Coronavirus

Wear a mask. You'll be fine.....Lol!

wear two masks. better safe than sorry

wear two masks. better safe than sorry

Like the old Valley Girl Joke: Why did the Valley Girl use 2 diaphragms??

She wanted to be For Sure, For Sure...

Then again, double masking isn't a bad idea...

Then again, double masking isn't a bad idea...

Except that it makes it difficult to breathe lol

Except that it makes it difficult to breathe lol

And peeps like me take pics of them and flood the internet with them.

inda Subway 2 years ago these were brand new, they are starting to scratch em out now.. what a waste of resources and shows how freaking dumb the MTA is, shaking in their boots…

my maintenance buddies were on a paid leave every other week… cellfish…
.

Is this till a thing :rolleyes::rolleyes:

Is this till a thing :rolleyes::rolleyes:

Translate

Translate

The topic of this thread

It has everything to do wit CV, wen the city was locked down and speaking of social distance crap…

It has everything to do wit CV, wen the city was locked down and speaking of social distance crap…

Guess you didnt understand my reply

Guess you didnt understand my reply

But im guessing you did but you just waNNA KEEP DOING WHAT YOU DO HUH

the city installed into the subway floor tiles those warning symbols of social distancing in every station, 6 feet apart, that’s a lot of effort & $$$$

the are starting to remove them now…
.

not sure where to put this post but it is virus related.

Just got back from a [U]wonderful [/U]land and sea cruise, Rome to Spain. Only time we were asked to mask at all was on the Viking hired tour busses in Italy, that we took all of twice, two round trips to visit Florence and Pisa. Never saw anyone masked in any taxi. Don't recall anyone masked at the Spanish Steps, or Trevi Fountain and maybe just a few elderly at the Vatican. Some people (way under 10%) on our cruise (900 persons on the Viking Sky) wore them every day, but they were either old or decrepit.) Of course I caught a minor cold about our fifth day (in Pisa) probably the result of ignoring masking etc. LOL. Never got sick enough to be more than an annoyance. We just took those free nasal swab china virus tests today that the gubmint mailed out by the dozen and we are both negative. We will use up another box in a week or so, just before SWMBO goes back to work her one day a week for a dentist. All in all, Europe has far less paranoid people about this "pandemic" than we have here, based on the percentage of masked at ShopRite, lol.

Great idea

[URL unfurl="true"]https://nypost.com/2022/10/17/boston-university-researchers-claim-to-have-developed-new-more-lethal-covid-strain-in-lab/[/URL]

Great idea

[URL unfurl="true"]https://nypost.com/2022/10/17/boston-university-researchers-claim-to-have-developed-new-more-lethal-covid-strain-in-lab/[/URL]

Apples and oranges, and actually the goal of the study to determine if mutations to the spike protein make the virus more transmissible. They found that it isn't the spike protein but other ones that make it more transmissible...

Boston University Pushes Back on Claims of New ‘Deadly' COVID Strain

**There's some friction between the federal government and Boston University researchers after the publication of a new COVID-19 study.

BU said reports by some publications saying they had created a new "deadly" COVID strain are misleading and untrue.

“First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-COV-2 virus strain (original virus from 2020) or make it more dangerous,” [BU said in a statement]('https://www.bu.edu/articles/2022/neidl-researchers-refute-uk-article-about-covid-strain/'), calling online reports Monday "false and inaccurate."

"In fact, this research made the virus replicate less dangerous," the university said.

The university's National Emerging Infectious Diseases Laboratories have been studying the omicron variant and the original strain. They reportedly wanted to see if omicron, while highly contagious, was still less likely to cause severe illness.

Researchers were working with this hybrid virus where they took the spiked protein of omicron and attached it to the original strain.

In mice, they found this new fused version killed 80% of mice infected. But that's lower than the 100% that died of the original strain. So their conclusion is that it's not the omicron spiked protein itself that causes the virus to spread so easily but other proteins.

BU researchers say identifying those proteins will help better diagnose and treat COVID.

The study caught the National Institute of Allergy and Infectious Diseases, which helps fund BU's research, off guard. But the university said the research was reviewed and approved by the Institutional Biosafety Committee, which consists of scientists and members of the local community, and that the Boston Public Health Commission had also approved the research.

