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Omicron in Brooklyn – Google Search https://shar.es/aW9gXq https://www.nytimes.com/2022/01/15/nyregion/brooklyn-omicron-cases.html …
What the Omicron Wave Looks Like at One Brooklyn E.R.
The nature of this variant, combined with widespread vaccine use, may make it seem less severe in some ways than earlier ones. It doesn’t always feel like that here.
nytimes.com
Omicron in Brooklyn – Google Search https://shar.es/aW9gXY https://gothamist.com/news/nycs-hospital-staffing-crisis-is-fueled-by-omicron-made-worse-by-employee-departures …
NYC’s Hospital Staffing Crisis Is Fueled By Omicron – Made Worse By Employee Departures
Adams says he’s getting the hospital staffing crisis under control. Health care workers say it’s not as simple as hiring temporary staff.
gothamist.com
Why Coney Island and Brighton Beach were hit so hard by omicron – Gothamist https://ino.to/R15bgtt
Why Coney Island and Brighton Beach were hit so hard by omicron
The iconic oceanside neighborhoods experienced a fatality rate nearly three times the citywide average. gothamist.com
End of COVID-19 hospital death reporting is “incomprehensible,” says US health official https://www.wsws.org/en/articles/2022/02/03/deat-f03.html …
End of COVID-19 hospital death reporting is “incomprehensible,” says US health official
On Wednesday, the US Department of Health and Human Services (HHS) officially ended its system for hospitals to report COVID-19 deaths daily to the federal government, amid a worldwide campaign to…
wsws.org
Michael Novakhov Retweeted
US Department of Health ENDS requirement for hospitals to report daily COVID deaths to federal government https://trib.al/vWLywkc
US ends requirement for hospitals to report daily COVID deaths
The reporting policy change went into effect on Wednesday. Although hospitals aren’t reporting to the HHS, the CDC will continue to collect and report COVID data from death certificates.
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Why Coney Island and Brighton Beach were hit so hard by omicron
Underneath the Q train, near the intersection of Coney Island and Brighton Beach Avenues, many of the passersby are older and speak in Russian. Last Wednesday, 64-year-old Irina Andreeva was among them, walking alongside her son, Alexander Astafurov, toward one of three COVID-19 testing vans parked side-by-side.
It was the first sunny day in weeks, but Andreeva was feeling under the weather.
“I have a temperature, and I’m shaking,” Andreeva, 64, said in Russian, as her son translated. She said several of her friends had caught the coronavirus in recent weeks as the omicron variant swept over New York City.
Some had more severe cases than others. One unvaccinated friend ended up being hospitalized at Maimonides Medical Center for a couple of weeks, Andreeva said. She felt more secure because she had had two doses of COVID-19 vaccine, but her son, who also lives in the neighborhood, said he now wants them both to get boosters to be on the safe side.
Omicron tore through New York City, with the five boroughs recording 1 million COVID-19 cases since the variant became dominant in mid-December. That’s four times as many cases as the city’s first wave in early 2020. But, as in previous surges, the burden has not been distributed evenly across people from different backgrounds and neighborhoods.
Some at-risk communities are still dealing with much higher rates of hospitalizations and deaths, despite the overall impression of a milder wave. These include people who are older, often fighting against pre-existing diseases. And as local organizations work to make sure these vulnerable groups get their booster shots, they continue to come up against those who don’t want to get vaccinated at all.
One of the city’s omicron hotspots centers on the southern tip of Brooklyn, spread across the neighborhoods of Brighton Beach, Manhattan Beach, Sheepshead Bay and iconic Coney Island.
Over the last month, these zip codes have experienced 75 COVID deaths per 100,000 people, a fatality rate nearly three times the citywide average.
The two zip codes encompassing this region — 11224 and 11235 — have experienced 75 deaths per 100,000 people over the last month, a fatality rate nearly three times the citywide average. The pair of zip codes ranked only behind East New York when it came to the pace of COVID deaths between December 24th and January 20th, while their hospitalization rates were also among the highest in the city.
These two zip codes in southern Brooklyn also have lower vaccination coverage than the city as a whole, a common thread between most of the places hit hardest this winter. The area is averaging 66% full vaccination, compared with 75% citywide. In adjacent Gravesend, fewer than two-thirds of residents are fully vaccinated, and meanwhile, some parts of the city are approaching universal coverage.
Most patients admitted to Coney Island Hospital during the latest surge were unvaccinated, as were the majority of the patients placed in intensive care. City officials described some of these trends in late January when they welcomed a military medical team to the beleaguered medical center.
Hospital leaders said undervaccination is having an outsized effect on these oceanside communities because the area’s demographics make residents prone to severe illness from COVID-19. In Brighton Beach and Coney Island, 26% of residents are over the age of 65, compared with about 14% in the borough as a whole. Many of those elderly residents also have underlying health conditions.
“One of the things about this neighborhood is the high preponderance of older adults who live in the various retirement buildings that are near here, many of whom have been pushed over the edge by COVID,” Dr. Mitchell Katz, president and CEO of NYC Health + Hospitals, which runs Coney Island Hospital, said at a press conference welcoming the military on January 24th. “And so that’s made the care very difficult for this hospital to do.”
About 2,300 New Yorkers are currently hospitalized with COVID-19, a big drop since citywide hospitalizations peaked in early January with 6,100 people. But state data show that the situation at Coney Island Hospital is only gradually starting to get better.
Since the military team arrived a couple of weeks ago, the medical center has gone from only 9% of its beds being available to 15% over the past seven days. But citywide, nearly a quarter of hospital beds were free over the past week. The intensive care unit at Coney Island Hospital also still hovers near capacity, at a time when nearly 20% of ICU beds are open citywide.
Public health experts say that getting people to stay up-to-date on their vaccines will be crucial moving forward to keep omicron and future variants from continuing to prey on high-risk groups.
Keeping Seniors Safe
Older New Yorkers were among the first cohorts eligible to get vaccinated against COVID-19, and several grassroots efforts popped up at the time to help them navigate the Byzantine online appointment-making process. A year later, some local groups continue to wage a tireless campaign to ensure this vulnerable population is vaccinated and boosted – particularly with the arrival of omicron.
One such organization is Brighton Neighborhood Association. Founder and executive director Pat Singer said her small nonprofit has recently doubled down on its vaccination efforts. The group coordinated with the city to station a vaccine van outside its office on Brighton Beach Avenue last week — and recently started working with a local pharmacy to deliver doses to seniors in their homes.
Speaking in her office, decorated with photos and memorabilia from her long career in the neighborhood, Singer said some of the elderly clients she serves who were initially hesitant had come around since the vaccines first became available. Others are harder to convince.
“They get an attitude like you’re the enemy,” Singer said. “They think the government is trying to tag them to watch what they’re doing.” She laughed, adding, “You’re not that interesting!”
Citywide, 89% of New Yorkers between ages 65 to 74 are fully vaccinated, but the rate drops to 63% for people older than 85. Municipal data also show coverage varies by region and by other demographics. For instance, just 62% of white seniors in the Bronx are fully vaccinated, and only 65% of Black seniors in Brooklyn.
JASA, a large nonprofit that provides senior housing and social services in neighborhoods across the city, has helped more than 4,000 individuals get COVID-19 shots so far, according to Danielle Palmisano, the organization’s chief program officer.
“We have been pretty successful in helping people make sure they get vaccinated, getting them to their booster appointments,” said Palmisano. She said during the latest surge, JASA has been hosting pop-up vaccine clinics in some of its senior residences, such as Scheuer House in Coney Island.
She said despite the statistics showing that older New Yorkers were more likely to be hospitalized from omicron, the view from the ground has been far less bleak compared to when the pandemic first hit New York City.
Back then, doctors barely knew how to treat the disease, and there were no vaccines. This wave, many residents and staff members got sick, Palmisano said, but “we were not seeing the same numbers of hospitalizations and severe illness and deaths.”
Why Vaccines Still Matter
Naum Nakhimovsky, one of the employees at the van where Andreeva got her COVID-19 test, said he was suspicious of the vaccines because he thought they were developed too quickly — a persistent talking point among those who oppose the shots.
“I don’t wear a mask, and people who don’t wear a mask, they have good immunity,” Nakhimovsky said. The 66-year-old said he was required to get vaccinated for another job. But he claimed many in the Russian community in Brighton Beach share his views.
Such views run contrary to evidence around vaccines versus so-called natural immunity, or what the body develops after an infection. Both routes can offer strong protection, but studies show vaccination is more consistent.
This subtle difference is hard to convey, as well as the idea that omicron still poses a threat. The number of COVID cases citywide has dropped from its peak in early January, but daily infections and deaths still rival last winter’s worst days.
A year ago, the city peaked at around 83 COVID deaths per day over a three-week period, notching 1,800 fatalities during that stretch. These days, the boroughs are averaging more than 100 daily deaths, a pattern that’s been in place for nearly a month and killed about 2,300 people.
I hesitate to think of how bad [omicron] could have been had we not had the opportunity to vaccinate as many people as we did.
Severe cases among high-risk groups continue to contribute to these tallies, even as New Yorkers try to put this surge behind them and resume a sense of normalcy.
Public health experts say, regardless of what happens over the coming months or as the pandemic evolves, vaccination will continue to be an important tool to protect people from the worst outcomes of the virus. But overcoming vaccine hesitancy in all its forms will also continue to be a challenge.
“I don’t know many who say we can project whether we’re going to have a new variant or not, or whether it’s going to be more virulent,” said Albert Ko, an epidemiologist with the Yale School of Public Health. “But the bottom line is the best way to protect our vulnerable populations is to get them vaccinated, and not only vaccinated, but up-to-date on their vaccinations.”
It remains uncertain what pattern the coronavirus will follow in the future, but many experts predict that it could become seasonal and endemic like the flu. And the flu offers a clue as to the challenges of getting people to take a vaccine on a regular basis, even for something very deadly.
Over the last decade, the number of people hospitalized for the flu in the United States has ranged from 140,000 to 710,000 annually, according to the CDC. During that time, the flu killed between 12,000 and 52,000 people each year. Yet, only half of adults got vaccinated during last year’s flu season, which was an improvement over prior years. Among adults over 65, coverage was much better – 75% — but there were still disparities between racial and ethnic groups.
In New York City, there are some 2,000 deaths each year from seasonal flu and pneumonia, routinely making it the third leading cause of death in the five boroughs, according to the city health department. But last year, just half of city adults got their flu shots – a record number.
Although the number of adults getting flu shots has increased during the pandemic, Ko said he feared that the U.S. had “taken steps backwards” in terms of vaccine hesitancy overall in the last 20 years. But, he said, “COVID has offered a new opportunity to learn.”
