The COVID-19 Science and Medicine Question Thread

Sad news and doesn't bode well for school openings...

The Coronavirus Infected Hundreds at a Georgia Summer Camp The camp took precautions but did not require campers to wear masks, the C.D.C. reported. Singing and cheering may have helped spread the virus.

By Roni Caryn Rabin July 31, 2020, NY Times

As schools and universities plan for the new academic year, and administrators grapple with complex questions about how to keep young people safe, a new report about a coronavirus outbreak at a sleepaway camp in Georgia provides fresh reasons for concern.

The camp implemented several precautionary measures against the virus, but stopped short of requiring campers to wear masks. The virus blazed through the community of about 600 campers and counselors, the Centers for Disease Control and Prevention reported on Friday.

The staff and counselors gathered at the overnight camp in late June. Within a week of the camp orientation, a teenage counselor developed chills and went home.

The camp, which the C.D.C. did not name, started sending campers home the next day, and shut down a few days later. By then, 76 percent of the 344 campers and staffers whose test results were available to C.D.C. researchers had been infected with the virus — nearly half the camp.

The study is notable because few outbreaks in schools or child care settings have been described to date, said Caitlin Rivers, an epidemiologist at the Johns Hopkins Bloomberg School of Public Health.

“The study affirms that group settings can lead to large outbreaks, even when they are primarily attended by children,” she said.

“The fact that so many children at this camp were infected after just a few days together underscores the importance of mitigation measures in schools that do reopen for in person learning,” Dr. Rivers added.

Physical distancing, universal mask use, hygiene and ventilation are essential to reducing transmission, she noted.

While the role children play in the spread of the virus has been questioned, the authors of the report said the research adds to evidence that children of all ages are not only susceptible to infection, but may play an important role in transmission.

Dr. Preeti Malani, the chief health officer at the University of Michigan who was not involved in the study, called the report “a cautionary tale.”

“It’s difficult when you have a gathering this large,” she said. “Young people want to be with other young people. They want to socialize. It just takes one person for it to spread to lots of people.”

Of the 344 campers and staff for whom test results were available, 260 tested positive. Of children ages 6 to 10, over half were infected; 44 percent of those ages 11 to 17 were infected, as were one-third of those ages 18 to 21. Only seven staffers were older than 22, and two of them tested positive.

Those who had been at the camp longest had the highest rate of infection; overall, more than half of the staff, who had arrived before the campers, were infected.

Additional cases may have been missed, because the researchers did not have access to data about 253 other campers and staff.

Though the camp was following the directives of an executive order issued in Georgia, it was not in full compliance with recommendations made by federal health officials at the C.D.C.

Campers and staff members were required to show proof that they had tested negative for the coronavirus no more than 12 days before arriving at the camp. Cleaning and disinfection of communal areas were enhanced; the camp required physical distancing outside cabins, and it staggered the use of communal spaces.

But while staff were required to wear cloth masks, the camp did not ask campers to do so, and did not open windows and doors to increase air circulation in buildings. The campers stayed overnight in cabins, with an average of 15 occupants in each.

Many camp activities — which took place indoors as well as outdoors — included “vigorous singing and cheering,” which can enhance spread of the virus, the report said.

The case highlights the limitations of asking for proof of negative coronavirus tests before large gatherings, Dr. Malani said.

“Testing doesn’t always mean safety,” she added. “It has to be combined with individuals adhering to strict quarantine. And that’s hard to do for young people, on a college campus, and in K through 12.”

Inconsistent mask wearing is also problematic, she said.

“Even if the staff were wearing masks around the campers, it’s likely that when they were back in their quarters at night, they weren’t — because that’s what happens,” Dr. Malani said. “It’s hard to do, because it’s not natural to have to distance all the time and wear a mask.”

In a recent study of an outbreak at a high school in Jerusalem that began 10 days after in-person classes resumed in late May, 13 percent of the student body and 16 percent of the staff ultimately tested positive.

Though the students were supposed to wear face masks and practice social distancing, researchers concluded crowded classrooms of up to 38 students made distancing impossible. Air conditioning may have accelerated the spread of the virus
 
Here's a nice article from the NYTimes that describes a possible reason that some people have the Coronavirus, but don't get really sick from it...


The Coronavirus Is New, but Your Immune System Might Still Recognize It

Some people carry immune cells called T cells that can capitalize on the virus’s resemblance to other members of its family tree.