“Ultimately, this research will provide a public benefit, by leading to better, targeted therapeutic interventions to help fight against future pandemics," the university's statement said.**

OMG, the National Enquir...errr, the NY Post was wrong ? Shocking !

Apples and Oranges lol. Let’s make a new modified reason to accidentally leak out so we can get the same idiots to get another shot $$$$
Better yet, how many nerds are absolutely nuts? Remember one of them mailing Anthrax just because.
Think the Enquirer or Post is more spot on.

Apples and Oranges lol. Let’s make a new modified reason to accidentally leak out so we can get the same idiots to get another shot $$$$
Better yet, how many nerds are absolutely nuts? Remember one of them mailing Anthrax just because.
Think the Enquirer or Post is more spot on.

Here, read this and maybe you can learn how some practice safe virological research and why this NY Post article was Shakespearean in scope, Much Ado About Nothing...

[HEADING=2]Gain of Function? Not So Fast.[/HEADING]

[[SIZE=5]https://www.science.org/content/blog-post/gain-function-not-so-fast[/SIZE]]('https://www.science.org/content/blog-post/gain-function-not-so-fast')

It's been a little while since I wrote about coronaviruses per se, but some recent news (and the coverage of it, especially) prompts today's post. I'm talking about [the preprint]('https://www.biorxiv.org/content/10.1101/2022.10.13.512134v1.full.pdf') out of a Boston University research group which is being described by many as "irresponsible gain-of-function" research. I think that that's not a good characterization of it, and I think that language is likely just to scare or enrage a lot of people who don't know much about viruses or virus research. On the other side of the coverage, here's one of the [best takes]('https://www.statnews.com/2022/10/17/boston-university-researchers-testing-of-lab-made-version-of-covid-virus-draws-government-scrutiny/') on it I've seen, predictably from Helen Branswell at Stat, who's been doing a great job on this sort of thing through the whole pandemic.

So here are the general details of the story: the BU group (at the university's National Emerging Infectious Diseases Laboratories) created a chimeric virus, taking an "original" strain from Wuhan and putting in a current Omicron-type spike protein (a BA1, to be specific). The Omicron strains have not only that version of the spike, but numerous other mutations throughout their sequence, so this is an experiment to see how much of the differences in the early virus strains and the current ones are due to just changes in the spike itself. Recall that the spike protein is the part of the virus that recognizes human cells to infect, specifically the human ACE2 surface protein, and that it's especially the "tip" of that protein (the receptor binding domain or RBD) that is at the business end of that process. And also recall that infectious viruses in general have human cell-surface proteins that they've evolved to recognize and use as leverage to move their contents across the cell membrane and start the infection cycle. There's nothing particularly remarkable about ACE2 or the fact that the current coronavirus strains use it or that they use such a mechanism - there's a whole list of such human proteins that viruses have stumbled onto over the last few hundred million years or so and have managed to exploit.

This research was partially funded by the National Institute of Allergy and Infectious Disease (NIAID), a part of the NIH, and the NIAID itself is not happy that they first learned of this work when the preprint came out. They claim that the grant application itself does not mention this experiment, but unfortunately I don't think any of us have seen it to know what it says or doesn't say or at what level of detail. It's important to realizes that this doesn't mean that this work was "illegal" or "unauthorized", either (although there's a lot of loose language like that being thrown around). As you can see from the Stat article linked above, about all the NIAID can say is that they wish the BU team would have informed them. The agency's granting policy is that work that could produce "enhanced pathogens of pandemic potential" needs to be evaluated by a committee doing a risk/benefit analysis and studying the proposed research plan. The NIAID is not saying that this work produced such a pathogen, or that it would have caused such a committee to be convened at all, just that they would have wanted to decide whether it warranted that level of examination or not. Meanwhile, the research was approved by BU's own biosafety review process and by the Boston Public Health Commission, so it's not like anyone who saw the proposed experiment would have immediately hit some sort of alarm button.

