does, and it has a dual action, is it alleviates the pressure by taking the foot off the gas pedal and putting a foot on the brake pedal.

A Mayo Clinic study looking at 12 patients found 92% of them saw improvement with the drug staying five days in the hospital instead of 11.

As for immunity, no one knows how long it lasts in patients who had the coronavirus. On the plus side, the disease mutates more slowly than flu viruses, whose viral-protein targets change so fast that annual flu shots are needed.

(credit: Humanigen)

MORE FROM CBSDFW

Here is the original post:

North Texas Doctors Testing Drug As Promising Treatment For Severe COVID-19 Complications - CBS Dallas / Fort Worth

CanSino Biologicss experimental COVID-19 vaccine is one of at least four using an adenovirus that some worry could increase HIV susceptibility.

By Jon CohenOct. 19, 2020 , 6:30 PM

Sciences COVID-19 reporting is supported by the Pulitzer Center and the Heising-Simons Foundation.

Certain COVID-19 vaccine candidates could increase susceptibility to HIV, warns a group of researchers who in 2007 learned that an experimental HIV vaccine had raised in some people the risk for infection with the AIDS virus. These concerns have percolated in the background of the race for a vaccine to stem the coronavirus pandemic, but now the researchers have gone public with a cautionary tale, in part because trials of those candidates may soon begin in locales that have pronounced HIV epidemics, such as South Africa.

Some approved and experimental vaccines have as a backbone a variety of adenoviruses, which can cause the common cold but are often harmless. The ill-fated HIV vaccine trial used an engineered strain known as adenovirus 5 (Ad5) to shuttle into the body the gene for the surface protein of the AIDS virus. In four candidate COVID-19 vaccines now in clinical trials in several countries, including the United States, Ad5 similarly serves as the vector to carry in the surface protein gene of SARS-CoV-2, the viral cause of the pandemic; two of these have advanced to large-scale, phase III efficacy studies in Russia and Pakistan.

In todays issue ofTheLancet, four veteran researchers raise a warning flag about those COVID-19 vaccine candidates by recounting their experience running a placebo-controlled AIDS vaccine trial dubbed STEP.An interim analysis of STEP found that uncircumcised men who had been naturally infected with Ad5 before receiving the vaccine became especially vulnerable to the AIDS virus. The vaccine, made by Merck, had been the leading hope for what was then a 20-year search for a shot that could thwart HIV. But after the STEP results appeared, the field went into a tailspin. It took a decade to recover, says one of the co-authors of theLancet correspondence, Lawrence Corey of the Fred Hutchinson Cancer Research Center.

Corey, who now co-leads the COVID-19 prevention network in the United States that is testing vaccines at the behest of the National Institutes of Health, says he and his co-authors went public because Ad5-based COVID-19 vaccines may soon be tested in populations with high HIV prevalence and thus a greater risk of accidental infection during a clinical trial. If I were in a sub-Saharan African country and making a decision as to what I would want for my country for a general population use of a SARS-CoV-2 vaccine, I dont see why I would pick an Ad5 vector [vaccine] when there are many other alternative choices, Corey says.

The backfire in STEPwhich evaluated the efficacy of the Merck vaccine in people at high risk of HIV infection in the Americas and Australiaalso appeared in a second study, dubbed Phambili, of the same vaccine. It was taking place simultaneously in South Africa and was stopped early because of the STEP data.

Precisely how Mercks Ad5 vaccine increased the risk of HIV transmission in STEP and Phambili remains murky. The Lancet editorial spells out several possibilities, including dampening of HIV immunity, enhancing replication of the AIDS virus, or setting up more target cells for it.

In addition to the Ad5 COVID-19 vaccine candidates, several other leading vaccines, including ones made by Johnson & Johnson and AstraZeneca/the University of Oxford, use different adenoviruses as vectors. Theres no evidence that any of those adenoviruses increases the risks of an HIV infection.

I dont see why I would pick an Ad5 vector [vaccine] when there are many other alternative choices.

Of the Ad5-based COVID-19 vaccine candidates, from China-based CanSino Biologics, has developed the furthest. In a Lancet report in May, researchers from the company recognized the controversial possibility of their vector increasing the risk of HIV infection and said they would watch for it in the candidates trials. CanSinos COVID-19 vaccine is being tested in efficacy trials in Russia and Pakistan that together hope to enroll more than 40,000 people, and the company is discussing starting studies in Saudi Arabia, Brazil, Chile, and Mexico.

