All COVID-19 Discussion GOES HERE

[Speedy]

First covid-19 reinfection documented in Hong Kong, researchers say

The 33-year-old man tested positive after returning from Europe, but showed no symptoms the second time round.

https://www.washingtonpost.com/health/20...hong-kong/

The study, by a team at the University of Hong Kong and accepted by the international medical journal Clinical Infectious Diseases, purports to be “the world’s first documentation” of a patient who recovered from covid-19 being reinfected. The fact that the man had no symptoms the second time suggests his immune system protected him from disease.

The findings have big potential implications for vaccine use, as well as policies based around the concept of herd immunity that presume those who recover from the virus are unlikely to be reinfected.

Robert Glatter, an emergency physician at Lenox Hill Hospital in New York City, said the research showed herd immunity from natural infection would be unlikely to eradicate the novel coronavirus. “The only safe and practical approach to achieve herd immunity is through vaccination," he said, although even those might not provide lifelong protection.

But immunologists also emphasized that the case was not a surprise, given what is already known about the response to the virus. “[T]his is a textbook example of how immunity should work,” Akiko Iwasaki, an immunology expert at Yale University, tweeted on Monday.

She noted the second infection was asymptomatic implying that the man’s immune response protected him from disease, although not reinfection, and calling its findings “no cause for alarm.”

The 33-year-old man, an unnamed IT worker from the city, was first hospitalized in late March after testing positive for covid-19. His symptoms included a fever and a cough.

The man was released from hospital in mid-April after testing negative for the virus and having no further symptoms. But after visiting Spain in August, he tested positive again upon returning to Hong Kong, despite appearing asymptomatic.

Physicians at first thought he might be a persistent carrier of the virus, the study’s authors write, but they sequenced the genome of his first and second infection to show the virus strains were different, indicating he had been reinfected.

[Speedy]

It helps to be a city of young people. Let the young get sick and (mostly) recover and you will have herd immunity. Except the USA is a country of old people.

https://www.washingtonpost.com/world/the...story.html

The hospital system was coming apart. Coronavirus patients were being turned away. Basic necessities — beds, stretchers, oxygen — had run out. Ambulances had nowhere to take patients. People were dying at home. Gravediggers couldn’t keep up.

The human destruction in the Brazilian city of Manaus would be “catastrophic,” physician Geraldo Felipe Barbosa feared.

But then, unexpectedly, it started to let up ­— without the interventions seen elsewhere.

Hospitalizations of coronavirus patients plummeted in the state from a peak of more than 1,300 in May to fewer than 300 in August. Excess deaths in Manaus fell from around 120 per day to practically zero. The city closed its field hospital.

In a country devastated by the novel coronavirus, where more than 3.6 million people have been infected and over 114,000 killed, the reversal has stunned front-line doctors. Manaus never imposed a lockdown or other strict containment measures employed successfully in Asia and Europe. And what policies did exist, many people ignored.

In the spring, the Amazonian city became a global symbol of the devastation the disease can wreak in the developing world. But now it has returned to near normalcy — far sooner than many expected — and scientists and public health officials are asking why. The question is part of a broader debate among scientists and public health officials over the mechanics of herd immunity and the level of transmission that must be crossed before the disease starts to recede.

[pdq]

It may be that NYC (for instance) already has herd immunity. The antibody tests are notoriously unreliable, and there has been no significant effort at widespread public testing for immunity/exposure, only current infection.

[Speedy]

‘The 1918 flu is still with us’: The deadliest pandemic ever is still causing problems today

https://www.washingtonpost.com/history/2...demic-end/

In 1918, a novel strand of influenza killed more people than the 14th century’s Black Plague.

At least 50 million people died worldwide because of that H1N1 influenza outbreak. The dead were buried in mass graves. In Philadelphia, one of the hardest-hit cities in the country, priests collected bodies with horse-drawn carriages.

In the middle of today’s novel coronavirus outbreak, some are turning to the conclusion of past pandemics to discern how and when life might “return to normal.” The Washington Post has received a few dozen questions from readers who want historical context for our current epidemic. But how did the deadliest pandemic ever recorded come to an end?