So what did the team find? Did they make a more dangerous version of the coronavirus? No. In fact, contrary to many of the people who are spouting off on this on social media, the new chimeric strain was less dangerous by comparison in animal tests. Some readers may have seen the figure of 80% of the mice exposed to the chimeric virus dying (because that one is sometimes passed around in ALL CAPS, it can be hard to miss). But before jumping out of your chair, consider that when these mice were exposed to the original Wuhan coronavirus that 100% of them died. This would also be a good time to mention that "exposed", in this experiment, means "large dose sprayed directly up their noses", not wafting around in the cage like some simulation of a mouse dinner party. And as [another real virologist]('https://twitter.com/MarionKoopmans/status/1582292244702597121?s=20&t=yTHFEUlvHSrm7W2L8Ms_xw') (Marion Koopmans of the Netherlands) notes from the data in the preprint, the chimeric virus actually had lower ability to replicate deep in the lung tissue, which may be some of the reason that it was less virulent than the ancestral strain.

[Here's a good Twitter thread]('https://twitter.com/florian_krammer/status/1582309667388411904?s=20&t=XMAwfgWjfbOVa6U2neFQNg') by a real virologist, Florian Krammer at Mount Sinai. He points out that the Omicron strains of the coronavirus are much less pathogenic in the mouse model than the originals, and that's what this chimeric strain showed as well: when these mice are exposed to the actual Omicron BA1 strain, they are not killed off by it at all. The BU experiment was trying to see if this weakening of Omicron in the mice was due to changes in the spike protein, and the answer is that that can't be the whole answer. The chimeric virus did get weaker than the original strain, but it didn't just drop down to mouse-nonlethal like a real Omicron strain would. So the majority of the Omicron-weakening effect in mice has to be coming from mutations in other parts of the virus.

And here's [another discussion]('https://twitter.com/stuartjdneil/status/1581759224597532672?s=20&t=pMX_TMwKEsZxIZUzSrxUgQ') from a real virologist, Stuart Neil at King's College, London. He emphasizes that this work was done not in just plain mice, but in an inbred mutated strain, K18-huACE2. That name means that the mice are expressing the human ACE2 protein (because the coronavirus doesn't really recognize the native mouse ACE2), and that this introduced protein is being expressed via the Keratin 18 promoter. If you're not a molecular biologist, all that means is that when you're getting some organism to produce a protein that's not in its own genome, you need to put some signaling sequences in as well when you splice in this new gene, to get the cellular machinery to pay attention and actually read off your new sequence instead of just ignoring it. The key thing here is that the K18 promoter makes sure that the human ACE2 protein is expressed strongly in pretty much all epithelial tissue, very much including the lining of the lungs. These mice are loaded with the stuff compared to humans - they have much wider and stronger expression of ACE2 than we do, so they are completely set up to be hit by the coronavirus. They are an animal model, in other words, not a direct reflection of the real world - in the real world, mice don't get sick from SARS-Cov-2. You will note, for example, that as the early strains of the coronavirus went into the human population that we did not see a 100% mortality rate like these transgenic mice did. The Black Death itself didn't hit 100%, even under medieval public health conditions. You build animal models like this to get fast, solid comparisons between mouse experiments, not to take the numbers from them and think that they will directly translate to human disease.

But what if? What if this chimeric strain turned out to be more lethal than expected in the human population? What happens if you take an older strain of the virus and swap in the Omicron-level spike; doesn't that have the potential for trouble? Well, we've already seen a "natural experiment" like that, as Florian Krammer [points out]('https://twitter.com/florian_krammer/status/1582311039395565568?s=20&t=XMAwfgWjfbOVa6U2neFQNg'). There was a strain [back in March]('https://twitter.com/PeacockFlu/status/1504158873938272269?s=20&t=XMAwfgWjfbOVa6U2neFQNg') called XD, which was a Delta that had the Omicron spike protein in it (via recombination). XD did not take off in the human population and did not seem to be more of a problem than the other strains, which is why you've probably never heard of it. That recombination domain-switching process very likely takes place in cases of infection with two viral strains at once. The various sequences can get swapped around under these circumstances while things are replicating and reassembling in the same cells, and you'd overall rather not see much of that, because it just gives the virus more lottery tickets to play with.