Eight months ago, the new coronavirus was unknown. But to some of our immune cells, the virus was already something of a familiar foe.

A flurry of recent studies has revealed that a large proportion of the population — 20 to 50 percent of people in some places — might harbor immunity assassins called T cells that recognize the new coronavirus despite having never encountered it before.

These T cells, which lurked in the bloodstreams of people long before the pandemic began, are most likely stragglers from past scuffles with other, related coronaviruses, including four that frequently cause common colds. It’s a case of family resemblance: In the eyes of the immune system, germs with common roots can look alike, such that when a cousin comes to call, the body may already have an inkling of its intentions.

The presence of these T cells has intrigued experts, who said it was too soon to tell whether the cells would play a helpful, harmful or entirely negligible role in the world’s fight against the current coronavirus. But should these so-called cross-reactive T cells exert even a modest influence on the body’s immune response to the new coronavirus, they might make the disease milder — and perhaps partly explain why some people who catch the germ become very sick, while others are dealt only a glancing blow.


“If you have a population of T cells that are armed and ready to protect you, you could control the infection better than someone who doesn’t have those cross-reactive cells,” said Marion Pepper, an immunologist at the University of Washington who is studying the immune responses of Covid-19 patients. “That’s what we’re all hoping for.”

T cells are an exceptionally picky bunch. Each spends the entirety of its life waiting for a very specific trigger, like a hunk of a dangerous virus. Once that switch is flipped, the T cell will clone itself into an army of specialized soldiers, all with their sights set on the same target. Some T cells are microscopic assassins, tailor-made to home in on and destroy infected cells; others coax immune cells called B cells into producing virus-attacking antibodies.

The first time a virus infects the body, this response is sluggish; it takes several days for the immune system to sort out which T cells are best suited for the job at hand. But subsequent encounters typically prompt a response that is stronger and faster, thanks to a reserve force of T cells, called memory T cells, that lingers after the initial threat has passed and can quickly be called into action again.


Usually, this process operates best when T cells must battle the same pathogen again and again. But these recruits are more flexible than they are often given credit for, said Laura Su, an immunologist and T cell expert at the University of Pennsylvania. Should these cells chance upon something that bears a strong resemblance to their germ of choice, they can still be roused to fight, even if the invader is a total newcomer.

In theory, cross-reactive T cells can “protect almost like a vaccine,” said Smita Iyer, an immunologist at the University of California, Davis, who is studying immune responses to the new coronavirus in primates. Previous studies have shown that cross-reactive T cells may guard people against different strains of the flu virus, and perhaps confer a trace of immunity against dengue and Zika viruses, which share a family tree.

The case for coronaviruses is less clear cut, said Alessandro Sette, an immunologist at the La Jolla Institute for Immunology who has led several studies examining cross-reactive T cells to the new coronavirus. Researchers have found people in the United States, Germany, the Netherlands, Singapore and the United Kingdom who have never been exposed to the new coronavirus but who carry T cells that react to it in the lab.

Researchers are eager to understand the history of these T cells, because that might help reveal who is more likely to have them. A growing body of evidence, including data published this week in Science by Dr. Sette and his colleagues, points to common-cold coronaviruses as a potential source. But even unrelated viruses can share similar features, and researchers may never know for sure what originally “drove their development,” said Avery August, an immunologist and T cell expert at Cornell University.


Whatever the origin of T cells, their mere existence could be encouraging news. There is much more to the immune system than T cells, but even a semblance of pre-existing immunity could mean that people who have recently grappled with the common cold may have an easier time fighting off a nastier member of the coronavirus clan.

Cross-reactive T cells alone probably would not be enough to completely stave off infection or disease. But they might alleviate symptoms of the coronavirus in people who happen to carry these cells, or extend the protection provided by a vaccine.

“That would be awesome,” Dr. Iyer said.

Children, who share lots of germs with their peers, might be good candidates for this hypothetical scenario.

But cross-reactive T cells are not necessarily a benevolent force. They could instead be ineffectual souvenirs of infections past, with “absolutely no relevance” to how well people fare against the new coronavirus, Dr. Sette said.

