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Salty Dog

 

12 hours ago, jaybee747 said:

Not sure what is exactly "covid-19 sufferer"

I don't know either, but I'm pretty sure it doesn't mean just deaths from Covid-19.

Though it could include deaths, if it is refering to everyone who has contracted the virus. In which case, it would include those who have recovered, still have it, and have died from it.

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From an on line Senior's website which I'm a Member  https://www.yourlifechoices.com.au/health/covid19/glasses-cut-covid-infections-study? This although not conclusive I found interesting as

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jaybee747
10 hours ago, cogon88 said:

I don't have subscription to the newspaper you quoted  but just by reading the first paragraph I can see that this is "fake news".

Just look at the raw data in the study that YOU linked -

62k (87%) of the 71k total deaths are people ages over 60  (33k deaths age over 80, 17k deaths age over 70, 12k deaths over age  60). Considering the lower percentage of older people in the population, this confirm my initial post that the Median age of Covid-19 death is 78 

If you have a STUDY with different numbers please give link, just quoting an article by journalists who are known to massage the data will not cut it...

Lies, damn lies and statistics...

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On 8/9/2020 at 8:57 AM, Dafey said:

Do you have a source for that?

I did see on the news a while back, some USA Vet. Admin, stating it is completely harmless and they still prescribe it to Vet's with Malaria and have been doing so for years.  And there are no side effects that are dangerous to anyone.  Does it work, no idea. 

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On 7/1/2020 at 2:12 PM, Ozepete said:

REALLY (again!)  With only 69 new cases and ONE case serious / critical,  the claim that "Aus has all but eradicated the virus." is very accurate.  (BTW in case this is just Aus slang, the term 'all but' relates to nearly, almost etc.)  

I was trying to emphasise the need to recognise the seriousness of this pandemic, the need for positive leadership and enforcement with each country enabled to act as a whole working together to prevent yet more thousands of deaths. That is what prevented big numbers in Aus and why all new cases are investigated and the source located and isolated. That is what the Aus press is telling you about 'hot spots' being isolated and that is what works... Look at the numbers! As of yesterday in the US you are 15,900 times more likely to be in an American hospital needing serious / critical care than if you was in Aus... This thing is SERIOUS! and it will only improve when the nit picking stops, we all face reality together with the facts, demand action from hopeless leaders and strictly enforce regulations. 

At least you get it Moe! :thumbsup:

Not nitpicking on Australia or any other country but your claim that Australia eradicated the virus is, to put it mildly, over hyped. The virus is here to stay, learn to live with it! The virus was able to escape a biosafety level 4 (BSL–4) laboratory in China, what make you think that it will not be able to penetrate Australia?

"More heartbreaking days ahead as Victoria's COVID-19 death rate triples

Infectious disease experts have warned Victoria to brace for more heartbreaking daily COVID-19 death tolls in coming days, after 25 more lives were reported lost to the virus on Monday – the state's deadliest day of the pandemic."

https://www.theage.com.au/national/victoria/more-heartbreaking-days-ahead-as-victoria-s-covid-19-death-rate-triples-20200817-p55mgn.html

 

Meanwhile in New Zealand...

"New Zealand's reputation as the country that beat coronavirus is in doubt as the country records new outbreak"

https://www.businessinsider.com/new-zealands-reputation-the-country-that-beat-coronavirus-in-doubt-2020-8

 

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Ozepete
1 hour ago, jaybee747 said:

Not nitpicking on Australia or any other country but your claim that Australia eradicated the virus is, to put it mildly, over hyped. The virus is here to stay, learn to live with it! The virus was able to escape a biosafety level 4 (BSL–4) laboratory in China, what make you think that it will not be able to penetrate Australia?

"More heartbreaking days ahead as Victoria's COVID-19 death rate triples

Infectious disease experts have warned Victoria to brace for more heartbreaking daily COVID-19 death tolls in coming days, after 25 more lives were reported lost to the virus on Monday – the state's deadliest day of the pandemic."

https://www.theage.com.au/national/victoria/more-heartbreaking-days-ahead-as-victoria-s-covid-19-death-rate-triples-20200817-p55mgn.html

 

Meanwhile in New Zealand...