Early data from New York City’s omicron surge show that those who didn’t get any shots were at least eight times more likely to end up in the hospital than those who were fully vaccinated. Shortly after omicron became dominant in Los Angeles, unvaccinated people were 23 times more likely to be hospitalized than those who had received booster shots and five times more likely to be admitted than those who were vaccinated without boosters, according to a new report from the Centers for Disease Control and Prevention.
“I hesitate to think of how bad [omicron] could have been had we not had the opportunity to vaccinate as many people as we did,” said Cameron Wolfe, an infectious disease expert at the Duke University School of Medicine.
Still, the COVID-19 vaccines were not as effective at stopping omicron infections in the first place as they had been for previous variants. Future versions of the shots could restore this defense, but the constantly evolving nature of the virus and the scientific knowledge around it complicates public health messaging, Wolfe said.
”I think you’ve got to keep the message clear as to, ‘What am I trying to do with vaccination?’” Wolfe said. One goal is “to protect those most at risk.”
Health Reporter
The US Department of Health and Human Services (HHS) is no longer requiring hospital systems to report daily COVID-19 deaths to the federal government.
The policy change, which was announced in January, went into effect last Wednesday, just days ahead of the US death toll surpassing 900,000.
Some health officials are calling the move ‘incomprehensible,’ alleging the hospital data has, over the last two years, ‘changed the response to the pandemic for the better’.
‘The hospitals have been doing this for going on two years,’ a federal health official told WSWS, speaking on the condition of anonymity.
‘It is the only consistent, reliable and actionable dataset at the federal level. Ninety-nine percent of hospitals report one hundred percent of the data every day.’
Although hospitals will no longer need to report the previous day’s COVID-19 deaths to the federal government each day, the Centers for Disease Control and Prevention (CDC) will continue to collect and report COVID data from official death certificates.
The CDC also notes the death data reported by hospitals to the HHS ‘is not a CDC-owned data source and does not impact our reporting’.
The organization instead compiles its numbers from death certificate reports sent to the National Center for Health Statistics (NCHS), with officials reiterating ‘there have been no changes to CDC data sources.’
The same day the HHS stopped collecting figures, the UK government announced plans to end its death toll reporting by April.

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The US Department of Health and Human Services (pictured) is no longer requiring hospital systems to report daily COVID-19 deaths to the federal government
On Sunday, the US reported 902,266 coronavirus deaths, an increase of 875, and a seven-day average of 2,455, according to data compiled by Johns Hopkins.
The US tally marks an increase of more than 100,000 fatalities nationwide since Dec. 12, coinciding with a surge of infections and hospitalizations driven by the Omicron variant.
The country also reported 104,104 new cases, bringing the total to 76,458,144. The US seven-day average case average was 313,028.
Nationally, the average daily confirmed COVID cases is half of what was reported less than two weeks ago and down from the peak of nearly 806,000 infections a day on Jan. 15.
Analysts with Reuters allege the US death tally is the highest number of COVID fatalities reported by any nation, followed by Russia, Brazil and India with more than 1.8 million deaths combined. In terms of coronavirus fatalities per capita, the United States ranks 20th, well below the top two – Peru and Russia.
Approximately 212,657,682 Americans are fully vaccinated against the virus, which accounts for 64.79 percent of the population.

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On Sunday, the US reported 902,266 coronavirus deaths, an increase of 875, and a seven-day average of 2,455, according to data compiled by Johns Hopkins

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The country also reported 104,104 new cases, bringing the total to 76,458,144. The US seven-day average case average was 313,028

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The US death tally is the highest number of COVID fatalities reported by any nation, according to analysts
Although CDC death data collection will continue, some health officials argue the information provided by America’s hospitals is more reliable and most beneficial to researchers.
‘The CDC has never really counted cases for things that a lot of people get like the flu,’ the health official said. ‘They get data from sentinel sites and then extrapolate what is happening.’
‘The hospitalization data coming out of HHS is now the best and most granular publicly available data on the pandemic. This information has changed the response to the pandemic for the better,’ echoed Alexis C. Madrigal, a co-founder of the COVID Tracking Project.
‘There was no hospital data at the federal level and even at many states. We had no idea who has capacity, who was in trouble, who had supply shortages, who was getting admissions so fast that they would need supplemental meds, who has staffing issues, etc. We also didn’t know anything about the people admitted in a timely manner, such as age.’

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Although hospitals will no longer need to report the previous day’s COVID-19 deaths to the federal government each day, the Centers for Disease Control and Prevention (CDC) will continue to collect COVID data from official death certificates

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Some health officials are calling the move ‘incomprehensible,’ alleging the hospital data has, over the last two years, ‘ changed the response to the pandemic for the better’
CDC acknowledges that Americans are ‘anxious’ to go back to normal
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However, American Hospital Association Vice President Nancy Foster claims the CDC’s reports are actually than the hospital data because it accounts for deaths that occurred outside of the hospital setting.
‘While it is likely that most individuals who die of COVID do so in the hospital, some die at home, in a nursing home, or elsewhere,’ Foster told KXTV.
‘We believe CDC looked at the conflicting sources of data on COVID deaths, chose the one that was most accurate, and moved to reduce the burden on hospitals to collect data that were less complete and, to the best of our knowledge, not being used.’
Nevertheless, the official who spoke to WSWS claimed the HHS dataset ‘is normalized to a specific hospital and can he compared to other data like capacity, number of admissions, ages of admissions, number in ICU, number of ventilated and a death count—not just for COVID but also influenza (which we have never had good insight into at this scale).’
The CDC has claimed the initial daily death counts are ‘provisional’ and ‘slowly updated over time,’ with death reports often being one to two weeks behind other data collected.
The health authority attributed the delay to the time it takes for death certificates to be filled out, the differing rates at which states report death certificate data and the time it takes extra time for the NCHS to code COVID-19 deaths.
On Wednesday, the US Department of Health and Human Services (HHS) officially ended its system for hospitals to report COVID-19 deaths daily to the federal government, amid a worldwide campaign to reduce the reporting of COVID-19 deaths and cases.
The end of the hospital death reporting came as the official US death toll from COVID-19 approached 900,000, and at least 60,000 people died from COVID-19 in January.
The same day as the US federal government stopped collecting figures on hospital deaths, the UK government announced plans to end reporting of the UK’s COVID-19 death toll by Easter.
The move by HHS, which was quietly announced on January 6, received no coverage until Dr. Jorge A. Caballero brought it to public attention on January 14. A tweet reporting Caballero’s warnings by this reporter went viral, prompting thousands of people to state their opposition to the move.
The end of hospital death reporting has been met with a wall of silence in the media. But among health experts, there is broad opposition to this measure, which would slash the most up-to-date metrics for assessing the current state of COVID-19 deaths and hospital capacity.
The move is “incomprehensible,” one federal health official told the WSWS.
“It is the only consistent, reliable and actionable dataset at the federal level,” the official said. “Ninety-nine percent of hospitals report one hundred percent of the data every day.”
Responding to claims that the HHS data is duplicative of death data collected by the Centers for Disease Control and Prevention (CDC), the official said, “deaths are reported by the counties/states but the process is very slow and many coroners are actually not wanting to cite COVID as the reason, while hospitals rely on diagnoses.” The official continued, “It is also timely as it is every day and many states have a delay anyway but now many are reporting less often.”
Prior to the ending of the HHS reporting system, there were two ways for COVID-19 deaths to be reported to the federal government.
The HHS system relied on direct reporting by hospitals, meaning that all deaths were reported by trained medical professionals on the basis of medical diagnoses. It was daily, timely and included a broad cross-section of relevant information.
With the end of this system, the only remaining means for the federal government to track COVID-19 deaths relies on the aggregation and reporting of death certificates on the state level. These statistics, which pass through America’s fragmented, archaic and politically manipulated system of coroners and medical examiners, are then aggregated by the CDC.
The office of coroner is a remnant of the Middle Ages, in which the officer’s primary responsibilities had to do with the collection of revenues for royal authorities. A 2009 National Academy of Sciences (NAS) report explained: “On behalf of the crown, the crowner [coroner] was responsible for inquests to confirm the identity of the deceased, determine the cause and manner of death, confiscate property, collect death duties, and investigate treasure troves.”
The report, commissioned by the US Department of Justice, stated that “more than 80 years ago, the [NAS] identified concerns regarding the lack of standardization in death investigations and called for the abolishment of the coroner’s office, noting that the office ‘has conclusively demonstrated its incapacity to perform the functions customarily required of it.’”
The 2009 review found that “About 36 percent of the population lives where minimal or no special training is required to conduct death investigations. Recently, an 18-year-old high school student was elected a deputy coroner in Indiana after completing a short training course.”
As the Economist recently warned, “Coroners reliant on voters who are skeptical about COVID have not been as scrupulous as their medical-examiner peers. One coroner in Missouri candidly told the press that he strikes COVID-19 from the death certificates at the request of the family of the deceased.”
Once the data goes through the coroner/medical examiner system, it will be aggregated by states, most of which do not report daily and are themselves moving rapidly to reduce the frequency of COVID-19 death reporting. Tennessee ended daily reporting in early January, and Pew reports that “experts expect other states to follow.”
The official added that the HHS dataset “is normalized to a specific hospital and can he compared to other data like capacity, number of admissions, ages of admissions, number in ICU, number of ventilated and a death count—not just for COVID but also influenza (which we have never had good insight into at this scale).”
The official said that the official explanation, that the ending of data aims to reduce “burdens” on the hospital system, is not believable, because the system is largely automated through the Electronic Medical Records (EMR) System.
Hospitals operate massive data infrastructure systems, with medical staff spending a substantial portion of their time entering data into these systems.
The HHS worked with major manufacturers of medical records software to automate the system, meaning that close to 85 percent of the data reporting was fully automated.
“The hospitals have been doing this for going on two years,” the official said. HHS “worked with all the major EMR vendors to automate the capture of this data.”
Last year, Alexis C. Madrigal, a co-founder of the COVID Tracking Project, writing in the Atlantic, called the HHS reporting system “America’s Most Reliable Pandemic Data,” writing, “The hospitalization data coming out of HHS are now the best and most granular publicly available data on the pandemic. This information has changed the response to the pandemic for the better.”
Explaining why the system was set up, the official said, “There was no hospital data at the federal level and even at many states. We had no idea who has capacity, who was in trouble, who had supply shortages, who was getting admissions so fast that they would need supplemental meds, who has staffing issues, etc. We also didn’t know anything about the people admitted in a timely manner, such as age.”
The ending of the HHS reporting system will likewise inflict collateral damage on the management of other diseases, including influenza. “The CDC has never really counted cases for things that a lot of people get like the flu,” the official said. “They get data from sentinel sites and then extrapolate what is happening.”
Stating that there existed a “correlation” between the calls for ending COVID-19 data reporting and the drive to make life with COVID-19 the “new normal,” the official warned, “I don’t know any scientists who want to have less data.”