So this was not a gain-of-function experiment, and it did not appear to make a more dangerous virus. It was approved by review committees, and it was done in a BSL3 lab facility (as any work with the pandemic coronaviruses should be!) Where things have gone wrong here is (as mentioned above) that the NIAID folks would like to know about such experiments beforehand, and to start from a sheer practical standpoint you don't want to irritate people who are providing some of your funding. But the larger problem is the way that this was rolled out. I don't think that this group through through the way that coronavirus news gets handed around in this day and age. There are extremely strong and loud opinions out there, and some of those are held by people who cannot be bothered to read the original paper. Hell, let's stop being polite about it: some of the loudest ones are held by people who are frankly unable to understand the original papers at all. So this is what happens. Rumor and misinformation is (as usual) lapping around the world while the truth is still looking for its shoes. I realize that this post falls into that category, but I felt like I needed to write it anyway. Calm down.

Predictable, but not to this extent...

[HEADING=2][SIZE=6]Whites are now more likely to die from covid than Blacks. Here’s why the pandemic shifted.[/SIZE][/HEADING]
[pressherald.com/2022/10/19/whites-now-more-likely-to-die-from-covid-than-blacks-why-the-pandemic-shifted/]('https://www.pressherald.com/2022/10/19/whites-now-more-likely-to-die-from-covid-than-blacks-why-the-pandemic-shifted/')

By Akilah Johnson and Dan Keating October 20, 2022

SOMERVILLE, Tenn. — Skill Wilson had amassed more than three decades of knowledge as a paramedic, first in Memphis and then in Fayette County. Two places that felt like night and day.

With only five ambulances in the county and the nearest hospital as much as 45 minutes away, Skill relished the clinical know-how necessary to work in a rural setting. Doing things like sedating patients to insert tubes into their airways.

But when it came to covid-19, despite more than 1 million deaths nationwide, Skill and his family felt their small town on the central-eastern side of Fayette County, with its fields of grazing cattle and rows of cotton and fewer than 200 covid deaths since the start of the pandemic, was a cocoon against the raging health emergency.

“It was a lot easier to stay away from others,” his widow, Hollie Wilson, said of the largely White and predominantly conservative county of about 42,000 residents. “Less people. Less chance of exposure.”
Covid seemed like other people’s problems – until it wasn’t.

The imbalance in death rates among the nation’s racial and ethnic groups has been a defining part of the pandemic since the start. To see the pattern, The Washington Post analyzed every death during more than two years of the pandemic. Early in the crisis, the differing covid threat was evident in places such as Memphis and Fayette County. Deaths were concentrated in dense urban areas, where Black people died at several times the rate of White people.

“I don’t want to say that we weren’t worried about it, but we weren’t,” said Hollie, who described her 59-year-old husband as someone who “never took a pill.” After a while, “you kind of slack off on some things,” she said.

Over time, the gap in deaths widened and narrowed but never disappeared – until mid-October 2021, when the nation’s pattern of covid mortality changed, with the rate of death among White Americans sometimes eclipsing other groups.

A Post analysis of covid death data from the Centers for Disease Control and Prevention from April 2020 through this summer found the racial disparity vanished at the end of last year, becoming roughly equal. And at times during that same period, the overall age–adjusted death rate for White people slightly surpassed that of Black and Latino people.

The nature of the virus makes the elderly and people with underlying health conditions – including hypertension, diabetes and obesity, all of which beset Black people at higher rates and earlier in life than White people – particularly vulnerable to severe illness and death.

That wasn’t Skill.

The virus also attacks unvaccinated adults – who polls show are more likely to be Republicans – with a ferocity that puts them at a much higher risk of infection and death.

That was Skill.

He joined the choir of critics opposing vaccination requirements, his rants in front of the television eventually wearing on Hollie, who, even if she agreed, grew tired of listening and declared their home “covid-talk free.”

So, she said, Skill commiserated with like-minded people in Facebook groups and on Parler and Rumble, the largely unmoderated social networking platforms popular with conservatives.

“We’re Republicans, and 100% believe that it’s each individual’s choice – their freedom” when it comes to getting a coronavirus shot, Hollie said in January. “We decided to err on the side of not doing it and accept the consequences. And now, here we are in the middle of planning the funeral.”