China has already approved a CanSino vaccine against Ebola that uses the Ad5 vector. Yu Xuefeng, CanSinos CEO, tells Science the risk of increased HIV susceptibility may be limited to Ad5 vaccines that produce an AIDS virus protein. Theres no clear answer yet, Yu says. We certainly havent seen anything with the Ebola vaccine. The companys Ebola vaccine was tested in a population in Sierra Leone that, he notes, had a relatively high HIV prevalence, making it more likely to have detected the problem if it existed.

Russias Gamaleya Research Institute has a COVID-19 vaccine candidate that uses a combination of Ad5 and Ad26 vectors; its now in an efficacy trial in that country.

Last week, ImmunityBio received approval from the U.S. Food and Drug Administration to begin human trials of its COVID-19 vaccine, which uses Ad5 as a vector. The first trial will take place in Newport Beach, California, but Patrick Soon-Shiong, the companys CEO, says he also hopes to test it in South Africa, where he grew up and went to medical school.

He calls the STEP study results very, very fuzzy and stresses that ImmunityBios Ad5 has four deleted genes that reduce the immune responses it triggers. Its 90% muted, he says.

ImmunityBio is discussing the risks with scientists and regulators in South Africa of a trial there to test its modified Ad5 COVID-19 vaccine. The informed consent process for that proposed study would tell participants about potential risks given the previous STEP and Phambili results.

Soon-Shiong emphasizes that his companys experimental COVID-19 vaccine, unlike every other candidate that uses an adenovirus vector, presents two different SARS-CoV-2 genes and mighttherefore offer more protection from infection or disease. Why only test this in wealthy enclaves of Southern California, he asks? Why not South Africa? Why not for the underserved people of the world?

Pediatrician Glenda Gray, who heads the South African Medical Research Council and was the protocol chair of Phambili, has taken part in several discussions with the ImmunoBio team.When [Soon-Shiong] contacted South Africa, we were obviously quite concerned, Gray says. All of us who were in Phambili and quite traumatized by what happened asked whether there was an appetite to do something in South Africa.

But after several months of deliberations, the South Africans concluded that regulators should consider a small trial of the vaccine there in people at low risk of HIV infection, Gray says. We decided not to throw the baby out with the bath water just yet, she adds. If it does go ahead in South Africa, there has to be huge consultation with communities, and we have to make doubly sure that the participants understand what happened in the past.

Gray says South Africa appreciates ImmunoBios offer to allow the country to manufacture the product. Were in the middle of a COVID-19 epidemic in South Africa, and we dont know if well ever get access to the current suite of vaccines produced elsewhere, she says.

The decision to move forward, she insists, has to be left to South African scientists, regulators, and ethics committees. Its incredibly patronizing for people to determine what science is good or bad for other countries, she says. Everyone knows about Phambili and STEP, and the scientists understand that theres an important need to be cautious.

Gray, who has co-authored papers about HIV vaccines with Corey and the other three authors of the Lancet correspondence, says there are no easy answers. What if this vaccine is the most effective vaccine? she asks. If this works out to be an important vaccine, well have some experience with it.

The rest is here:

Could certain COVID-19 vaccines leave people more vulnerable to the AIDS virus? - Science Magazine

Need to stay updated on coronavirus news in Texas? Our evening roundup will help you stay on top of the day's latest updates. Sign up here.

Cases of COVID-19 in parts of Texas surged to near catastrophic levels this summer as some hospitals were forced to put beds in hallways, intensive care units exceeded capacity and health officials struggled to stem the tide of the virus.

After peaking in late July and August, cases fell and leveled off in September, and the states seven-day positivity rate or the proportion of positive tests reached its lowest point since early June.

But health officials are now eyeing a worrying trend: New infections are rising again, and the number of patients hospitalized with COVID-19 is also ticking upward. The state reported 2,273 new cases Monday, and the seven-day average was up by 862 from the previous week. On Monday, at least 4,319 patients were hospitalized with COVID-19, far below the more than 10,000 in July, but that number has steadily risen during the last month.

Im no longer pondering if were going to see a surge, said Dr. James McDeavitt, dean of clinical affairs at the Baylor College of Medicine. Were already seeing it.

Eight months since Texas recorded its first case, experts say the state is more prepared to handle another wave, but they fear that if the state fails to control the outbreak, it could quickly spiral out of control.

The question is whether itll be a modest surge, or something like we saw in July, or worse, McDeavitt said.

The majority of new cases recently have been in people in their 20s and 30s who are generally healthier and less likely to face serious health complications, McDeavitt said. Thats a shift from the spring and summer surges, when older people and those with preexisting health conditions were hit hardest.

I suspect this surge will not be as medically intensive as the past, McDeavitt added.