BERLIN — (AP) — German Chancellor Olaf Scholz set off Sunday for Washington seeking to reassure Americans that his country stands alongside the United States and other NATO partners in opposing any Russian aggression against Ukraine.
Scholz has said that Moscow would pay a “high price” in the event of an attack, but his government’s refusal to supply lethal weapons to Ukraine, bolster Germany’s troop presence in Eastern Europe or spell out which sanctions it would support against Russia has drawn criticism abroad and at home.
“The Germans are right now missing in action. They are doing far less than they need to do,” Sen. Richard Blumenthal, a Democrat and member of the Armed Services Committee, recently told an audience of Ukrainian Americans in his state, Connecticut.
This sentiment was echoed by Republican Sen. Rob Portman, who questioned why Berlin hadn’t yet approved a request to let NATO member Estonia pass over old German howitzers to Ukraine. “That makes no sense to me, and I’ve made that very clear in conversations with the Germans and others,” Portman told NBC.
Ahead of his trip, Scholz defended Germany’s position not to supply Kyiv with lethal weapons, but insisted that his country is doing its bit by providing significant economic support to Ukraine.
Asked about the future of the Nord Stream 2 pipeline that seeks to bring Russian natural gas to Germany under the Baltic Sea, bypassing Ukraine, Scholz refused to make any explicit commitments.
“Nothing is ruled out,” he told German public broadcaster ARD.
Germany has come under criticism over its heavy reliance on Russian energy supplies and the gas pipeline has long been opposed by the United States. But it is strongly supported by some in Scholz’s center-left Social Democratic Party, including former chancellor Gerhard Schroeder.
The 77-year-old Schroeder is close to Russian President Vladimir Putin and heads the shareholders’ committee of Nord Stream AG and the board of directors of Nord Stream 2.
In a move likely to embarrass Scholz ahead of his first official trip to Washington, the Russian state-owned gas company Gazprom announced Friday that Schroeder — who has accused Ukraine of “saber-rattling” in its standoff with Russia — has been nominated to join its board of directors.
Scholz’s spokesman declined repeated requests for comment on Schroeder’s ties to Putin.
Despite Germany’s reluctance to officially put the new pipeline — which has yet to receive an operating permit — on the negotiating table with Russia, the United States has made clear that even without Berlin’s agreement the project is dead should Moscow launch an attack.
“One way or the other, if Russia invades Ukraine, Nord Stream 2 will not move forward,” U.S. national security adviser Jake Sullivan told “Fox News Sunday.”
Scholz will meet President Joe Biden and members of Congress on Monday to try to smooth out differences. The 63-year-old’s performance in Washington could have broad implications for U.S.-German relations and for Scholz’s standing at home.
While former President Donald Trump frequently slammed Germany, accusing it of not pulling its weight internationally, his successor has sought to rebuild relations with Berlin.
“Biden has taken some real risks, including on the the issue of the German-Russian gas pipeline,” said Jeff Rathke, president of the American Institute for Contemporary German Studies.
“(Scholz’s) visit to Washington is an opportunity for him to try to turn that page,” said Rathke.
Having succeeded long-time German leader Angela Merkel last year, Scholz also needs to appease doubters at home who accuse him of pulling a diplomatic vanishing act compared to his European counterparts. With the phrase “Where is Scholz?” trending on social media last week, German conservative opposition leader Friedrich Merz called for “clear words” from the government on the Ukraine crisis.
“We must rule nothing out as a reaction to a further military escalation,” the leader of Merkel’s center-right bloc said, though he too has been skeptical about sending possible German arms shipments to Ukraine.
Others in Scholz’s three-party governing coalition have struck a harsher tone toward Russia.
Speaking alongside her Russian counterpart in Moscow last month, German Foreign Minister Annalena Baerbock of the Green Party branded Russia’s troop deployment at the border with Ukraine a “threat.” She plans to visit Ukraine on Monday and Tuesday and inspect the front line between Ukrainian troops and areas held by Russian-based separatists in the east.
Marie-Agnes Strack-Zimmermann, a member of the Free Democrats who chairs Germany’s parliamentary defense committee, said Schroeder’s work for Moscow “harms the country he should serve” and suggested removing the privileges he enjoys since leaving office.
Whatever Germany does to support Ukraine will likely come at a cost.
Berlin’s approval of 5,000 helmets for Ukrainian troops last week drew widespread mockery. Kyiv has since asked Germany for more military hardware, including medium-range and portable anti-aircraft missile systems, as well as ammunition.
Meanwhile, some German officials worry that any mention of further sanctions against Russia, let alone a full-blown conflict, could drive up Europe’s already high gas prices. Constanze Stelzenmueller, a specialist on trans-Atlantic relations at the Brookings Institution, noted that Europe will bear the brunt of blowback costs from economic sanctions against Russia.
“You have populists in Europe always looking for ways to exploit political differences and tensions,” she said. “That’s what’s at stake here.”
In an uncharacteristic outburst at the start of the coronavirus pandemic, Scholz — who was then Germany’s finance minister — announced that he would be pulling out a figurative “bazooka” to help businesses cope with the crisis by setting aside more than 1 trillion euros ($1.1 trillion) in state aid.
Scholz may need to make a similarly expansive gesture to ease concerns in Washington and beyond, said Rathke.
“Germany is going to have to show that it is not only committed to the sovereignty and territorial integrity of Ukraine, but that it’s putting real resources behind it now, not just pointing to what it’s done in the past,” he said.
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Geir Moulson in Berlin and Ellen Knickmeyer and Nathan Ellgren in Washington contributed to this report.
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Follow Frank Jordans on Twitter at http://twitter.com/wirereporter
Copyright 2022 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed without permission.
Abstract
The rapid accumulation of mutations in the SARS-CoV-2 Omicron variant that enabled its outbreak raises questions as to whether its proximal origin occurred in humans or another mammalian host. Here, we identified 45 point mutations that Omicron acquired since divergence from the B.1.1 lineage. We found that the Omicron spike protein sequence was subjected to stronger positive selection than that of any reported SARS-CoV-2 variants known to evolve persistently in human hosts, suggesting a possibility of host-jumping. The molecular spectrum of mutations (i.e., the relative frequency of the 12 types of base substitutions) acquired by the progenitor of Omicron was significantly different from the spectrum for viruses that evolved in human patients but resembled the spectra associated with virus evolution in a mouse cellular environment. Furthermore, mutations in the Omicron spike protein significantly overlapped with SARS-CoV-2 mutations known to promote adaptation to mouse hosts, particularly through enhanced spike protein binding affinity for the mouse cell entry receptor. Collectively, our results suggest that the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans, indicating an inter-species evolutionary trajectory for the Omicron outbreak.
Keywords: Evolutionary origins; Molecular spectrum of mutations; Omicron; Receptor-binding domain; SARS-CoV-2; Spike-ACE2 interaction.
Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.
Abstract
Despite claims from prominent scientists that SARS‐CoV‐2 indubitably emerged naturally, the etiology of this novel coronavirus remains a pressing and open question: Without knowing the true nature of a disease, it is impossible for clinicians to appropriately shape their care, for policy‐makers to correctly gauge the nature and extent of the threat, and for the public to appropriately modify their behavior. Unless the intermediate host necessary for completing a natural zoonotic jump is identified, the dual‐use gain‐of‐function research practice of viral serial passage should be considered a viable route by which the novel coronavirus arose. The practice of serial passage mimics a natural zoonotic jump, and offers explanations for SARS‐CoV‐2’s distinctive spike‐protein region and its unexpectedly high affinity for angiotensin converting enzyme (ACE2), as well as the notable polybasic furin cleavage site within it. Additional molecular clues raise further questions, all of which warrant full investigation into the novel coronavirus’s origins and a re‐examination of the risks and rewards of dual‐use gain‐of‐function research.
Keywords: coronavirus, COVID‐19, gain‐of‐function, intermediate host, pandemic, SARS‐CoV‐2, serial passage, virology
Abstract
This article from a father–son team explores whether the history and methodology of viral serial passage gain‐of‐function research provides a parsimonious explanation for SARS‐CoV‐2, contrasting it with the theory that the novel coronavirus emerged naturally. It also examines the precedents of performing gain‐of‐function research on bat‐borne coronaviruses, and calls for a re‐examination of the risks inherent with gain‐of‐function research.
1. Introduction
To date, the origins of SARS‐CoV‐2 remain in doubt, and its behavior enigmatic: It has been reported that “the virus acts like no microbe humanity has ever seen.”[ 1 ] Although based on sequence analysis many prominent virologists and other eminent scientists have concluded that the novel coronavirus causing the current pandemic was not designed or manipulated in a laboratory and was the result of a natural zoonotic jump,[ 2 ] this assertion fails to fully account for all possible origins of two unique genomic characteristics found in SARS‐CoV‐2, and ignores the long history of serial passage as a method to manipulate viral genomes. The long‐standing practice of serial passage is a form of gain‐of‐function research that forces zoonosis between species, and requires the same molecular adaptations necessary for a natural zoonotic jump to occur within a laboratory, leaving the same genetic signatures behind as a natural jump but occurring in a much shorter period of time.
The genetic signatures in question includes two distinctive features possessed by SARS‐CoV‐2’s spike‐protein: the unique sequence in the receptor binding domain (RBD), a region known to be critical for SARS‐CoV‐2’s utilization of human angiotensin converting enzyme (ACE2), which is the cell surface receptor used by both SARS‐CoV and SARS‐CoV‐2 for fusion with target cells and subsequent cell entry. The second feature is the presence of a polybasic furin cleavage site, which is also known as a multibasic cleavage site (MBS)—a four amino acid insertion with limited sequence flexibility—within the coronavirus’s novel spike‐protein, that is not found in SARS‐CoV or other lineage B coronaviruses. This furin cleavage site, which is poly or multibasic by definition since its composed of multiple basic amino acids, is an important virulence feature observed to have been acquired by fusion proteins of avian influenza viruses and Newcastle Disease Virus either grown under experimental conditions or isolated from commercial animal farms—settings that mimic the conditions of serial laboratory passage. In fact, no influenza virus with a furin cleavage site has ever been found in nature,[ 3 ] and it is a feature that has been thoroughly investigated in the literature since it appears to allow the influenza viruses that carry it to establish a systemic multiorgan infection using different cell types including nerve cells,[ 3 ] is correlated with high pathogenicity, and also plays a key role in overcoming the species barrier.[ 4 ] More generally, despite the fact that not all serially passed viruses have demonstrated an increase in pathogenicity, the fact remains that every highly pathogenic avian influenza virus, defined by having a furin cleavage site, has either been found on commercial poultry farms that create the pseudo‐natural conditions necessary for serial passage, or created in laboratories with gain‐of‐function serial passage experiments.[ 3 ]
Although they only emerge under artificial conditions in influenza viruses, these furin cleavage sites are found within several branches of the coronavirus family tree. However SARS‐CoV‐2 is the only lineage B coronavirus found with one, and the only other coronaviruses known to have them are only at most 60% identical to this novel coronavirus.[ 5 ] An intriguing clinical correlate is that furin cleavage sites within influenza viruses are associated with lymphopenia in infected mice, and with neurological conditions following replication in the brains of ferrets,[ 6 ] both of which are clinical manifestations observed in hospitalized patients infected by SARS‐CoV‐2 and suffering from COVID‐19.[ 1 ] This indicates that furin cleavage sites may be an example of the convergent evolution that dominates virus–host interactions, since viral proteins evolve convergently and often accumulate many of the same linear motifs that mediate many functionally diverse biophysical interactions in order to manipulate complex host processes.[ 7 ] It is possible that this novel coronavirus gained its furin cleavage site through recombination in an intermediate host species, however there are also two laboratory processes that may have imbued SARS‐CoV‐2 with its furin cleavage site which will be discussed below.