Over time, those who contracted the virus developed an immunity to the novel strand of influenza, and life returned to normal by the early 1920s, according to historians and medical experts. Reports at the time suggest the virus became less lethal as the pandemic carried on in waves.

But the strand of the flu didn’t just disappear. The influenza virus continuously mutated, passing through humans, pigs and other mammals. The pandemic-level virus morphed into just another seasonal flu. Descendants of the 1918 H1N1 virus make up the influenza viruses we’re fighting today.

“The 1918 flu is still with us, in that sense,” said Ann Reid, the executive director of the National Center for Science Education who successfully sequenced the genetic makeup of the 1918 influenza virus in the 1990s. “It never went away.”

It’s not clear exactly how or where the 1918 influenza outbreak began, but, at some point, the novel H1N1 virus passed from birds to humans.

From start to finish, the flu could burn through a town or city in a matter of weeks. Very few people had ever contended with a concoction of influenza like this before, which is why it was so potent, Reid said. In crowded cities, it wasn’t a matter of who got sick but, rather, when they would.

“Everybody got the flu, and everybody got it bad,” Reid said.

Even President Woodrow Wilson contracted the virus while negotiating the end of World War I.

Seasonal influenza tends to kill the oldest and youngest in a society but in 1918, roughly half of those who died were men and women in their 20s and 30s. People were getting sick and dying in the prime of their lives.

“As many as 8 to 10 percent of all young adults then living may have been killed by the virus,” historian John M. Barry wrote in his best-selling book “The Great Influenza.”

All the while, World War I continued. The bloody trench warfare across Europe left 8.5 million or more soldiers dead. The tight quarters during the war only aided the spread of the virus, said Howard Markel, a physician and medical historian at the University of Michigan.

The 1918 outbreak has been called the Spanish flu because Spain, which remained neutral during World War I, was the first country to publicly report cases of the disease. China, France and the United States already had cases of the flu, but wartime censorship largely kept the outbreaks out of the newspapers.

Then, the king of Spain — Alfonso XIII — and several other members of his government contracted the flu. This series of unfortunate events left a permanent mark, tying the country to the deadly outbreak.

“There was a very common habit, which has persisted to this day, of blaming an epidemic on one country or one group of people,” Markel said. “It goes back centuries.”

Spain hated being linked to the deadly 1918 flu pandemic. Trump’s ‘Chinese virus’ label echoes that.

The longer the influenza virus existed in a certain community, the less lethal the sickness was. An epidemiological study cited by Barry in “The Great Influenza” noted that “the virus was most virulent or most readily communicable when it first reached the state, and thereafter it became generally attenuated.”

Experts say there’s this natural progression where a virus often — but not always — becomes less lethal as time wears on. It’s in the best interest of the virus for it to spread before killing the host.

“The natural order of an influenza virus is to change,” Barry told The Post. “It seems most likely that it simply mutated in the direction of other influenza viruses, which is considerably milder.”

By 1920, the influenza virus was still a threat, but fewer people were dying from the disease. Some scientists at the time started to move on to other research. Barry wrote that William Henry Welch, a famous pathologist from Johns Hopkins who was studying the virus, found it “humiliating” that the outbreak was passing away without experts truly understanding the underlying cause of the disease.

What Welch didn’t predict was that the virus never truly went away. In 2009, David Morens and Jeffery Taubenberger — two influenza experts at the National Institutes of Health — co-authored an article with Anthony S. Fauci explaining how the descendants of the 1918 influenza virus have contributed to a “pandemic era” that has lasted the past hundred years. At the time the article was published, the H1N1 influenza virus in public circulation was a fourth-generation descendant of the novel virus from 1918.

“All those pandemics that have happened since — 1957, 1968, 2009 — all those pandemics are derivatives of the 1918 flu,” Taubenberger told The Post. “The flu viruses that people get this year, or last year, are all still directly related to the 1918 ancestor.”

Because of this, the 1918 influenza outbreak doesn’t come with a neat bookend. Society moved on, but the virus continued in some form or fashion.