Dr. David Persse, the city of Houstons chief medical officer, said that cases in a younger demographic would not stay concentrated within that population.

Its true that the biggest increase in cases is in younger people, he said. Its true that they tend to become less sick. The thing to keep in mind, however, is that those same people are at risk for spreading it to the 50-, 60-, 70-, 80-year-olds.

At Houston Methodist, one of the regions largest health care systems, medical staff were stretched thin this summer, said President Marc Boom. At its peak in July, the systems staff treated nearly 850 patients with COVID-19 each day. Since then, Boom said, the medical communitys understanding of the virus has evolved, along with how to treat the disease.

Remdesivir, an antiviral medication, has shown promising results in minimizing the severity of illness, especially when administered shortly after symptoms develop. Houston Medical was the first hospital to use convalescent plasma, a therapy in which antibody-rich blood from people who have recovered from COVID-19 is administered to ill patients, Boom said.

Weve had tons of experience gained, better outcomes, shorter lengths of stay, Boom said. But this is still a serious illness.

While health authorities are better equipped to deal with new spikes, including an adequate supply of protective gear and sizable quantities of drugs like Remdesivir, a fall surge could still be equally as taxing on hospitals, said Carrie Kroll, vice president of advocacy, quality and public health at the Texas Hospital Association. As colder weather forces people inside and families gather for the holiday season, the chances for transmission increase, she said.

We certainly have been tested, and we know the beast that it is, and have shown that we were able to make it through those first two spikes, Kroll said. But we dont want to test the limit by putting patients into hospitals.

Hospitalizations from COVID-19 have already begun to tick upward in areas of the state including West Texas, the Dallas-Fort Worth area and the Panhandle. But nowhere is the situation as dire as in El Paso.

A record 496 people were hospitalized Monday, and only 16 intensive care unit beds were available among facilities in El Paso, Hudspeth and Culberson counties, according to city and state data. El Paso Mayor Dee Margo scaled back business capacity from 75% to 50% last week and banned home gatherings. Gov. Greg Abbott also dispatched an emergency team of doctors and nurses to assist local health care facilities.

El Paso Health Director Angela Mora said that while she is concerned with hospital capacity, shes confident the city can handle the influx of cases. Officials are instead focusing on reminding residents to follow simple precautions, such as wearing masks in public, washing hands frequently and avoiding gatherings.

Somebody mentioned that the pandemic is out of control, Mora said. We are the ones who are out of control, because we are not practicing preventive measures that really work.

Experts attribute this latest surge in part to pandemic fatigue thats leading more people to ignore precautions that help slow the virus.

We know what works, our community knows what works, weve seen the results when everyone sticks to it, said Dr. Philip Huang, who leads the Dallas County Health Department.

Last week, Dallas County Judge Clay Jenkins increased the countys coronavirus threat level to red indicating high community spread. Hospitals in the region are closely monitoring the trend and are able to quickly scale up capacity, said Stephen Love, president of the Dallas-Fort Worth Hospital Council.

In response to rising hospitalizations in Amarillo and Lubbock, Abbott sent additional medical resources, including personnel, ventilators and IV pumps, last week. This came even as the governor allowed bars to reopen in parts of the state where patients with COVID-19 make up less than 15% of hospitalizations and local officials opted in.

Local officials in most major cities have so far been reluctant to lift restrictions, fearing packed bars and restaurants could lead to a dangerous rise in cases.

This is a super slick virus thats broken all the rules, said Dr. Umair Shah, executive director of the Harris County Health Department. We may be tired of this virus, but the virus is not tired of us.

Disclosure: Texas Hospital Association has been a financial supporter of The Texas Tribune, a nonprofit, nonpartisan news organization that is funded in part by donations from members, foundations and corporate sponsors. Financial supporters play no role in the Tribune's journalism. Find a complete list of them here.

Continued here:

Texas is better prepared for the next COVID-19 surge, experts say - The Texas Tribune

Two studies published Wednesday in the journal Blood Advances add to a growing body of evidence showing there may be a correlation between a person's blood type and their risk of developing a severe case of Covid-19and suggest one blood type in particular may be tied to a lower risk.

Cheat sheets: Evidence-based medicine 101

Early in the novel coronavirus pandemic, research suggested that individuals with Type A blood were at an especially high risk of developing a severe case of Covid-19 or dying from the disease.

For example, one preprint study released in June examined blood samples from 1,610 Covid-19 patients who developed severe cases of Covid-19, which the researchers classified as needing oxygen or a ventilator as part of their treatment. The researchers found that many of the patients who had severe cases of Covid-19 possessed the same variant on a gene that determines a person's blood type, and that having blood type A was linked with a 50% increase in the likelihood a patient would develop a severe case of Covid-19.