Without incorporating the historical and biological implications of serial viral passage either through lab animals in vivo or through cell cultures in vitro, it is impossible to comprehensively evaluate whether SARS‐CoV‐2 is the result of a laboratory leak or a natural zoonotic jump. Moreover, despite the published consensus being that SARS‐CoV‐2 arose naturally, because these publications universally ignore the scenario of the widely used practice of laboratory serial passage, this latter scenario deserves a thorough investigation. Especially since serial passage through a live animal host simply forces the same molecular processes that occur in nature to happen during a zoonotic jump, and in vitro passage through cell culture mimics many elements of this process—and neither necessarily leaves any distinguishing genetic traces.
2. The History of Viral Serial Passage
The dual‐use gain‐of‐function research tool of serial passage was first applied to a strain of H1N1 Swine Flu, a variant of the pandemic influenza virus that was genetically modified before it either leaked out of a Soviet lab or was introduced as part of an attenuated vaccine trial in 1977. Although no one has ever taken responsibility for the introduction of this virus, it would become the first known example of a virus created by serial passage leaving a lab, which was later determined due to its inexplicable genetic distance from any known sister strain.[ 8 ] This extra distance would be expected since serial passages artificially accelerates genetic divergence between taxa, resulting in the accumulation of genetic distance at a much faster rate than it occurs in a natural setting.
Then in 1979, just 2 years after the introduction of this modified H1N1 Swine Flu, a different Soviet lab leaked weaponized anthrax out through an improperly maintained exhaust filter, and Soviet authorities convincingly blamed the deaths on contaminated local meat. This cover up withstood a formal inquiry conducted in 1986, and was not revealed to be a fabrication until 1992, when an analysis of dispersion patterns revealed that the victims were not those working with the supposedly contaminated meat, but instead all lived downwind from the Sverdlovsk weapons lab and its improperly maintained exhaust vent. Therefore, there is a history of denying laboratory leaks on the commercial meat industry that dates back about 40 years, an effective excuse that provided the Soviets with an alibi that held up for nearly 2 decades.
The Soviet strain of serially passaged H1N1 Swine Flu was likely being developed as part of a vaccine program, one of the humane goals of gain‐of‐function research that exist alongside riskier and more troublesome ones like developing bioweapons. Its emergence ignited the debate between the risks and rewards of dual‐use gain‐of‐function research—causing it to became the poster virus for the dangers this protocol posed.[ 8 ]
This debate would largely fade in the decades that followed, until two separate teams used genetic manipulation followed by serial passage between ferrets to create mammal‐transmissible H5N1 Bird Flu strains of influenza virus in 2011 that had the gain‐of‐function of being transmissible by aerosol. The first team was led by Dr. Ron Fouchier and conducted at the Erasmus Medical Center in the Netherlands, and demonstrated that as few as five mutations prior to serial passage were sufficient to create a modified strain of the H5N1 Bird Flu that could be transmitted by aerosol while remaining highly lethal.[ 9 ] The creation of this highly virulent strain that was said by a reporter to be able to “make the deadly 1918 pandemic look like a pesky cold,”[ 10 ] and was contentious enough to cause the scientists working on them to prepare for a media storm[ 11 ]—a storm that rolled in on the back of a second similar experiment.
Instead of only tweaking the H5N1 Bird Flu in a few places before serial passage, Dr. Yoshihiro Kawaoka of the Universities of Tokyo and Wisconsin used genetic engineering to combine genes from the H1N1 Swine Flu as well as the H5N1 Bird Flu to create a chimeric virus that was then serially passed through ferrets, creating another airborne virus with potentially pandemic properties.[ 12 ] Both experiments created a modified genome that appeared to be the result of natural, albeit accelerated, selection since the process of serial passage forces the mutations selected for in natural zoonotic jumps, and masks the direct genetic engineering done on the viruses. These experiments were viewed by many as being sufficiently dangerous that they should not be published,[ 13 ] however they were both eventually released with certain methodological and sequence details left out.
In the years that followed, gain‐of‐function serial passage through ferrets was used to increase the virulence of the H7N1 Bird Flu as well as allowing for its aerosol transmission without first introducing any mutations.[ 14 ] Additionally, the H1N1 Bird Flu was also found to become airborne and increase in virulence after in vivo passage through swine.[ 15 , 16 ] And although serial passage in the laboratory does not invariably increase viral pathogenicity, highly pathogenic influenza viruses all contain furin cleavage sites,[ 16 ] which only emerge after serial passage in laboratories or pseudo‐naturally on commercial animal farms.
The process of sequential passage through animal hosts or cell cultures leaves a genome that appears natural and not purposefully manipulated since it effectively mimics the natural process of zoonosis, and leaves a genome that appears to be the result of natural selection so long as its relationship to related strains of virus is ignored. However, the artificial generations added by forced serial passage creates the artificial appearance of evolutionary distance, which was the characteristic of the H1N1 Swine Flu Soviet leak in the 1970s that lead researchers to conclude it had been constructed in a lab, and is exactly what is found with SARS‐CoV‐2, which is distant enough from any other virus that it has been placed in its own clade.[ 17 ]
2.1. Serial Passage and Its Molecular Signatures
Although serial passage mimics many of the natural zoonotic processes that occur during a natural zoonotic jump, because serial passage artificially condenses a natural phenomenon into a small temporal window, some subtle differences can be found. In addition to the inexplicable genetic distance from its sister strains, which screams out for an intermediate relative to complete the phylogenetic picture, SARS‐CoV‐2 has a remarkably strong affinity for spike‐protein binding to ACE2—some 10–20 times higher than SARS‐CoV’s.[ 18 ] That affinity may have emerged after mutational events either in an intermediate natural host or after a zoonotic jump into humans that theoretically could have occurred earlier than the first documented infection, which would give it time to increase that significantly. So logically, it could also have emerged via selection after serial passage through laboratory cell cultures or laboratory animals as well. And regarding the second distinctive feature found in the novel coronavirus: If other viruses have been observed to acquire furin cleavage sites by passage under experimental laboratory conditions, then such a mechanism is theoretically possible for SARS‐CoV‐2 as well.[ 2 ]
In the case of influenza viruses like those mentioned above, their gain‐of‐function furin cleavage sites are thought to be a result of two different molecular processes. The first is either nucleotide insertions or substitutions that are able to be rescued and then eventually selected for due to the high multiplicity of infection found in serial passage protocols.[ 19 ] And the second is the recombination of multiple viral RNAs inside a host cell,[ 20 ] which may also include additional viruses introduced through accidental laboratory co‐infections.
Unlike influenza viruses, serial passage through ferrets has not been recorded in the literature for coronaviruses. However, since several branches of coronavirus have furin cleavage sites, a molecular pathway for their emergence must exist and may reemerge during serial passage. Several factors weigh into the probability that coronaviruses can gain furin cleavage sites following serial passage: The frequency of evolutionary motifs meant to deal with virus–host interactions that are often shared between viruses, the observations that when the infectious bronchitis coronavirus (IBV) coronavirus is serially passed through chickens it developed notable mutations along its spike‐protein genes,[ 21 ] and the fact that when a lineage A bovine coronavirus was subject to in vitro serial passage through cell lines, a 12‐nucleotide insert found within only a small minority of the pooled viruses spike‐protein region was strongly selected for and quickly emerged as the dominate strain.[ 22 ] These findings all point to the possibility that SARS‐CoV‐2 may have gained its furin cleavage site the same way influenza viruses do—through the in vivo serial passage between the live hosts that presents the immune challenges and intense selective pressure necessary for the recombination and mutations that lead to its emergence to occur. And just like influenza viruses are only able to preserve their furin cleavages in artificial environments since the heightened virulence they impart kills their hosts before they can propagate in a natural setting, based on the known taxonomy lineage B coronaviruses do not appear to be able to support furin cleavages in nature.
There is no doubt that the acquisition of the furin cleavage site was one of the key adaptations that enable SARS‐CoV‐2 to efficiently spread in the human populations compared to other lineage B coronaviruses, and provides a gain‐of‐function.[ 23 ] In addition to the possibility of obtaining a furin cleavage site through natural recombination in a secondary host or through serial passage either in a laboratory or on a commercial farm, one could have been spliced directly into the novel coronavirus’s backbone in a laboratory using classic recombinant DNA technology that has been available for nearly 20 years. This allows for the removal of the restriction site junctions that are the telltale sign of direct genetic manipulation and permits reassembly without introducing nucleotide changes—creating a virus without any evidence of manipulation using the aptly named “No See’m technology.”[ 24 ] So although the entire spike‐protein RBD was not assembled from scratch, it is certainly plausible that the 12‐nucleotide‐long furin cleavage site could have been spliced directly into SARS‐CoV‐2. Furin cleavages already have been successfully spliced into other coronaviruses, including the IBV,[ 25 ] and even into SARS‐CoV, where it increased cell‐to‐cell fusion in in vitro experiments that only examined only the spike‐protein’s function, which would presumably heighten its infectivity in vivo.[ 26 ]
Moreover, when a furin cleavage site was introduced to the IBV coronavirus spike‐protein via recombination, just like influenza viruses hosting this feature, it appeared to impart it with increased lethality as well as inflict neurological symptoms that had never previously been reported in studies of the murine IBV coronavirus.[ 25 ] The presence of this cleavage site also increased damage to the respiratory and urinary systems, paralleling SARS‐CoV‐2 systemic multiorgan symptoms—especially reports that infection with the novel coronavirus not only targets the lungs where it binds to ACE2 receptors, but also the entire cardiovascular system,[ 27 ] the nervous system,[ 28 ] and our kidneys as well.[ 29 ] It might be more than a coincidence that the Vero cells often used in serial passage are derived from kidney epithelial cells extracted from African green monkeys, which have ACE2 receptors very similar to those found in humans and would be shared by the humanized mice that are also used for serial passage research.