“We are living in a pandemic era that began around 1918,” Taubenberger wrote with Fauci and Morens back in 2009 for the New England Journal of Medicine. “Ever since 1918, this tenacious virus has drawn on a bag of evolutionary tricks to survive.”

We continue to turn back to the 1918 outbreak as a point of comparison, said Jeremy Greene, a historian of medicine at Johns Hopkins. Some of the public health measures a hundred years ago are still put in place today. To “flatten the curve,” cities and towns have more or less shut down. That said, Greene cautions against drawing the parallels “too closely.”

There are similarities to draw between today’s pandemic and the influenza outbreak a hundred years ago. Both come from winged animals — one from birds and the other from bats. Both are respiratory viruses. Both led people to wear masks in public. Both forced cities and schools to shut down for periods of time. And, finally, in both cases, the country’s leaders exacerbated problems by ignoring the early warning signs.

Despite all that, influenza viruses and coronaviruses are not the same. There’s very little someone can draw from influenza to then provide treatment for the infectious disease named covid-19, said Paul Offit, the director of the Vaccine Education Center at Children’s Hospital of Philadelphia.

“They’re really different viruses,” Offit added.

Influenza is consistent and relatively quick when compared with the novel coronavirus. If you get exposed to the flu, you’ll start showing symptoms in one to four days after the infection. According to the Centers for Disease Control and Prevention, it tends to take five days for those infected with SARS-CoV-2 to start showing symptoms of covid-19, but the timing can fluctuate from two days to two weeks.

The novel coronavirus is not moving on the same time frame as the 1918 influenza, Greene told The Post. Everything is longer with the novel coronavirus — the symptoms, the sickness and even the long-term complications. Doctors are concerned covid-19 can lead to lasting cardiovascular complications.

Then there are asymptomatic carriers of the disease. That one detail makes it harder to mitigate the spread of the virus by simply taking temperatures. Symptoms are not a be-all-end-all solution to tracking the disease. With that in mind, the novel coronavirus is acting more like polio, where those with mild cases don’t know they’re sick, Greene said.

“It immediately raises a different set of problems for managing a disease,” Greene said. “One needs to relearn the way to think about who is dangerous, and that becomes, basically, everybody.”

Recognizing both the similarities and differences to past pandemics can provide a “meaningful mirror” for the present, Greene added. The million-dollar question is: What can the 1918 influenza outbreak tell us about how our current pandemic may end?

“The sad answer is not very much,” Markel said. “The operative word in this particular pandemic is ‘novel’ coronavirus. We’re learning as we go along, but we don’t really know that much.”

[Speedy]

An update on the progress of some 200 vaccines:

https://www.washingtonpost.com/graphics/...ronavirus/

[Speedy]

Massive genetic study shows coronavirus mutating and potentially evolving amid rapid U.S. spread

No paywall:

https://www.washingtonpost.com/health/20...mutations/

Scientists in Houston on Wednesday released a study of more than 5,000 genetic sequences of the coronavirus that reveals the virus’s continual accumulation of mutations, one of which may have made it more contagious.

The new report, however, did not find that these mutations have made the virus deadlier or changed clinical outcomes. All viruses accumulate genetic mutations, and most are insignificant, scientists say.

Coronaviruses such as SARS-CoV-2 are relatively stable as viruses go, because they have a proofreading mechanism as they replicate. But every mutation is a roll of the dice, and with transmission so widespread in the United States — which continues to see tens of thousands of new, confirmed infections daily — the virus has had abundant opportunities to change, potentially with troublesome consequences, said study author James Musser of Houston Methodist Hospital.

“We have given this virus a lot of chances,” Musser told The Washington Post. “There is a huge population size out there right now.”

[pdq]

Over time, these things all eventually become less deadly and more contagious.

But not necessarily in that order...

[Speedy]

https://www.thelily.com/anika-chebrolu-j...t-shes-14/

Anika Chebrolu just discovered a potential covid-19 treatment. She’s 14.
She won $25,000 and America’s top young scientist prize

Lena Felton
As the world’s biggest pharmaceutical companies race to find treatments for the novel coronavirus, one scientist has been working for months on a potential treatment in her bedroom. Her name is Anika Chebrolu, and she’s only 14.