"New Zealand's reputation as the country that beat coronavirus is in doubt as the country records new outbreak"

https://www.businessinsider.com/new-zealands-reputation-the-country-that-beat-coronavirus-in-doubt-2020-8

 

For a start I did NOT say quote: Australia eradicated the virus". What I said "all but eradicated the virus." is very accurate.  I followed that with a terminology explanation my quote: (BTW in case this is just Aus slang, the term 'all but' relates to nearly, almost etc.)  In Oz the number of cases total 23560 with a death rate of 16 per million while the US has 5,612,00 cases and a death rate of 528 per million and a few other countries have worse pro-rata results.  Those Oz figures justify the term 'all but eradicated, surely!

I agree, like the flu this thing is here to stay and needs to be contained as well as possible and some countries are fortunate that their logistics, governance and leadership have contributed to far better numbers than others. 

Most states in Oz have a new case / day rate of less than 10 but the idiot premier of Victoria refused the Federal governments offer of ADF personal to assist in maintaining order in hotels with quarantined persons, opting to employ his lefty union mates and the outcome has been a spread of Covit 19 state wide. Victoria is now bordered off with City folk housebound and an 8.00PM to 5.00AM curfew, all because one idiot state leader wanted to play politics.. (Does that sound familiar?)  If a country can't pull together to ward off this virus then it is stuffed! It requires a NATIONAL effort overriding states. 

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Salty Dog

The Pandemic’s Biggest Mystery Is Our Own Immune System

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Immunology Is Where Intuition Goes to Die

Which is too bad because we really need to understand how the immune system reacts to the coronavirus.

ED YONG | AUGUST 5, 2020

There’s a joke about immunology, which Jessica Metcalf of Princeton recently told me. An immunologist and a cardiologist are kidnapped. The kidnappers threaten to shoot one of them, but promise to spare whoever has made the greater contribution to humanity. The cardiologist says, “Well, I’ve identified drugs that have saved the lives of millions of people.” Impressed, the kidnappers turn to the immunologist. “What have you done?” they ask. The immunologist says, “The thing is, the immune system is very complicated …” And the cardiologist says, “Just shoot me now.”

The thing is, the immune system is very complicated. Arguably the most complex part of the human body outside the brain, it’s an absurdly intricate network of cells and molecules that protect us from dangerous viruses and other microbes. These components summon, amplify, rile, calm, and transform one another: Picture a thousand Rube Goldberg machines, some of which are aggressively smashing things to pieces. Now imagine that their components are labeled with what looks like a string of highly secure passwords: CD8+, IL-1β, IFN-γ. Immunology confuses even biology professors who aren’t immunologists—hence Metcalf’s joke.

Even the word immunity creates confusion. When immunologists use it, they simply mean that the immune system has responded to a pathogen—for example, by producing antibodies or mustering defensive cells. When everyone else uses the term, they mean (and hope) that they are protected from infection—that they are immune. But, annoyingly, an immune response doesn’t necessarily provide immunity in this colloquial sense. It all depends on how effective, numerous, and durable those antibodies and cells are.

Immunity, then, is usually a matter of degrees, not absolutes. And it lies at the heart of many of the COVID-19 pandemic’s biggest questions. Why do some people become extremely ill and others don’t? Can infected people ever be sickened by the same virus again? How will the pandemic play out over the next months and years? Will vaccination work?

To answer these questions, we must first understand how the immune system reacts to SARS-CoV-2 coronavirus. Which is unfortunate because, you see, the immune system is very complicated.

It works, roughly, like this.

The first of three phases involves detecting a threat, summoning help, and launching the counterattack. It begins as soon as a virus drifts into your airways, and infiltrates the cells that line them.

When cells sense molecules common to pathogens and uncommon to humans, they produce proteins called cytokines. Some act like alarms, summoning and activating a diverse squad of white blood cells that go to town on the intruding viruses—swallowing and digesting them, bombarding them with destructive chemicals, and releasing yet more cytokines. Some also directly prevent viruses from reproducing (and are delightfully called interferons). These aggressive acts lead to inflammation. Redness, heat, swelling, soreness—these are all signs of the immune system working as intended.

This initial set of events is part of what’s called the innate immune system. It’s quick, occurring within minutes of the virus’s entry. It’s ancient, using components that are shared among most animals. It’s generic, acting in much the same way in everyone. And it’s broad, lashing out at anything that seems both nonhuman and dangerous, without much caring about which specific pathogen is afoot. What the innate immune system lacks in precision, it makes up for in speed. Its job is to shut down an infection as soon as possible. Failing that, it buys time for the second phase of the immune response: bringing in the specialists.