2.2. Natural Origin, or Gain‐of‐Function Lab Escape?
Gain‐of‐function research on bat‐borne coronaviruses has been ongoing for nearly a decade everywhere from the University of North Carolina to the Wuhan’s Institute of Virology, which is supported by related facilities such as Wuhan’s Center for Disease Control and Prevention as well as Wuhan University. A coronavirus that targets the ACE2 receptor like SARS‐CoV‐2 was first isolated from a wild bat in 2013 by a team out of Wuhan. This research was funded in part by EcoHealth Alliance,[ 30 ] and set the stage for the manipulation of bat‐borne coronavirus genomes that target this receptor and can become airborne. Many more viruses have been collected in Wuhan over the years, and one research expedition captured as many as 400 wild viruses,[ 31 ] which were added to a private repository that has since grown to over 1500 strains of virus,[ 32 ] meaning that the Wuhan Center for Disease Control and Prevention has a massive catalogue of largely undisclosed viruses to draw from for experiments. And in subsequent years, EcoHealth Alliance received funding for project proposals outlining gain‐of‐function research to be done in Wuhan, hoping to use cell cultures and humanized mice as well as “[spike]‐protein sequence data, infectious clone technology, in vitro and in vivo infection experiments and analysis of receptor binding”[ 33 ] to manipulate bat coronavirus genomes—all of which are consistent with the wet‐work that would be needed to engineer this novel coronavirus in a laboratory. But for whatever reason, the Wuhan Institute of Virology has refused to release the lab notebooks of its researchers, which are ubiquitous in even the simplest laboratories and are expected to be meticulously detailed given the sensitive and delicate work that takes place in BSL‐4 research labs intent on documenting their intellectual property, despite the fact that these notebooks would likely be enough to exonerate the lab from having any role in the creation of SARS‐CoV‐2.[ 34 ]
Although it does not prove a laboratory origin, another gain‐of‐function experiment demonstrates one possible step along the way to engineering SARS‐CoV‐2: the synthetic reconstruction of the SARS coronavirus to impart this virus with a high affinity for ACE2. This involved isolating a progenitor coronavirus from civets and then serially passing it through mammalian ACE2 receptor‐expressing cells—serial passage through host cell lines instead of entire hosts, which imparted a strong affinity for ACE2,[ 35 ] and another novel strain of coronavirus that was also presumably airborne. A few years after this study, more gain‐of‐function research was performed that involved the creation of a chimeric bat‐borne coronavirus by directly manipulating the bat coronavirus spike‐protein gene,[ 36 ] which created a coronavirus so virulent that it evoked the following dire warning from Simon Wain‐Hobson, a virologist with the Pasteur Institute in Paris: “If the [new] virus escaped, nobody could predict the trajectory.”[ 37 ]
Although SARS‐CoV‐2’s efficient solution for ACE2 binding has been accurately described as something that could not be intentionally engineered nucleotide‐by‐nucleotide,[ 2 ] it could well be selected for after serial passage through ferrets or cell cultures in a lab. The only origin for the SARS‐CoV‐2 spike‐protein RBD that the sequence data excludes is the deliberate manufacturing and introduction of the entire SARS‐CoV spike‐protein RBD sequence to create SARS‐CoV‐2. Otherwise, there are no genetic data to distinguish among natural and engineered possibilities at the present time.
2.3. Ferreting Out the Signs of Serial Passage
Curiously, studies examining SARS‐CoV‐2’s infectivity in ferrets found that it spreads readily among them, and also appears airborne in that animal model.[ 38 ] This lends support to the idea that ferrets may have been used for serial passage since viruses typically take a significant many months if not years to acclimate enough to spread at all among any new species, nonetheless become airborne, which requires further mutations.
This relationship was further supported by reports out of the Netherlands that the novel coronavirus had spread among thirteen different mink farms there, and also to at least one farm in Denmark[ 39 ] and to another in Spain where 87% of the mink were infected.[ 40 ] Minks are a closely related subspecies of ferret that can produce fertile offspring together, and so the fact that not only did the virus spread to fifteen different farms in three countries, but also appears to have spread from minks into farm workers[ 41 ] indicates that accidental commercial serial passage through minks could have played a role in its creation, as an alternative to laboratory ferrets. Nevertheless, regardless of where any possible serial passage occurred, the fact that SARS‐CoV‐2 spreads from humans to minks and then back to humans demonstrates a high affinity for both species, despite neither nominally being a natural reservoir. Further support for the possibility that serial passage through lab ferrets or throughout mink farms played a role in the genesis of this novel coronavirus is provided by a preprint that notes the obvious ease with which it passes through the air between ferrets, since SARS‐CoV‐2 was transmitted through the air to three out of four indirect recipient ferrets monitored for airborne passage of the novel coronavirus.[ 42 ] It seems reasonable to think that SARS‐Cov‐2’s apparent affinity for ferrets and minks should lead to an investigation of mink farms in the Hubei province were the novel coronavirus was discovered, since a viable pathway for its emergence could be infected bats defecating on commercial mink farms, which would loosely parallel the emergence of MERS‐CoV from herds of camels following putative fecal contamination by local bats.[ 43 ]
The prospect that serial passage through lab animals or on commercial farms may have played a role in the creation of SARS‐CoV‐2 is also raised by an April 2020 preprint, which appears to have been retracted after Chinese authorities implemented the censorship of any papers relating to the origins of the novel coronavirus.[ 44 ] This paper found that coronaviruses that target the ACE2 receptor bind with ferret cells more tightly than any other species except the tree shrew, which only scored about 2% higher. Tree shrews have also been used for serial viral passage, and have been promoted as a preferable animal host for laboratory experimentation since they are cheaper, smaller, easier to handle, and closer to humans evolutionarily and physiologically than ferrets.[ 45 ] However, one does not exclude the other as a possible host, and a recent preprint examining SARS‐CoV’s binding affinity in humans raises additional questions about its initial emergence. It found that the novel coronavirus appears to be far more adapted to human ACE2 receptors than those found in bats, which is unexpected given that bats are the virus’s assumed source, and which lead the lead research to observe that SARS‐CoV‐2 was perfectly adapted to infect humans since its first contact with us, and had no apparent need to for any adaptive evolution at all.[ 46 ]
Although the novel coronavirus also appears to have a high affinity for the pangolin ACE2 receptor,[ 47 ] phylogenetic analysis of the neutral sites that best determine shared heritage[ 48 ] and a distinctive amino acid sequence both indicate that pangolins are unlikely to have served as an intermediate host,[ 47 ] so this affinity is likely due to the convergent motifs that often mark viral evolution and not shared heritage. The unexpected immediate affinity for humans was also reflected by another preprint, which observed that SARS‐CoV‐2 appeared just as adapted to humans at the very start of its epidemic as SARS‐CoV was in the latest stages of its emergence,[ 49 ] an unexpected finding since viruses are expected to mutate substantially as they acclimate to a new species.[ 50 ] SARS‐CoV‐2’s muddled origins are made even more Gordian by a study published March 2018 that examined people who live in villages about a kilometer away from bat caves. This study revealed that only 2.7% of those villagers had antibodies indicating any past exposure to bat coronaviruses. The authors also sampled people living in Wuhan, and found no evidence of exposure to SARS‐CoV‐like coronaviruses at all.[ 51 ]
This means there is very little serological evidence of any exposure to these coronaviruses even in Chinese villagers living in close proximity to bat caves, and at the epicenter of the current outbreak—no previous exposure was found at all. These data do not support the idea that SARS‐CoV‐2 was circulating in humans prior to the outbreak began in Wuhan in the early winter or fall of 2019, making a zoonotic jump even more unlikely since natural jumps leave wide serological footprints in their new host populations as early variants of a prospective virus make limited and unsuccessful jumps into individuals of the new host species, a trial‐and‐error that must occur before mutations that allow adaptation to a new host species are selected.[ 50 ] However these results do not rule out a much earlier jump into humans somewhere outside Hubei province, an alternative that is awaiting empirical support.
Taken together, the available evidence does not point definitively toward a natural origin for SARS‐CoV‐2, rather, much of it is more consistent with what would be found if the novel coronavirus had arisen from serial passage of a “precursor” progenitor virus in a lab, or from bats infecting a commercial mink farm somewhere in China, which would also provide the conditions for serial passage. However, more evidence is required before a conclusive judgement can be made one way or the other.
Further research around SARS‐CoV‐2’s affinity to ferrets and minks, as well as other possible intermediate hosts seems warranted, and certainly the examination of all past gain‐of‐function serial passage research by the scientific community at large should occur to determine what other definitive genomic signatures serial passage leaves besides the creation of furin cleavage sites, in case more of those can be found in this novel coronavirus. Two additional unique genomic signature are already being researched, as one preprint indicates that SARS‐CoV‐2 possesses a genomic region not found in other coronaviruses that appears to cloak the novel coronavirus from white blood cells, a characteristic also found with HIV.[ 52 ] And the second preprint identifies a region on the spike‐protein gene found in no other bat‐borne coronavirus that is nearly identical to superantigenic and neurotoxic motifs found in some bacteria, which may contribute to the immune overreaction that leads to the Kawasaki‐like multisystem inflammatory syndrome in children, and cytokine storms in adults.[ 53 ] Given the unique traits found in SARS‐CoV‐2 and all the open questions there still are around its emergence, until either a natural or laboratory origin is conclusively demonstrated both avenues should be robustly investigated by the scientific community.
3. Conclusions and Outlook
The history of gain‐of‐function research is one of science’s most significant and troubling, especially since the Nuremberg Code, research scientists’ Hippocratic Oath, dictates that experiments that could endanger human life should only occur if the potential humanitarian benefits significantly outweigh the risks.[ 54 ] It seems ill‐advised to rule out the possibility that gain‐of‐function techniques such as serial passage may have played a role in the creation of SARS‐CoV‐2 until more definitive data are collected, and when the Center for Arms Control and Non‐Proliferation has calculated that the odds that any given potential pandemic pathogen might leak from a lab could be better than one in four.[ 55 ]
The release of the H1N1 Swine Flu in 1977 first initiated the discussion about the moral and physical hazards involved with dual‐use gain‐of‐function research, and it was the creation of extraordinarily virulent H5N1 Bird Flu strains—using the same technique of serial passage through an animal host in a lab—that contributed to the NIH imposing a moratorium on dual‐use gain‐of‐function research from 2014 until 2017, after which it was relaxed explicitly to allow influenza strains as well as coronaviruses to be studied. This moratorium was meant to limit “the potential to create, transfer, or use an enhanced potential pandemic pathogen.”[ 56 ] However, just as an increased pace of research into influenza vaccines increased the odds that a leak would occur leading up to the 1977 release of H1N1 Swine Flu, which is the most often cited as originating from a laboratory leak,[ 8 ] it would follow that an increased pace of research into coronaviruses over the past few years would have increased the odds that a lab leak of one would occur; after all, these viruses were pinpointed back in 2006 as a viable vector for an HIV vaccine[ 57 ] and research into a pan‐coronavirus vaccine has been ongoing for decades.