Capt. Julian Greaves Wilson Jr., known to everybody as Skill, died of covid Jan. 23, a month after becoming infected with the coronavirus. He fell ill not long after transporting a covid patient to the hospital. At the time he died, infection rates in Fayette County had soared to 40.5% among people taking coronavirus tests.

‘A DIFFERENT CALCULUS’
When the coronavirus appeared in the United States, it did what airborne viruses do – latched onto cells in people’s respiratory tract, evaded innate immune responses and multiplied. The pathogen, free of politics or ideology, had a diverse reservoir of hosts and found fertile pathways for growth in the inequalities born from centuries of racial animus and class resentments.

Unequal exposure, unequal spread, unequal vulnerability and unequal treatment concentrated harm in communities that needed protection the most yet had the least. Cumulatively, Black, Latino and Native American people are 60 % more likely to die of covid.

But as the pandemic progressed, the damage done by the virus broadened, and the toxicity of modern-day politics came to the fore.

The message was unmistakable outside a business in Reagan, Tenn., on June 6, 2022. Brandon Dill/The Washington Post

The Post analysis revealed the changing pattern in covid deaths. At the start of the pandemic, Black people were more than three times as likely to die of covid as their White peers. But as 2020 progressed, the death rates narrowed – but not because fewer Black people were dying. White people began dying at increasingly unimaginable numbers, too, the Post analysis found.

In summer 2021, the nation saw some of the pandemic’s lowest death rates, as vaccines, shoring up the body’s immune response, became widely available.

Then came the delta variant. The virus mutated, able to spread among the vaccinated. As it did, an erosion of trust in government and in medicine – in any institution, really – slowed vaccination rates, stymieing the protection afforded by vaccines against severe illness and death.

After delta’s peak in September 2021, the racial differences in covid deaths started eroding. The Post analysis found that Black deaths declined, while White deaths never eased, increasing slowly but steadily, until the mortality gap flipped. From the end of October through the end of December, White people died at a higher rate than Black people did, The Post found.

That remained true except for a stretch in winter 2021-2022, when the omicron variant rampaged. The Black death rate jumped above White people’s when the spike in cases and deaths overwhelmed providers in the Northeast, resulting in a bottleneck of testing and treatment.

When the surge subsided, the Black death rate once again dropped below the White rate.

“Usually, when we say a health disparity is disappearing, what we mean is that . . . the worse-off group is getting better,” said Tasleem Padamsee, an assistant professor at Ohio State University who researched vaccine use and was a member of the Ohio Department of Health’s work group on health equity. “We don’t usually mean that the group that had a systematic advantage got worse.”

That’s exactly what happened as the White death rate surpassed that for Black people, even though Black Americans routinely confront stress so corrosive it causes them to age quicker, become sicker and die younger.

The shift in covid death rates “has vastly different implications for public health interventions,” said Nancy Krieger, professor of social epidemiology at Harvard University’s T.H. Chan School of Public Health. Officials must figure out how to connect with “communities who are ideologically opposed to the vaccine” while contending with “the cumulative impact of injustice” on communities of color.

“Think about the fact that everyone who is age 57 and older in this country was born when Jim Crow was legal,” she said. “What that did was intersect with covid-19, meaning that embodied history is part of this pandemic, too.”

So what contributed to the recent variation in death rates? And why?

The easy explanation is that it reflects the choices of Republicans not to be vaccinated, but the reasons go deeper. The Post interviewed historians and researchers who study the effects of White racial politics and social inequality on health, spoke with relatives and friends of those lost to covid, and compiled data from federal databases and academic studies.

Many Republicans decided they would rather roll the dice with their health than follow public health guidance – even when provided by President Donald Trump, who was booed after saying he had been vaccinated and boosted.

Researchers at Ohio State found Black and White people were about equally reluctant to get the coronavirus vaccine when it first became available, but Black people overcame that hesitancy faster. They came to the realization sooner that vaccines were necessary to protect themselves and their communities, Padamsee said.

As public health efforts to contain the virus were curtailed, the pool of those most at risk of becoming casualties widened. The No. 1 cause of death for 45-to-54-year-olds in 2021 was covid, according to federal researchers.