Amid all the fighting in your airways, messenger cells grab small fragments of virus and carry these to the lymph nodes, where highly specialized white blood cells—T-cells—are waiting. The T-cells are selective and preprogrammed defenders. Each is built a little differently, and comes ready-made to attack just a few of the zillion pathogens that could possibly exist. For any new virus, you probably have a T-cell somewhere that could theoretically fight it. Your body just has to find and mobilize that cell. Picture the lymph nodes as bars full of grizzled T-cell mercenaries, each of which has just one type of target they’re prepared to fight. The messenger cell bursts in with a grainy photo, showing it to each mercenary in turn, asking: Is this your guy? When a match is found, the relevant merc arms up and clones itself into an entire battalion, which marches off to the airways.

Some T-cells are killers, which blow up the infected respiratory cells in which viruses are hiding. Others are helpers, which boost the rest of the immune system. Among their beneficiaries, these helper T-cells activate the B-cells that produce antibodies—small molecules that can neutralize viruses by gumming up the structures they use to latch on to their hosts. Roughly speaking—and this will be important later—antibodies mop up the viruses that are floating around outside our cells, while T-cells kill the ones that have already worked their way inside. T-cells do demolition; antibodies do cleanup.

Both T-cells and antibodies are part of the adaptive immune system. This branch is more precise than the innate branch, but much slower: Finding and activating the right cells can take several days. It’s also long-lasting: Unlike the innate branch of the immune system, the adaptive one has memory.

After the virus is cleared, most of the mobilized T-cell and B-cell forces stand down and die off. But a small fraction remain on retainer—veterans of the COVID-19 war of 2020, bunkered within your organs and patrolling your bloodstream. This is the third and final phase of the immune response: Keep a few of the specialists on tap. If the same virus attacks again, these “memory cells” can spring into action and launch the adaptive branch of the immune system without the usual days-long delay. Memory is the basis of immunity as we colloquially know it—a lasting defense against whatever has previously ailed us.

This account is what should happen when the new coronavirus enters the body, based on general knowledge about the immune system and how it reacts to other respiratory viruses. But what actually happens? Well … sigh … the thing is, the immune system is very complicated.

In general, the immune system’s reaction to SARS-CoV-2 is “what I would expect if you told me there was a new respiratory infection,” says Shane Crotty from the La Jolla Institute of Immunology. The innate immune system switches on first, and the adaptive immune system follows suit. In several studies, most people who are infected develop reasonable levels of coronavirus-specific T-cells and antibodies. “The bottom line is that there are no big surprises,” says Sarah Cobey, an epidemiologist from the University of Chicago.

Still, “any virus that can make people sick has to have at least one good trick for evading the immune system,” Crotty says. The new coronavirus seems to rely on early stealth, somehow delaying the launch of the innate immune system, and inhibiting the production of interferons—those molecules that initially block viral replication. “I believe this [delay] is really the key in determining good versus bad outcomes,” says Akiko Iwasaki, an immunologist at Yale. It creates a brief time window in which the virus can replicate unnoticed before the alarm bells start sounding. Those delays cascade: If the innate branch is slow to mobilize, the adaptive branch will also lag.

Many infected people still clear the virus after a few weeks of nasty symptoms. But others don’t. Maybe they initially inhaled a large dose of virus. Maybe their innate immune systems were already weakened through old age or chronic disease. In some cases, the adaptive immune system also underperforms: T-cells mobilize, but their levels recede before the virus is vanquished, “almost causing an immunosuppressed state,” Iwasaki says. This dual failure might allow the virus to migrate deeper into the body, toward the vulnerable cells of the lungs, and to other organs including the kidneys, blood vessels, and the gastrointestinal and nervous systems. The immune system can’t constrain it, but doesn’t stop trying. And that’s also a problem.

Immune responses are inherently violent. Cells are destroyed. Harmful chemicals are unleashed. Ideally, that violence is targeted and restrained; as Metcalf puts it, “Half of the immune system is designed to turn the other half off.” But if an infection is allowed to run amok, the immune system might do the same, causing a lot of collateral damage in its prolonged and flailing attempts to control the virus.

This is apparently what happens in severe cases of COVID-19. “If you can’t clear the virus quickly enough, you’re susceptible to damage from the virus and the immune system,” says Donna Farber, a microbiologist at Columbia. Many people in intensive-care units seem to succumb to the ravages of their own immune cells, even if they eventually beat the virus. Others suffer from lasting lung and heart problems, long after they are discharged. Such immune overreactions also happen in extreme cases of influenza, but they wreak greater damage in COVID-19.