There is even a small chance that pre-existing T cells could raise the risk for serious symptoms of Covid-19, although experts consider this possibility unlikely. T cells that are primed to recognize common-cold coronaviruses might marshal only a lackluster response to the current coronavirus, potentially sapping resources from other populations of immune cells that have a better shot at defeating the new invader. “Now you have your immune system distracted,” Dr. Iyer said.

T cells are also expert orchestrators. Depending on the signals they send out, they can synchronize cells and molecules from disparate parts of the immune system into a tag-teamed attack, or quell these assaults to return the body to baseline. If it turns out that cross-reactive T cells tend toward quieting the response, they could suppress a person’s immune defense before it has a chance to kick into gear, Dr. August said.

Then again, many types of T cells exist, and all operate as part of a complex immune system. “It’s almost like some people are trying to say this is ‘good’ or ‘bad,’” Dr. Su said. “It’s probably more nuanced than that.”

Teasing it all apart will not be easy. Unlike antibodies, which are inanimate proteins that often circulate in the blood, T cells are living cells that often hole up in hard-to-reach tissues. That makes them much more difficult to extract, maintain and analyze, Dr. Pepper said.

Researchers could learn more by testing whether cross-reactive T cells are more abundant in patients who have had mild or serious cases of Covid-19, although such studies cannot prove cause and effect. A more laborious effort might involve measuring cross-reactive T cell levels in large groups of healthy people, then waiting to see if they became infected or sick from the current coronavirus, Dr. Sette said.
Strong evidence could also come from an animal model, like the rhesus macaques that Dr. Iyer studies in her lab. Researchers could dose primates with common-cold coronaviruses, and then see how their immune responses stack up against the new coronavirus.

Less than a year into this pandemic, plenty of questions remain unanswered, Dr. Pepper said. Immunologists cannot fully forecast how the human immune system will respond to this new virus; even with science at its speediest, that interaction must be studied in real time.
It’s a frustrating reality, Dr. Pepper said: “Until we see it in real life, we just don’t know.”
 
Interesting, but yet to be peer-reviewed. Blurb pulled out of a NYTimes article...

Skeptics of the notion that the coronavirus spreads through the air — including many expert advisers to the World Health Organization — have held out for one missing piece of evidence: proof that floating respiratory droplets called aerosols contain live virus, and not just fragments of genetic material.

Now a team of virologists and aerosol scientists has produced exactly that: confirmation of infectious virus in the air.

“This is what people have been clamoring for,” said Linsey Marr, an expert in airborne spread of viruses who was not involved in the work. “It’s unambiguous evidence that there is infectious virus in aerosols.”

A research team at the University of Florida succeeded in isolating live virus from aerosols collected at a distance of seven to 16 feet from patients hospitalized with Covid-19 — farther than the six feet recommended in social distancing guidelines.
 
Another NY Times summary article. I left out the gory immunological details, but as we learn more about the variations in folks' responses to infection, there's greater potential for better treatments while awaiting widespread vaccine deployment. Suffice it to say that this helps to explain the Cytokine Storm seen in very severe, and often fatal cases.


Scientists are beginning to untangle one of the most complex biological mysteries of the coronavirus pandemic: Why do some people get severely sick, whereas others quickly recover?

In certain patients, according to a flurry of recent studies, the virus appears to make the immune system go haywire.

Unable to marshal the right cells and molecules to fight off the invader, the bodies of the infected instead launch an entire arsenal of weapons — a misguided barrage that can wreak havoc on healthy tissues, experts said.
 
Another NY Times summary article. I left out the gory immunological details, but as we learn more about the variations in folks' responses to infection, there's greater potential for better treatments while awaiting widespread vaccine deployment. Suffice it to say that this helps to explain the Cytokine Storm seen in very severe, and often fatal cases.


Scientists are beginning to untangle one of the most complex biological mysteries of the coronavirus pandemic: Why do some people get severely sick, whereas others quickly recover?

In certain patients, according to a flurry of recent studies, the virus appears to make the immune system go haywire.

Unable to marshal the right cells and molecules to fight off the invader, the bodies of the infected instead launch an entire arsenal of weapons — a misguided barrage that can wreak havoc on healthy tissues, experts said.

Ah on this thread, I can, and will, edit all BS.

Got a citation? Please share.

Have stories? If they're fish related file a fishing report. Related to Coronavirus, please share on the other free for all thread...
 
Last edited by a moderator:
Ah on this thread, I can, and will, edit all BS.

Got a citation? Please share.