After it became clear that communities of color were being disproportionately affected, racial equity started to become the parlance of the pandemic, in words and deeds. As it did, vaccine access and acceptance within communities of color grew – and so did the belief among some White conservatives, who form the core of the Republican base, that vaccine requirements and mask mandates infringe on personal liberties.

“Getting to make this decision for themselves has primacy over what the vaccine could do for them,” said Lisa R. Pruitt, a law professor at the University of California at Davis who is an expert in social inequality and the urban-rural divide. “They’re making a different calculus.”

It’s a calculation informed by the lore around self-sufficiency, she said, a fatalistic acceptance that hardships happen in life and a sense of defiance that has come to define the modern conservative movement’s antipathy toward bureaucrats and technocrats.

“I didn’t think that that polarization would transfer over to a pandemic,” Pruitt said.
It did.

A lifesaving vaccine and droplet-blocking masks became ideological Rorschach tests.

The impulse to frame the eradication of infectious disease as a matter of personal choice cost the lives of some who, despite taking the coronavirus seriously, were surrounded by enough people that the virus found fertile terrain to sow misery. That’s what happened in northern Illinois, where a father watched his 40-year-old son succumb to covid-19.

For Robert Boam, the increase in White deaths is politics brought to bear on the body of his son, though he’s reluctant “to get into the politics of it all, but it all goes back to that.”

Brian Boam was a PE teacher at an elementary school in suburban Chicago. On Christmas Eve, the entire family gathered at the elder Boam’s home in an Illinois town where the first Lincoln-Douglas debate was held. Brian Boam was there with his 10-year-old daughter and 6-year-old son.

Robert Boam said his son had survived covid the year before, so “we got on his butt to get that booster shot when he was here for Christmas.” And he did – but got sick again, the 73-year-old said. “Being vaccinated, and all that, and getting covid again kind of bummed him out.”

Just after the new year, Brian Boam, who was hypertensive, went to a hospital feverish and vomiting. It took 10 hours to be seen and even longer for a bed to become available. As he waited, he sent what would be his last text message to his parents. Thanks for all you do. I love you.

He went into cardiac arrest in the emergency room and was transferred to Rush University Medical Center in Chicago, one of the nation’s top academic hospitals. There, his family hoped he would be healed, but his organs began to fail. He died Jan. 8.

“The thing that gets me is the people who still don’t believe it’s serious or even real, but when they get sick, they run to the hospital,” Robert Boam said. “You’re taking away from heart attack patients and stroke patients.”

The pandemic, he said, “should’ve been taken seriously from the very beginning, and it wasn’t. It was denied. It was downplayed. And it all goes back to one person, as far as I’m concerned.”

Asked who that was, Boam would say only: “I’ll give you three guesses. The first two don’t count.”.

Had to clip article, too long to post entire thing...

... METHODOLOGY
The Post applied the standard technique used by the Centers for Disease Control and Prevention to calculate age-adjusted covid death rates by race using the CDC’s provisional covid death data that includes race, ethnicity, age and date of death. Under that procedure, The Post calculated death rates for age groups by dividing the number of deaths by the population in that age group. The Post then used a standardized age distribution to create an overall rate for each race-ethnicity group.

Age-adjusted rates are especially necessary for understanding covid deaths because the majority of people killed by covid are age 75 or older, even though that group represents less than 9% of the U.S. population. Additionally, more than 90% of covid deaths are in people age 50 and older.

The covid death age pattern is important in reviewing deaths by race because White people are disproportionately older. More than 40% of White people are age 50 or older, but less than 30% of Black people are in those older age groups. Hispanics are even younger, with less than 25% age 50 or older.

The age-adjusted rates offset that difference in age distribution to compare deaths as if the races or ethnic groups had the same age distribution.

Whites, Blacks, Asians, American Indians and Alaskan Natives are non-Hispanic. Hispanics are of any race, so the racial groups and the Hispanic groups do not overlap.

For maps, The Post calculated age-adjusted covid death rates for each race in each state over the course of the pandemic using provisional covid death data by state.

So I here study’s out of UK are showing the mortality rate in those with three shots is now higher then those with none.

Also seen the CDC has admitted these shots never stopped either catching or transmitting the virus and new it all along.

Got to suck knowing all these peeps have (ADE). I’m shedding a tear right now like the Indian in the pollution commercial. NOT!