And whether or not gain‐of‐function research is determined to have played a role in SARS‐CoV‐2’s emergence, the fact that it creates opportunities for pandemic viruses to leak out of labs calls for a re‐examination of the moratorium against this practice, because the emergence of this novel coronavirus has demonstrated that the international public health community is not prepared to handle the leak of a pandemic virus. Furthermore, none of the gain‐of‐function research conducted since 2014 has provided humanity with any tools at all to fight back against the ongoing pandemic caused by this novel coronavirus.
Did omicron come from rodents? – Google Search
Did Omicron acquire the unusual 57 mutations as the result of the serial passages in lab rodents?
Was Sars-Cov-2 Omicron weaponized by serial passages in lab rodents?
Was Sars-Cov-2 Omicron weaponized? By the serial passages in lab rodents?
Might SARS‐CoV‐2 Have Arisen via Serial Passage through an Animal Host or Cell Culture?
Abstract
Despite claims from prominent scientists that SARS‐CoV‐2 indubitably emerged naturally, the etiology of this novel coronavirus remains a pressing and open question: Without knowing the true nature of a disease, it is impossible for clinicians to appropriately shape their care, for policy‐makers to correctly gauge the nature and extent of the threat, and for the public to appropriately modify their behavior. Unless the intermediate host necessary for completing a natural zoonotic jump is identified, the dual‐use gain‐of‐function research practice of viral serial passage should be considered a viable route by which the novel coronavirus arose. The practice of serial passage mimics a natural zoonotic jump, and offers explanations for SARS‐CoV‐2’s distinctive spike‐protein region and its unexpectedly high affinity for angiotensin converting enzyme (ACE2), as well as the notable polybasic furin cleavage site within it. Additional molecular clues raise further questions, all of which warrant full investigation into the novel coronavirus’s origins and a re‐examination of the risks and rewards of dual‐use gain‐of‐function research.
Abstract
This article from a father–son team explores whether the history and methodology of viral serial passage gain‐of‐function research provides a parsimonious explanation for SARS‐CoV‐2, contrasting it with the theory that the novel coronavirus emerged naturally. It also examines the precedents of performing gain‐of‐function research on bat‐borne coronaviruses, and calls for a re‐examination of the risks inherent with gain‐of‐function research.
(NEXSTAR) – Where did omicron come from? It’s a question scientists worldwide are still working to understand as the COVID-19 variant continues its reign as the dominant strain globally. While much is known about its symptoms and differences to other variants, its origins remain unclear.
Researchers say omicron is so different from previous strains, like delta, that they’re unsure how it even came to be, Nature scholarly journal reports. In an analysis still awaiting peer review, authors explain omicron’s closest estimated relative was from mid-to-late 2020 – as if this particular SARS-CoV-2 strain developed completely independently of previously widespread ones.
What’s more: omicron has over 50 mutations, more than any other strain. Many of these particular mutations, authors of the analysis say, are very rare or altogether never-before-seen. Some researchers say that simple person-to-person spread would not result in so much viral change. Could it be rodent-human transmission?
A December study of 45 omicron mutations published in the Journal of Genetics and Genomics found the types of changes in those cells resembled those found when coronaviruses previously evolved in mice, researchers said. Single-nucleotide substitutions for RNA viruses in humans typically flip from G to U – but omicron shows a switch from C to A.
Some scientists theorize that coronavirus may have been transmitted from a person to a rat and then back to a person, accounting for some of omicron’s unique mutations, which Scripps Research infectious disease researcher Kristian Andersen says have rarely been seen in humans.
Rats, mice and disease
Rodents are especially good at spreading disease because they live and/or frequent places where germs accumulate, Dr. Bobby Corrigan, urban rodentologist, tells Prevention. Mice and rats live and visit trash bins and sewers, touching everything with little hands that never get washed.
Rats and mice can transfer dozens of diseases to humans in two ways: directly or indirectly. Direct exposure happens when a human comes into contact with rodent feces, urine or even the creatures themselves. This happens easily, since Corrigan says rats and mice are “constantly urinating and defecating” inside human homes.
Indirect transmission happens when rodent parasites – like ticks or fleas – infect humans with various diseases, including West Nile virus and Lyme disease.
Omicron symptoms include cold or flu-like symptoms, including runny nose, fatigue, sneezing and sore throat – night sweats, itchy eyes, nausea and vomiting have also been reported.
COVID-19 Videos: Review Of News And Ideas | Covid-19 – YT Search | Omicron Covid | Coronavirus
Because an immunocompromised host doesn’t produce a lot of antibodies, many viruses are left to propagate. And new mutant viruses that resist the antibodies can multiply.
A mutation that allows a virus to evade antibodies isn’t necessarily advantageous. It could make the virus’s spike protein unstable so that it can’t latch quickly onto a cell, for example. But inside someone with a weak immune system, viruses may be able to gain a new mutation that stabilizes the spike again.
Similar mutations could have built upon themselves again and again in the same person, Dr. Pond speculates, until Omicron evolved a spike protein with just the right combination of mutations to allow it to spread supremely well among healthy people.
“It certainly seems plausible,” said Sarah Otto, an evolutionary biologist at the University of British Columbia who was not involved in the study. But she said scientists still needed to run experiments to rule out alternative explanations.
It’s possible, for example, that the 13 spike mutations offer no benefit to Omicron at all. Instead, some of the other spike mutations could be making Omicron successful, and the 13 are just along for the ride.
“I would be cautious about interpreting the data to indicate that all of these previously deleterious mutations have been adaptively favored,” Dr. Otto said.
Dr. Pond also acknowledged that his hypothesis still has some big gaps. For example, it’s not clear why, during a chronic infection, Omicron would have gained an advantage from its new “bubble” method for getting into cells.
“We just lack imagination,” Dr. Pond said.
James Lloyd-Smith, a disease ecologist at U.C.L.A. who was not involved in the study, said that the research revealed just how hard it is to reconstruct the evolution of a virus, even one that arose recently. “Nature is certainly doing its part to keep us humble,” he said.
M.N.: My answer is : YES, THIS IS PROBABLY CORRECT. And I thought so too …
This thesis has to be carefully examined by the statisticians, epidemiologists, and good medical thinkers of which there is the most obvious and the most dangerous shortage, ain’t it so, dear Dr. Fauci?
I still cannot get an answer, if the differential diagnostic work is properly performed in the hospitals in the cases of severe illness with signs of coagulopathy ascribed to “Covid-19”, and in the cases of severe respiratory syndrome, previously called the “Atypical Pneumonia of unknown origin”.
There might be the different various underlying illnesses, with coincidental or “comorbid” positive tests for Sars-Cov-2, which reportedly, at least in the beginning of this Pandemic, was asymptomatic in about 85% of all positive antigen tests.
The Informational aspect of this Pandemic, the Info-Demic, to which WHO referred to, has to be very carefully examined.
Our politicians, on all levels, should be aware of the significant complexities of these issues, and should keep their minds critical and open.
The quality and depth of our medical thinking is not what it used to be, for various reasons. The talk about the severe crisis of American Medicine is not baseless. The comprehensive and adequate Health Care Reform still is one of the most urgent problems and needs in this country, and it is closely related to the issue of the adequate physicians’ training.
Without considering the option of understanding the Covid-19 as the INFO-Pandemic, which includes the signs and the aspects of the Biowarfare, the picture will be incomplete.
I think we need the new, radical, in-depth, truly scientific reassessment of the “Covid Phenomenon”, and the input from the Intelligence Community can be very, very valuable.
Michael Novakhov | 12.21.21
Opinion | What We Can Learn From How the 1918 Pandemic Ended
Most histories of the 1918 influenza pandemic that killed at least 50 million people worldwide say it ended in the summer of 1919 when a third wave of the respiratory contagion finally subsided.
Yet the virus continued to kill. A variant that emerged in 1920 was lethal enough that it should have counted as a fourth wave. In some cities, among them Detroit, Milwaukee, Minneapolis and Kansas City, Mo., deaths exceeded even those in the second wave, responsible for most of the pandemic’s deaths in the United States. This occurred despite the fact that the U.S. population had plenty of natural immunity from the influenza virus after two years of several waves of infection and after viral lethality in the third wave had already decreased.
Nearly all cities in the United States imposed restrictions during the pandemic’s virulent second wave, which peaked in the fall of 1918. That winter, some cities reimposed controls when a third, though less deadly wave struck. But virtually no city responded in 1920. People were weary of influenza, and so were public officials. Newspapers were filled with frightening news about the virus, but no one cared. People at the time ignored this fourth wave; so did historians. The virus mutated into ordinary seasonal influenza in 1921, but the world had moved on well before.
We should not repeat that mistake.
True, right now we have every reason for optimism. First, Omicron cases are declining in parts of the country. Second, nearly the entire U.S. population will soon have been either infected or vaccinated, strengthening their immune systems against the virus as we know it now. Third, although Omicron is extraordinarily good at infecting the upper respiratory tract, which makes it so transmissible, it seems less able to infect the lungs than earlier variants so it is less virulent. It is entirely possible and perhaps even likely that, spurred by a better immune response, the virus will continue to decrease in lethality; indeed, there is a theory that the 1889-92 influenza pandemic was actually caused by a coronavirus called OC43, which today causes the common cold.
All of which makes overconfidence, indifference or weariness, after two years of battling the virus — and one another — a danger now.
Signs of weariness — or misguided hope — are everywhere. Although more than 70 percent of the adult population is fully vaccinated, progress has stagnated, and as of Jan. 27, only 44 percent had received boosters, which provide vital protection against severe illness. Although most of us, especially parents, want schools to stay open, parents have gotten only about 20 percent of children ages 5 to 11 fully vaccinated. As in 1920, people are tired of taking precautions.
This is ceding control to the virus. The result has been that even though Omicron appears to be less virulent, the seven-day average for daily Covid-19 deaths in the United States has now surpassed the Delta peak in late September.
Worse, the virus may not be finished with us. Although there’s a reasonable likelihood that future variants will be less dangerous, mutations are random. The only thing certain is that future variants, if they are to be successful, will elude immune protection. They could become more dangerous.
That was the case not only in 1920 with the last gasp of the 1918 virus, but also in the 1957, 1968 and 2009 influenza pandemics. In 1960 in the United States, after much of the population had achieved protection from infection and a vaccine, a variant caused peak mortality to exceed the pandemic levels in 1957 and 1958. In the 1968 outbreak, a variant in Europe caused more deaths the second year, even though, once again, a vaccine was available and many people had been infected.
In the 2009 pandemic, variants also emerged that caused breakthrough infections; one study in Britain found “greater burden of severe illness in the year after the pandemic” but “much less public interest in influenza.” Researchers blamed the government’s approach for that. In the first year, the public health response was “highly assertive,” chiefly in providing information; there were no lockdowns. In the second year, they found, “the approach was laissez-faire.” As a result, “a large number of deaths, critical care and hospital admissions occurred, many of these in otherwise healthy people of working age.”