Have stories? If they're fish related file a fishing report. Related to Coronavirus, please share on the other free for all thread...

Fair enough Dom.

Can we ask questions on this thread?
 
That's why the lid is supposed to be down when flushing and your toothbrush far away from the bowl.
 
Do doody particles really go into the air?

Yes if you're asking about feces...


Aerosolization is the process or act of converting some physical substance into the form of particles small and light enough to be carried on the air i.e. into an aerosol. Aerosolization refers to a process of intentionally oxidatively converting and suspending particles or a composition in a moving stream of air for the purpose of delivering the oxidized particles or composition to a particular location.[1]

The term is often used in medicine to refer specifically to the production of airborne particles (e.g. tiny liquid droplets) containing infectious virus or bacteria. The infectious organism is said to be aerosolized. This can occur when an infected individual coughs,[2] sneezes[3] exhales,[4] or vomits,[5] but can also arise from flushing a toilet,[6] or disturbing dried contaminated feces.[7] Aerosolization becomes critical in cases of Coronavirus and Pneumonic plague because of the high lethality of these diseases and human-to-human transmission disease vector.
 
Thanks.
Can you explain in simple terms, the chemical/biological difference between the common flu we get every year vs. the Covid-19? Just some basics, like are their small differences that make this one more intense, probably, contagious etc.. I'm not sure of the scientific terms, but what are the major differences in Covid's composition/makeup vs a common everyday Flu. In language we can understand.

Thank you.
 
Thanks.
Can you explain in simple terms, the chemical/biological difference between the common flu we get every year vs. the Covid-19? Just some basics, like are their small differences that make this one more intense, probably, contagious etc.. I'm not sure of the scientific terms, but what are the major differences in Covid's composition/makeup vs a common everyday Flu. In language we can understand.

Thank you.


From the World Health Organization from 30,000 ft. Still much to be learned on COVID-19 and this was penned in mid-March. Another key difference is the whole method of target cell infection. Coronavirus use the "spike protein" that gives them the crown (Corona) looking appearance and binds to one particular cell membrane protein. Influenza uses different proteins and a different cell membrane target.


Q&A: Influenza and COVID-19 - similarities and differences
17 March 2020 | Q&A

As the COVID-19 outbreak continues to evolve, comparisons have been drawn to influenza. Both cause respiratory disease, yet there are important differences between the two viruses and how they spread. This has important implications for the public health measures that can be implemented to respond to each virus.

How are COVID-19 and influenza viruses similar?

Firstly, COVID-19 and influenza viruses have a similar disease presentation. That is, they both cause respiratory disease, which presents as a wide range of illness from asymptomatic or mild through to severe disease and death.

Secondly, both viruses are transmitted by contact, droplets and fomites. As a result, the same public health measures, such as hand hygiene and good respiratory etiquette (coughing into your elbow or into a tissue and immediately disposing of the tissue), are important actions all can take to prevent infection.

How are COVID-19 and influenza viruses different?

The speed of transmission is an important point of difference between the two viruses. Influenza has a shorter median incubation period (the time from infection to appearance of symptoms) and a shorter serial interval (the time between successive cases) than COVID-19 virus. The serial interval for COVID-19 virus is estimated to be 5-6 days, while for influenza virus, the serial interval is 3 days. This means that influenza can spread faster than COVID-19.

Further, transmission in the first 3-5 days of illness, or potentially pre-symptomatic transmission –transmission of the virus before the appearance of symptoms – is a major driver of transmission for influenza. In contrast, while we are learning that there are people who can shed COVID-19 virus 24-48 hours prior to symptom onset, at present, this does not appear to be a major driver of transmission.

The reproductive number – the number of secondary infections generated from one infected individual – is understood to be between 2 and 2.5 for COVID-19 virus, higher than for influenza. However, estimates for both COVID-19 and influenza viruses are very context and time-specific, making direct comparisons more difficult.

Children are important drivers of influenza virus transmission in the community. For COVID-19 virus, initial data indicates that children are less affected than adults and that clinical attack rates in the 0-19 age group are low. Further preliminary data from household transmission studies in China suggest that children are infected from adults, rather than vice versa.

While the range of symptoms for the two viruses is similar, the fraction with severe disease appears to be different. For COVID-19, data to date suggest that 80% of infections are mild or asymptomatic, 15% are severe infection, requiring oxygen and 5% are critical infections, requiring ventilation. These fractions of severe and critical infection would be higher than what is observed for influenza infection.