There’s a further twist. Normally, the immune system mobilizes different groups of cells and molecules when fighting three broad groups of pathogens: viruses and microbes that invade cells, bacteria and fungi that stay outside cells, and parasitic worms. Only the first of these programs should activate during a viral infection. But Iwasaki’s team recently showed that all three activate in severe COVID-19 cases. “It seems completely random,” she says. In the worst cases, “the immune system almost seems confused as to what it’s supposed to be making.”

No one yet knows why this happens, and only in some people. Eight months into the pandemic, the variety of COVID-19 experiences remains a vexing mystery. It’s still unclear, for example, why so many “long-haulers” have endured months of debilitating symptoms. Many of them have never been hospitalized, and so aren’t represented in existing studies that have measured antibody and T-cell responses. David Putrino of Mount Sinai tells me that he surveyed 700 long-haulers and a third had tested negative for antibodies, despite having symptoms consistent with COVID-19. It’s unclear if their immune systems are doing anything differently when confronted with the coronavirus.

We should expect such mysteries to build. The immune system’s reaction to the virus is a matter of biology, but the range of reactions we actually see is also influenced by politics. Bad decisions mean more cases, which means a wider variety of possible immune responses, which means a higher prevalence of rare events. In other words, the worse the pandemic gets, the weirder it will get.

A few patterns offer easier possible explanations. “Kids have very trigger-happy innate immune systems,” says Florian Krammer of Mount Sinai’s Icahn School of Medicine, which might explain why they rarely suffer severe infections. Elderly people are less fortunate. They also have smaller standing pools of T-cells to draw from, as if the mercenary-filled bar from the earlier metaphor is only sparsely packed. “It takes longer for the adaptive response to mobilize,” Farber says.

There are also preliminary hints that some people might have a degree of preexisting immunity against the new coronavirus. Four independent groups of scientists—based in the U.S., Germany, the Netherlands, and Singapore—have now found that 20 to 50 percent of people who were never exposed to SARS-CoV-2 nonetheless have significant numbers of T-cells that can recognize it. These “cross-reactive” cells likely emerged when their owners were infected by other, related coronaviruses, including the four mild ones that cause a third of common colds, and the many that infect other animals.

But Farber cautions that having these cross-reactive T-cells “tells you absolutely nothing about protection.” It’s intuitive to think they would be protective, but immunology is where intuition goes to die. The T-cells might do nothing. There’s an outside chance that they could predispose people to more severe disease. We can’t know for sure without recruiting lots of volunteers, checking their T-cell levels, and following them over a long period of time to see who gets infected—and how badly.

Even if the cross-reactive cells are beneficial, remember that T-cells act by blowing up infected cells. As such, they’re unlikely to stop people from getting infected in the first place, but might reduce the severity of those infections. Could this help to explain why, politics aside, some countries had an easier time with COVID-19 than others? Could it explain why some people incur only mild symptoms? “You can go pretty crazy pretty quickly with the speculations,” says Crotty, who co-led one of the studies that identified these cross-reactive cells. “A lot of people have latched onto this and said it could explain everything. Yes, it could! Or it could explain nothing. It’s a really frustrating situation to be in.”

“I wish it wasn’t,” he adds, “but the immune system is really complicated.”

One of the most pressing mysteries is what happens after you’re infected—and whether you could be again. Crucially, researchers still don’t know how much protection the leftover antibodies, T-cells, and memory cells might offer against COVID-19, or even how to measure that.

In July, a team of British researchers released a study showing that many COVID-19 patients lose substantial levels of their coronavirus-neutralizing antibodies after a few months. An earlier Chinese study, published in June, found similar results. Both prompted cascades of alarming headlines, which raised concerns that people could be infected repeatedly, or even that a vaccine—many of which work by readying neutralizing antibodies—won’t provide long-term protection. But many of the immunologists I spoke with weren’t too concerned, because—and reassuringly this time—the immune system is really complicated.

First, declines are expected. During an infection, antibodies are produced by two different groups of B-cells. The first group is fast and short-lived, and quickly unleashes a huge antibody tsunami before dying off. The second group is slower but long-lasting, and produces gentler antibody swells that continuously wash over the body. The transition from the first group to the second means that antibody levels usually decline over the course of an infection. “There’s nothing scary about it,” Krammer says.