Such precedents should make us wary. Vaccines, the new antiviral drug Paxlovid and others could end the pandemic, once billions of doses become widely available globally and if the virus does not develop resistance. But the end is not going to arrive anytime soon. The immediate future still depends on the virus and how we wield our current arsenal: vaccines, masks, ventilation, the antiviral drug remdesivir and steroids and the one monoclonal treatment that still works against Omicron, social distancing and avoiding crowds. As a society, we have largely abandoned the public health measures on that list. As individuals, we can still act.
John M. Barry is a distinguished scholar at the Tulane University School of Public Health and Tropical Medicine and the author of “The Great Influenza: The Story of the Deadliest Pandemic in History.”
The Omicron wave is now receding in states where the extremely contagious variant arrived later, and some governors are saying it’s time for pandemic-fatigued Americans to try to restore a sense of normalcy and learn to live with the virus.
The United States remains in a precarious position, as hospitals are overstretched and daily deaths are above 2,500 and rising. Case counts are now declining in some interior states, including Arizona, Utah, Colorado, North Dakota, Louisiana and Mississippi, where Omicron swept through more recently, and while new cases are falling nationally, too, they remain far higher than in any other period of the pandemic. And the spread of an Omicron subvariant that appears to be even more contagious has some experts warning that it could take longer than expected for the winter wave to wane.
The daily average of U.S. cases remains about 519,000 a day — more than double the worst statistics from last winter. Hospitalizations, which lag cases, seem to have peaked nationally, though they remain higher than last winter’s peak. Deaths, which lag more, are also at record levels in some states.
In a few states, like Washington and Montana, cases are still rising.
A few state leaders said Sunday that while more variants and, inevitably, another surge remain a threat, Omicron has brought the country closer to the endemic stage of the virus.
“We’re not going to manage this to zero,” Gov. Philip D. Murphy of New Jersey, a Democrat, said to Chuck Todd on NBC News’ “Meet the Press” on Sunday. “We have to learn how to live with this.”
Public health experts say the next phase of the virus in the United States will depend on what variants emerge and whether a sluggish vaccination campaign picks up speed. Herd immunity to the coronavirus, experts say, is unlikely to be achieved.
The spread of an Omicron subvariant is yet another reminder of the unpredictable path the pandemic could take next.
Scientists warn that the new member the Omicron viral family, known BA.2, could drag out the Omicron surge in much of the world. So far, BA.2 doesn’t appear to cause more severe disease, and vaccines are just as effective against it as they are against other forms of Omicron. But BA.2 does show signs of spreading more readily.
“This may mean higher peak infections in places that have yet to peak, and a slowdown in the downward trends in places that have already experienced peak Omicron,” Thomas Peacock, a virologist at Imperial College London, told The Times’s Carl Zimmer.
Dr. Anthony S. Fauci, the chief Covid adviser to President Biden, recently offered words of cautious optimism, saying he believed outbreaks could become much more manageable in the coming months — to a point where “they’re there, but they don’t disrupt society.”
As Omicron declines, Gov. Asa Hutchinson of Arkansas, a Republican, said the United States should move toward treating the virus as if it’s endemic, but remain vigilant. He acknowledged that more variants are inevitable and called on the federal government to help states ramp up testing capacity and access to treatments.
“That’s where the federal government needs to step up,” he said on “Meet the Press.” “Let’s take advantage of this going down to be prepared for what’s around the corner.”
Roni Caryn Rabin, Carl Zimmer and Maggie Astor contributed to this report.
The WHO has said calls to treat the coronavirus as endemic are premature as cases in parts of the world remain high.
On March 11, 2020, the World Health Organization declared COVID-19 a pandemic – a new disease that has spread around the world, affecting a large number of people.
The term pandemic comes from the Greek word “pan” meaning “all” and “demos” meaning “people”.
In comparison, an endemic – with the prefix en- meaning “in or within”- is the constant presence of a disease within a region, making its spread more predictable.
Many experts expect COVID-19 will not be eradicated, and the disease will become endemic and stay with us, in a milder form.
While the conditions to reclassify COVID-19 as endemic are not precisely defined, many countries – particularly in Europe – have begun lifting restrictions as they move towards living with the disease.
Last week, Spanish Prime Minister Pedro Sanchez called on European officials to treat COVID-19 as endemic due to falling death rates.
Classifying COVID-19 as such could mean that fewer resources would be allocated to combat the disease and people would be subject to less testing as it would likely no longer be considered a severe public health emergency.
But the World Health Organization (WHO) has said it is too early to treat the coronavirus as endemic as cases in parts of the world remain high.
Comparing endemic diseases
Endemic diseases are all around us, from the common cold to more severe diseases including HIV, malaria and tuberculosis.
Epidemiologists, scientists who study the spread of diseases, consider a disease endemic when its levels are consistent and predictable. Endemic diseases are constantly present in a population within a particular region.
Below we compare the number of cases and deaths per year from endemic diseases.
For COVID-19 to become endemic, several factors would need to be considered, including how the disease continues to evolve as well as the type of immunity people acquire through infection and vaccines.
The dominant Omicron variant
Like all viruses, the SARS-COV-2 coronavirus has been mutating since it emerged in late 2019.
Mutations – changes in genetic code – in a virus’s spike protein can affect its ability to infect cells.
Omicron, a more transmissible variant first detected in November 2021, has now been detected in at least 165 countries and territories worldwide.
It has pushed COVID-19 cases to record highs around the world with at least 100 countries recording their all-time highest daily confirmed cases since the start of 2022. There are also an unknown number of people who may have been infected with Omicron but were not tested.
Varying worldwide immunity levels
The WHO predicts more than half of the people in Europe could catch Omicron by March which, coupled with high vaccine rates, should lead to higher levels of immunity.
Herd immunity occurs when a large proportion of a community becomes immune to a disease through infection or vaccines, halting the disease from spreading.
As variants become more infectious, the herd immunity threshold increases. This is why the threshold percentage has gradually been increasing from about 60-70 percent during the original strain to 85 percent with Delta and upwards of 90 percent with Omicron.
Meanwhile, many poorer countries that are still waiting for vaccines may be a long way from seeing the end of the pandemic.
Only 5 percent of people in low-income countries are fully vaccinated according to the latest figures by Our World In Data.
Scientists and health officials around the world are keeping their eyes on a descendant of the omicron variant that has been found in more than 50 countries, including the United States.
This version of the coronavirus, which scientists call BA.2, is widely considered stealthier than the original version of omicron because particular genetic traits make it somewhat harder to detect. Danish scientists reported this week that preliminary information suggests it may be 1 1/2 times more contagious then the original variant.
But scientists say there’s a lot they still don’t know about it, including whether it causes more severe disease.
WHERE HAS IT SPREAD?
More than 18,000 genetic sequences of BA.2 have been uploaded to GISAID, a global platform for sharing coronavirus data, according to data collected by Scripps Research labs. The strain has been detected in at least 54 countries and 24 U.S. states.
“Thus far, we haven’t seen it start to gain ground” in the U.S., said Dr. Wesley Long, a pathologist at Houston Methodist in Texas, which identified three cases as of earlier this week.
The mutant appears much more common in Asia and Europe. In Denmark, it has spread quickly and become the dominant variant, according to State Serum Institute, which falls under the Danish Ministry of Health.
“Preliminary calculations indicate that BA.2 is one and a half times more contagious than BA.1,” the original omicron, the institute’s Dr. Tyra Grove Krause said in a press release earlier this week. If it is more contagious, “it may mean that the wave of infections will be higher and will extend further into February compared to the previous projections.”
WHAT’S KNOWN ABOUT THIS VERSION OF THE VIRUS?
BA.2 has lots of mutations. About 20 of them in the spike protein that studs the outside of the virus are shared with the original omicron. But it also has additional genetic changes not seen in the initial version.
It’s unclear how significant those mutations are, especially in a population that has encountered the original omicron, said Dr. Jeremy Luban, a virologist at the University of Massachusetts Medical School.
For now, the original omicron BA.1 and its descendant BA.2 are considered subsets of omicron. But global health leaders could give it its own Greek letter name if it is deemed a globally significant “variant of concern.”
Scientists at the UK Health Security Agency found that vaccine effectiveness against symptomatic disease appears similar for BA.1 and BA.2. Looking at all vaccine brands combined, scientists found they were about 70% effective against symptomatic disease from BA.2 two or more weeks after a booster shot.
An initial analysis by scientists in Denmark shows no differences in hospitalizations for BA.2 compared with the original omicron. They are also looking into how well current vaccines work against it. It’s also unclear how well treatments will work against it.
Doctors also don’t yet know for sure if someone who’s already had COVID-19 caused by omicron can be sickened again by BA.2. But they’re hopeful, especially that a prior omicron infection might lessen the severity if that happens.
The two versions of omicron have enough in common that it’s possible that infection with the original mutant “will give you cross-protection against BA.2,” said Dr. Daniel Kuritzkes, an infectious diseases expert at Brigham and Women’s Hospital in Boston.
Scientists will be conducting tests to see if antibodies from an infection with the original omicron “are able to neutralize BA.2 in the laboratory and then extrapolate from there,” he said.
HOW CONCERNED ARE HEALTH AGENCIES?
The World Health Organization classifies omicron overall as a variant of concern, its most serious designation of a coronavirus mutant, but it doesn’t single out BA.2 with a designation of its own. Given its rise in some countries, however, the agency says investigations into its characteristics “should be prioritized.”
The UK agency, meanwhile, has designated BA.2 a “variant under investigation,” citing the rising numbers found in the U.K. and internationally.
WHY IS IT HARDER TO DETECT?
The original version of omicron had specific genetic features that allowed health officials to rapidly differentiate it from delta using a certain PCR lab test because of what’s known as “S gene target failure.”
BA.2 doesn’t have this same genetic quirk. So on the test, Long said, it looks like delta.
“It’s not that the test doesn’t detect it; it’s just that it doesn’t look like omicron,” he said.
WHAT SHOULD YOU DO TO PROTECT YOURSELF?
Doctors advise the same precautions they have all along: Get vaccinated and follow public health guidance about wearing masks, avoiding crowds and staying home when you’re sick.
“The vaccines are still providing good defense against severe disease, hospitalization and death,” Long said.
The latest version is another reminder that the pandemic hasn’t ended.
“We all wish that it was over,” Long said, ”but until we get the world vaccinated, we’re going to be at risk of having new variants emerge.”
___
The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.