Those most at risk for severe influenza infection are children, pregnant women, elderly, those with underlying chronic medical conditions and those who are immunosuppressed. For COVID-19, our current understanding is that older age and underlying conditions increase the risk for severe infection.

Mortality for COVID-19 appears higher than for influenza, especially seasonal influenza. While the true mortality of COVID-19 will take some time to fully understand, the data we have so far indicate that the crude mortality ratio (the number of reported deaths divided by the reported cases) is between 3-4%, the infection mortality rate (the number of reported deaths divided by the number of infections) will be lower. For seasonal influenza, mortality is usually well below 0.1%. However, mortality is to a large extent determined by access to and quality of health care.

What medical interventions are available for COVID-19 and influenza viruses?

While there are a number of therapeutics currently in clinical trials in China and more than 20 vaccines in development for COVID-19, there are currently no licensed vaccines or therapeutics for COVID-19. In contrast, antivirals and vaccines available for influenza. While the influenza vaccine is not effective against COVID-19 virus, it is highly recommended to get vaccinated each year to prevent influenza infection.
 
MANY COVID-19 PATIENTS MAY BE DYING FROM THEIR IMMUNE RESPONSE TO THE VIRUS, NOT FROM THE VIRUS ITSELF. CAN SCIENCE FIGURE OUT HOW TO SAVE THEM?

Interesting...


One hypothesis follows from the animals’ adaptations to flight. Flapping wings requires immense amounts of energy, causing bat cells to spew out large quantities of a metabolic byproduct called reactive oxygen species, which might be thought of as cellular exhaust. In other animals, that cellular waste, which bears some resemblance to a viral infection, might trigger overwhelming inflammation — a cytokine storm. But bats have evolved ways to keep that inflammation in check.
 
MANY COVID-19 PATIENTS MAY BE DYING FROM THEIR IMMUNE RESPONSE TO THE VIRUS, NOT FROM THE VIRUS ITSELF. CAN SCIENCE FIGURE OUT HOW TO SAVE THEM?

Interesting...

One hypothesis follows from the animals’ adaptations to flight. Flapping wings requires immense amounts of energy, causing bat cells to spew out large quantities of a metabolic byproduct called reactive oxygen species, which might be thought of as cellular exhaust. In other animals, that cellular waste, which bears some resemblance to a viral infection, might trigger overwhelming inflammation — a cytokine storm. But bats have evolved ways to keep that inflammation in check.

Cytokine storm mentioned in one of the articles above. Now that physicians are alerted to be on watch for it, things are more optimistic because they can take steps to keep it in check before it blows up.
 
Decided to put this in this COVID thread instead of the other one. It just shows how data can be skewed to support whatever a person wants when they don't have proper controls in place, and more importantly, when a scientist comments the unspeakable crime of misrepresenting other groups' data, the scientific community will be relentless in taking the offender to task.

I have visited almost every major academic medical center in this country and IMHO the one that stands out above the other excellent institutions is Mayo Clinic. Nobody messes with their data without suffering the consequences...

Now please don't think I'm saying convalescent plasma is not effective for COVID-19, it is. We just don't know exactly how effective it is and how to best administer this treatment, items which Commissioner Hahn should have stated during the press conference instead of reading a script prepared by folks more suited to writing commercial advertisement copy. I do applaud him for owning up to his mistake instead of doubling down, which some folks feel is the proper way to respond to getting caught lying...

FDA chief apologizes for overstating benefits of virus plasma therapy
pressherald.com/2020/08/25/fda-commissioner-admits-he-overstated-benefits-of-virus-therapy/

By DEB RIECHMANNAssociated PressAugust 25, 2020
WASHINGTON — Responding to an outcry from medical experts, Food and Drug Administration Commissioner Stephen Hahn on Tuesday apologized for overstating the life-saving benefits of treating COVID-19 patients with convalescent plasma.

Scientists and medical experts have been pushing back against the claims about the treatment since President Trump’s announcement on Sunday that the FDA had decided to issue emergency authorization for convalescent plasma, taken from patients who have recovered from the coronavirus and rich in disease-fighting antibodies.

Trump hailed the decision as a historic breakthrough even though the treatment’s value has not been established. The announcement on the eve of Trump’s Republican National Convention raised suspicions that it was politically motivated to offset critics of the president’s handling of the pandemic.