In addition, another preprint study conducted by researchers in China found that, out of 2,173 Covid-19 patients, blood type A was associated with a higher risk of death from Covid-19 and a higher risk of contracting the new coronavirus. Those researchers also noted that patients with blood type O appeared to be the least likely to contract the virus.

However, later research revealed a more complicated picture, suggesting that the link between Covid-19 a person's blood type might not be significant enough to actually alter a person's risk.

For instance, after reviewing the medical records of 7,770 people who tested positive for the novel coronavirus, Nicholas Tatonetti, a data scientist at Columbia University, and graduate student Michael Zietz said they found that having blood Type A blood was associated with a lower risk of being placed on a ventilator, while having blood type AB was associated with a higher risk of needing ventilation. But overall, Tatonetti said connections between individuals' blood type and their Covid-19 risk were not strong enough to consider blood type as a risk factor for contracting the new coronavirus or developing a severe case of Covid-19.

"No one should think they're protected" because of their blood type, he said.

Separately, researchers at Massachusetts General Hospital (MGH) in a study published in Annals of Hematology, which has open access options, found that people with Type O blood appeared to have a slightly lower risk of contacting the novel coronavirusbut they also found that a patient's blood type was not associated with their risk of needing ventilation or dying because of Covid-19. Anahita Dua, a vascular surgeon at MGH and senior author of the study, said the link she and her colleagues found between blood type and coronavirus risk was so weak that she "wouldn't even" consider using blood type as a risk factor for the virus or Covid-19.

But now, two new studies offer more evidence suggested there is, in fact, a correlation between a person's blood type and their Covid-19 riskand that people with blood Type O are less susceptible to the coronavirus overall.

For one study, researchers in Denmark analyzed data on 473,654 people who were tested for the new coronavirus between February and July. In total, 7,422 of those people tested positive for the virus.

The researchers found that 38.4% of those who tested positive for the coronavirus had blood Type Oa finding that seemed low when considering that 41.7% of the untested Danish population had that blood type. In comparison, 44.4% of those who tested positive for the virus had blood Type A, while people with that blood type comprised 42.4% of the untested population.

The researchers wrote that their findings demonstrate that blood Type O "is significantly associated with reduced susceptibility to" the novel coronavirusthough they also noted that their study had several limitations and called for further research on the topic.

For the second study, researchers in Canada analyzed data on 95 patients in Vancouver who tested positive for the coronavirus between February and April. All of the patients were hospitalized for Covid-19 in an ICU.

Among those patients, the researchers found that those with Type A or AB blood had a median ICU stay of 13.5 days, compared to with a median ICU stay of nine days among patients with blood Type O or B. The researchers also found that the patients with Type A or AB blood were more likely to require mechanical ventilation, at 84%, than patients with blood Type O or B, at 61%.

The researchers wrote that, overall, their findings "demonstrate that critically ill Covid-19 patients with blood [Type] A or AB are associated with an increased risk for requiring mechanical ventilation and prolonged ICU length of stay compared with patients with blood [Type] O or B." However, they also noted that their research had several limitations and called for more studies on the topic. "Further research is required to delineate the biological mechanisms underpinning these findings," they wrote.

While experts generally agreed that the new findings are interesting, they cautioned that the results are correlationalnot causational.

Roy Silverstein, chair of medicine at the Medical College of Wisconsin, called the new studies' findings "interesting cocktail party conversation," and he added that, with further study, they "could lead to new approaches for prevention or therapy." However, he said, "at the present time, there is no reason to think that if you have type O blood, you're protected from Covid-19."

Similarly, Mypinder Sekhon, an intensive care physician at Vancouver General Hospital and an author of the Canadian study, said, "As a clinician [blood type] is at the back of my mind when I look at patients and stratify them. But in terms of a definitive marker we need repeated findings across many jurisdictions that show the same thing."

Sekhon added that he doesn't believe blood type "supersedes other risk factors of severity" for Covid-19, such as a person's age or comorbidities.

"If one is blood group A, you don't need to start panicking," Sekhon said. "And if you're blood group O, you're not free to go to the pubs and bars" (Edwards, NBC News, 10/14; Fox8, 10/14; Hunt/Howard, CNN, 10/14; Bogetofte Barnkob et al., Blood Advances, 10/14; Hoiland, Blood Advances, 10/14).

Read the original:

Does your blood type affect your Covid-19 risk? Here's the latest evidence. - The Daily Briefing