Coronavirus News: Study suggests coronavirus lingers in organs for months | The Deep Mystery Of Omicron: Was It Weaponized Further? | Is The Omicron Surge Mostly Due To Massively Increased Testing? – by Tyler Durden | M.N.: My answer is : YES, HE IS PROBABLY CORRECT. And I thought so too … | The crisis of American Medicine
News Review: Study suggests coronavirus lingers in organs for months
- Study suggests coronavirus lingers in organs for months <a href=”http://WOODTV.com” rel=”nofollow”>WOODTV.com</a>
- COVID virus can spread to heart, brain days after infection, study says New York Post
- SARS-CoV-2-induced kidney damage News-Medical.Net
- Study finds coronavirus can persist for months in almost every organ system: a step towards understanding lon PennLive
- Study: Coronavirus can persist for months after traversing entire body Bangor Daily News
- View Full Coverage on Google News
The crisis of American Medicine – Google Search
COVID-19 Information: Public health information (CDC) | Research information (NIH) | SARS-CoV-2 data (NCBI) | Prevention and treatment information (HHS) | Español
Is The Omicron Surge Mostly Due To Massively Increased Testing?
M.N.: My answer is : YES, HE IS PROBABLY CORRECT. And I thought so too …
This thesis has to be carefully examined by the statisticians, epidemiologists, and good medical thinkers of which there is the most obvious and the most dangerous shortage, ain’t it so, dear Dr. Fauci?
I still cannot get an answer, if the differential diagnostic work is properly performed in the hospitals in the cases of severe illness with signs of coagulopathy ascribed to “Covid-19”, and in the cases of severe respiratory syndrome, previously called the “Atypical Pneumonia of unknown origin”.
There might be the different various underlying illnesses, with coincidental or “comorbid” positive tests for Sars-Cov-2, which reportedly, at least in the beginning of this Pandemic, was asymptomatic in about 85% of all positive antigen tests.
The Informational aspect of this Pandemic, the Info-Demic, to which WHO referred to, has to be very carefully examined.
Our politicians, on all levels, should be aware of the significant complexities of these issues, and should keep their minds critical and open.
The quality and depth of our medical thinking is not what it used to be, for various reasons. The talk about the severe crisis of American Medicine is not baseless. The comprehensive and adequate Health Care Reform still is one of the most urgent problems and needs in this country, and it is closely related to the issue of the adequate physicians’ training.
Without considering the option of understanding the Covid-19 as the INFO-Pandemic, which includes the signs and the aspects of the Biowarfare, the picture will be incomplete.
I think we need the new, radical, in-depth, truly scientific reassessment of the “Covid Phenomenon”, and the input from the Intelligence Community can be very, very valuable.
Michael Novakhov | 12.21.21
Is The Omicron Surge Mostly Due To Massively Increased Testing?
Reported infections in the U.K. have suddenly spiked in the last three days, up from 59,610 on Tuesday to 78,610 on Wednesday, 88,376 on Thursday and 93,045 on Friday. Looking at the data regionally, the spike is currently much more pronounced in London, the South East, the East of England, the East Midlands and the North West than it is in the North East, Yorkshire and the Humber, the South West and the West Midlands. It’s not clear at this point if it is going to continue to rise, though the last three days’ counts don’t appear to indicate continued sharp growth.
However, as The Daily Sceptic’s Will Jones details, it is also so far largely an artefact of massively increased testing, as the graph below with data for the U.K. up to December 16th shows. Similar is true for Scotland. Positive tests have spiked.
But positivity is up only a little due to the large increase in testing.
How significant is it that the spike began on Monday December 13th, the day after Boris Johnson’s Sunday press conference when he warned everyone about Omicron and told them to get their booster jab? There was a huge surge in demand for booster doses starting that Monday and continuing throughout the week. Could the fact that this surge coincided with a similar surge in both testing and positive tests be more than coincidence? Perhaps people got tested before getting their booster, or just because of the dire warning of a new threat.
People lined up to get a COVID-19 test
MishTalk’s Mike Shedlock has some new rules:
- Testing the masses for Covid is worse than useless. Standing in line spreads it.
- The number of Omicron asymptomatic cases tells us that isolation is not the answer either. People not realizing they have it now spread Omicron like mad.
- We need to accept a fair percentage of the people simply will not get vaccinated.
- Given the vast majority of severe complications happen in the unvaccinated group, we should not let them clog up the hospitals.
- Hospital priority should go first to those with a booster, second to those with two shots, third to those with one shot, and last to the unvaccinated, with exceptions for those under the age of 12.
- If the unvaccinated don’t care, we should not care about them. Nor should insurance cover them.
- Finally, at long last, it makes sense to say “No worse than the Flu, at least for the vaccinated.” More accurately, for the vaccinated, it now appears to be “Nowhere near as bad as the flu”.
Tl,dr; The best thing to do now appears to be nothing.
As Raul Ilragi Meijer concludes at The Automatic Earth blog, if and when you’re suffering under yet another lockdown and/or any other restrictions, you should know they are for naught. There is no indication to date that Omicron will fill up hospitals, or ICUs, or that it will kill millions of people.
But that for now refuted scenario is still why those restrictions are being put in place, why you are being told not to hug your intensely lonely grandma for Christmas. Useless. And why everyone is told to get a booster, and soon another. Also useless.
It’s time for all of you to grow a spine and a pair of balls (sorry, ladies, just a manner of speech) and start living your lives again. Time to get rid of Fauci, and of Pfizer, and SAGE, and fill in your local/national bunch of experts. Because as long as they are there, they will hog the limelight, and you will never be able to start to live your life again.
A simple Christmas message.
Tyler Durden Tue, 12/21/2021 – 05:00
Gauteng in South Africa, where Omicron started, may be interpreted as the Telling Name (the way of affixing the criminal signature, to assure the credit): “Go (Gau) fly, the Chinese dragon Teng, bring us another pot of gold from Gauteng!”
The Russian Mob, allied with the Extreme (global?) Left (teeming with revenge for 1917?), with the New Abwehr as their brains and managers, appear to be the most likely actors.
The News And Times – newsandtimes.net | Post Link
Gauteng is the Telling Name:
“Go (Gau) fly, the Chinese dragon Teng, bring us pot of gold from Gauteng!”
The Russian Mob, allied with the Extreme Global Left (teeming with revenge for 1917?), with the New Abwehr as their brains & managers, appear to be the most likely actors.
‘Omicron is a long way from its ancestors and has an unusual combination of multiple changes …’
“What happened in between these two periods [mid-2020 and October 2021] is the mystery behind what has made Omicron so different.”
Note the date the Omicron variant took off like a rocket: around November 7 – the anniversary of the Russian “Great Socialist” October Revolution (11.7.1917)- the major date in the Communist calendar. Did it happen by design?
Did Omicron evolve in a RODENT? https://shar.es/aWz1jW
CoronaVirus – Omicron | Omicron and rodents – Google Search
CoronaVirus – Omicron | Omicron and rodents – Google Search
The News And Times – http://newsandtimes.net
Was Sars-Cov-2 weaponized into Omicron by multiple back and forth humans – rodents passages? – Google Search https://shar.es/aWyO72
Was Sars-Cov-2 (further) weaponized into Omicron by multiple back and forth humans – rodents passages (in the lab or the special facilities)?
12.16.21 – Omicron Human – Rodents Transmissions – Selected Articles And Searches
- Omicron Variant: Study Says Mice Could Be Mutation Source – NBC New York
- covid omicron interspecies transfer theory – Google Search
- Study Says Mice Could Be a Source of Mutation – NBC New York | Daily NewYork Journal
- covid plague rodents – Google Search
- Was Sars-Cov-2 weaponized into omicron by multiple back and forth humans – rodents passages? – Google Search
- covid in rodents – Google Search
- covid – Google Search
- University of Washington and Italy’s National Institute of Molecular Genetics study of omicron – Google Search
- University of Washington and Italy’s National Institute of Molecular Genetics omicron – Google Search
- Krisitan G Andersen omicron – Google Search
- Ученые заявили, что «омикрон» перекинулся на переносчиков чумы | Здравоохранение | Общество | Аргументы и Факты
Omicron Variant Might Come From Transmission Between Humans and Mice, Study Says
Omicron Variant Might Come From Transmission Between Humans and Mice, Study Says
The omicron variant of the virus that causes COVID-19 has so many mutations, it may be the result of “ping-pong” transmission between humans and mice or other rodents, according to a new paper… <a href=”http://nbcnewyork.com” rel=”nofollow”>nbcnewyork.com</a> –
Covid origins – Google Search
Coronavirus Origins Are Still Uncertain – US Intel Probe
Coronavirus Origins Are Still Uncertain – US Intel Probe
(NEXSTAR) – Where did omicron come from? It’s a question scientists worldwide are still working to understand as the COVID-19 variant continues its reign as the dominant strain globally. While much is known about its symptoms and differences to other variants, its origins remain unclear.
Researchers say omicron is so different from previous strains, like delta, that they’re unsure how it even came to be, Nature scholarly journal reports. In an analysis still awaiting peer review, authors explain omicron’s closest estimated relative was from mid-to-late 2020 – as if this particular SARS-CoV-2 strain developed completely independently of previously widespread ones.
What’s more: omicron has over 50 mutations, more than any other strain. Many of these particular mutations, authors of the analysis say, are very rare or altogether never-before-seen. Some researchers say that simple person-to-person spread would not result in so much viral change. Could it be rodent-human transmission?
A December study of 45 omicron mutations published in the Journal of Genetics and Genomics found the types of changes in those cells resembled those found when coronaviruses previously evolved in mice, researchers said. Single-nucleotide substitutions for RNA viruses in humans typically flip from G to U – but omicron shows a switch from C to A.
Some scientists theorize that coronavirus may have been transmitted from a person to a rat and then back to a person, accounting for some of omicron’s unique mutations, which Scripps Research infectious disease researcher Kristian Andersen says have rarely been seen in humans.
Rats, mice and disease
Rodents are especially good at spreading disease because they live and/or frequent places where germs accumulate, Dr. Bobby Corrigan, urban rodentologist, tells Prevention. Mice and rats live and visit trash bins and sewers, touching everything with little hands that never get washed.
Rats and mice can transfer dozens of diseases to humans in two ways: directly or indirectly. Direct exposure happens when a human comes into contact with rodent feces, urine or even the creatures themselves. This happens easily, since Corrigan says rats and mice are “constantly urinating and defecating” inside human homes.
Indirect transmission happens when rodent parasites – like ticks or fleas – infect humans with various diseases, including West Nile virus and Lyme disease.
Omicron symptoms include cold or flu-like symptoms, including runny nose, fatigue, sneezing and sore throat – night sweats, itchy eyes, nausea and vomiting have also been reported.
Brooklyn News Review | In Brief | Page | The Brooklyn News And Times Blog | Blog RSS – Page
Brooklyn News Review | In Brief | Page | The Brooklyn News And Times Blog | Blog RSS – Page
Brooklyn News Review | In Brief | Page | The Brooklyn News And Times Blog | Blog RSS – Page