Hahn had echoed Trump in saying that 35 more people out of 100 would survive the coronavirus if they were treated with the plasma. That claim vastly overstated preliminary findings of Mayo Clinic observations.
Virus_Outbreak_Trump_50192
President Trump listens as Dr. Stephen Hahn, commissioner of the U.S. Food and Drug Administration, speaks during a media briefing in the James Brady Briefing Room of the White House on Sunday. Alex Brandon/Associated Press

Hahn’s mea culpa comes at a critical moment for the FDA which, under intense pressure from the White House, is responsible for deciding whether upcoming vaccines are safe and effective in preventing COVID-19.

The 35 percent figure drew condemnation from other scientists and some former FDA officials, who called on Hahn to correct the record.

“I have been criticized for remarks I made Sunday night about the benefits of convalescent plasma. The criticism is entirely justified. What I should have said better is that the data show a relative risk reduction not an absolute risk reduction,” Hahn tweeted.

The FDA made the decision based on data the Mayo Clinic collected from hospitals around the country that were using plasma on patients in wildly varying ways – and there was no comparison group of untreated patients, meaning no conclusions can be drawn about overall survival. People who received plasma with the highest levels of antibodies fared better than those given plasma with fewer antibodies, and those treated sooner after diagnosis fared better than those treated later.

Hahn and other Trump administration officials presented the difference as an absolute survival benefit, rather than a relative difference between two treatment groups. Former FDA officials said the misstatement was inexcusable, particularly for a cancer specialist like Hahn.

“It’s extraordinary to me that a person involved in clinical trials could make that mistake,” said Dr. Peter Lurie, a former FDA official under the Obama administration who now leads the nonprofit Center for Science in the Public Interest. “It’s mind-boggling.”

The 35 percent benefit was repeated by Health and Human Services Secretary Alex Azar at Sunday’s briefing and promoted on Twitter by the FDA’s communication staff. The number did not appear in FDA’s official letter justifying the emergency authorization.

Hahn has been working to bolster confidence in the agency’s scientific process, stating in interviews and articles that the FDA will only approve a vaccine that meets preset standards for safety and efficacy.

Lawrence Gostin of Georgetown University said Hahn’s performance Sunday undermined those efforts.
“I think the integrity of the FDA took a hit. If I were Stephen Hahn I would not have appeared at such a political show,” said Gostin, a public health attorney.

Hahn pushed back Tuesday morning against suggestions that the plasma announcement was timed to boost Trump ahead of the Republican convention.
“The professionals and the scientists at FDA independently made this decision, and I completely support them,” Hahn said, appearing on “CBS This Morning.”

Trump has recently accused some FDA staff, without evidence, of deliberately holding up new treatments “for political reasons.” And Trump’s chief of staff, Mark Meadows, said over the weekend that FDA scientists “need to feel the heat.”

The administration has sunk vast resources into the race for a vaccine, and Trump aides have been hoping that swift progress could help the president ahead of November’s election.

At Sunday’s briefing Hahn did not correct Trump’s description of the regulatory move as a “breakthrough.” He also did not contradict Trump’s unsupported claim of a “deep state” effort at the agency working to slow down approvals.

Former FDA officials said the political pressure and attacks against the FDA carry enormous risk of undermining trust in the agency just when it’s needed most. A vaccine will only be effective against the virus if it is widely taken by the U.S. population.

“I think the constant pressure, the name-calling, the perception that decisions are made under pressure is damaging,” said Dr. Jesse Goodman of Georgetown University, who previously served as FDA’s chief scientist. “We need the American people to have full confidence that medicines and vaccines are safe.”

Convalescent plasma is a century-old approach to treating the flu, measles and other viruses. But the evidence so far has not been conclusive about whether it works, when to administer it and what dose is needed.

The FDA emergency authorization is expected to increase its availability to additional hospitals. But more than 70,000 Americans have already received the therapy under FDA’s “expanded access” program. That program tracks patients’ response, but cannot prove whether the plasma played a role in their recovery.
Some scientists worry the broadened FDA access to the treatment will make it harder to complete studies of whether the treatment actually works. Those studies require randomizing patients to either receive plasma or a dummy infusion.

Associated Press writer Lauran Neergaard contributed to this report.
 
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