A freshman at Independence High School in Frisco, Tex., Chebrolu this week won the 3M Young Scientist Challenge and $25,000 for her discovery: a compound that can bind to the coronavirus, inhibiting its ability to infect people. She beat out nine other finalists — whose own projects ranged from a robotic glove to a device that detects invisible particles in water — to be named America’s top young scientist.

Chebrolu first started working on her project last year when she was in eighth grade, initially looking to find a treatment for the influenza virus. But then the pandemic hit. With her mentor, 3M corporate scientist Mahfuza Ali, she changed tack. She’s just finalized her research, and she’s hoping to start reaching out to virologists to develop her finding into an antiviral drug.

[ FDA approves first covid-19 drug: Antiviral remdesivir]

With more than 220,000 people in the United States dead because of covid-19, viable treatments are crucial. On Thursday, remdesivir, a drug that inhibits a substance the virus uses to make copies of itself, became the first medicine to win full Food and Drug Administration approval for treating covid-19.

We caught up with Chebrolu days after she found out she was this year’s winner.

[Ca Bob]

Very impressive for somebody this young. The study seems to be a computer search of the shape of the spike protein vs. many possible molecules, any one of which might be a good fit for some part of the spike. There are computer programs that look for a 3D fit of the one target (Coronaviral spike) against each of the molecules in the data base. The programs aren't perfect, but they are a good place to start.

As an aside, this is a standard approach to drug design that is used in a lot of places. Locally, UCLA has a center that is designed to do this. We have seen quite a few good projects of this nature at the high school science fair state finals.

[Speedy]

Experimental hormone therapy may speed recovery for COVID patients

https://www.startribune.com/hormone-boos...572944532/

DULUTH — Every time the phone rang, it seemed to Kristine Smoley like more bad news about her husband, who contracted COVID-19 and was in a hospital intensive care unit on a ventilator because he couldn’t breathe on his own.

Smoley was prepared for the worst when a nurse from Duluth’s Essentia Health called with hope — albeit with risks and no solid evidence it would save her husband.

“They asked if I wanted to consider signing off on an experimental treatment for him,” Smoley said. “A treatment that had never been done before.”

Essentia’s Dr. Tim Rich and the University of Minnesota Medical School’s Dr. David Ingbar had studied for years whether a common thyroid hormone could be repurposed for the treatment of acute respiratory distress syndrome (ARDS), an often fatal type of lung failure. The doctors received federal approval late last year to test the therapy, so when COVID-19 caused a sudden surge in ARDS, they were ready for their first patient — Smoley’s husband, Bob Schlicht.

“It was scary,” Smoley said. “But I don’t know that I really had an option. Because the other option wasn’t good.”

The turnaround that followed was so remarkable that Rich and Ingbar have advanced their research — unique for a regional medical provider in a world of urban and academic COVID-19 studies — to a phase 2 U.S. Food and Drug Administration (FDA) study. The doctors have optimism about the impact their treatment could have amid the pandemic.

“There has been a lot of highly technical science to understand this biology, but the elegance now is in its simplicity,” said Rich, a pulmonologist. “This is not a designer drug. This is something we know the lung needs and uses.”

New therapies are needed against a pandemic that has caused 150,672 known infections, 10,334 hospitalizations and 2,475 deaths among Minnesotans. Only the antiviral remdesivir has received full FDA approval as a COVID-19 therapy for hospitalized patients, while treatments such as plasma infusions remain experimental and available only under emergency authorization.

Rich and Ingbar made a key discovery during the H1N1 pandemic of 2009, when families of those who died from influenza-related ARDS permitted autopsies. Rich found the victims’ lungs lacked T3, a thyroid hormone that would normally be detectable.

Ingbar said T3 reduces inflammation and coaxes epithelial cells in the lungs to absorb fluids — which is vital for patients with ARDS.

“A part of this acute lung injury with ARDS is the lungs get leaky, and they tend to fill with fluid,” Ingbar said. “That makes it really hard to get oxygen in or carbon dioxide out.”