Taia Wang of Stanford is a little less sanguine. She tells me several studies, including upcoming ones, consistently show that many people seem to lose their neutralizing antibodies after a couple of months. “If you asked me to guess six months ago, I would have thought that they would last longer,” she says. “The durability is not what we’d like.”

But “the fact that you don’t have measurable antibodies doesn’t mean that you aren’t immune,” Iwasaki says. T-cells could continue to provide adaptive immunity even if the antibodies tap out. Memory B-cells, if they persist, could quickly replenish antibody levels even if the current stocks are low. And, crucially, we still don’t know how many neutralizing antibodies you need to be protected against COVID-19.

Wang agrees: “There’s a common notion that antibody quantity is all that matters, but it’s more complicated than that,” she says. “The quality of the antibody is as important.” Quality might be defined by which part of the virus the antibodies stick to, or how well they stick. Indeed, many people who recover from COVID-19 have low levels of neutralizing antibodies overall, but some of them neutralize very well.  “Quantity is easier to measure,” Wang adds. “There are more ways to characterize quality and we don’t know which ones are relevant.” (This problem is even worse for T-cells, which are much harder than antibodies to isolate and analyze.)  

These uncertainties strengthen the need for large, careful vaccine trials: Right now it’s hard to know whether the promising signs in early trials will actually lead to substantial protection in practice. (Developing and deploying vaccines is a subject for another piece, which my colleague Sarah Zhang has written.) Scientists are trying to work out how to measure COVID-19 immunity by studying large groups of people who have either been infected naturally or taken part in a vaccine trial. Researchers will repeatedly measure and analyze the volunteers’ antibodies and T-cells over time, noting if any of them become infected again. Krammer expects that results will take a few months, or possibly until the end of the year. “There’s no way to speed that up,” he says. Because … well, you know.

In the meantime, anecdotal reports have described alleged reinfections—people who apparently catch COVID-19 a second time, and who test positive for the coronavirus again after months of better health. Such cases are concerning, but hard to interpret. Viral RNA—the genetic material that diagnostic tests detect—can stick around for a long time, and people can test positive for months after they’ve cleared the actual virus. If someone like that caught the flu and went to their doctor, they might get tested for coronavirus again, get a positive result, and be mistakenly treated as a case of reinfection. “It’s really hard to prove reinfection unless you sequence the genes of the virus” both times, Iwasaki says. “No one has that data, and it’s unreasonable to expect.”

Immunity lasts a lifetime for some diseases—chickenpox, measles—but eventually wears off for many others. As the pandemic drags on, we should expect at least a few instances in which people who’ve beaten COVID-19 must beat it again. So far, the fact that reinfections are still the subject of smattered anecdotes suggests that “it’s happening at a very low rate, if at all,” Cobey says. But remember: A bigger pandemic is a weirder pandemic. When there are almost 5 million confirmed cases, something that occurs just 0.1 percent of the time will still affect 5,000 people.

If people endure a second bout with COVID-19, the outcome is again hard to call. For some diseases, like dengue, an antibody response to one infection can counterintuitively make the next infection more severe. So far, there’s no evidence this happens with SARS-CoV-2, says Krammer, who expects that any reinfections would be milder than the first ones. That’s because the coronavirus has a longer incubation time—a wider window between infection and symptoms—than, say, the flu. That could conceivably provide more time for memory cells to mobilize a new force of antibodies and T-cells. “Even if there’s some immunity loss in the future, it’s not that we’d have to go through this pandemic again,” Cobey says.

What will determine our future with the virus is how long protective immunity lasts. For severe coronaviruses like MERS and the original SARS, it persists for at least a couple of years. For the milder coronaviruses that cause common colds, it disappears within a year. It’s reasonable to guess that the duration of immunity against SARS-CoV-2 lies within those extremes, and that it would vary a lot, much like everything else about this virus. “Everyone wants to know,” says Nina Le Bert from the Duke-NUS in Singapore. “We don’t have the answer.”

Most people still haven’t been infected a first time, let alone a second. The immediate uncertainty around our pandemic future “doesn’t stem from the immune response,” Cobey says, but from “policies that are enacted, and whether people will distance or wear masks.” But for next year and beyond, modeling studies have shown that the precise details of the immune system’s reactions to the virus, and to a future vaccine, will radically affect our lives. The virus could cause annual outbreaks. It might sweep the world until enough people are vaccinated or infected, and then disappear. It could lie low for years and then suddenly bounce back. All of these scenarios are possible, but the range of possibilities will narrow the more we learn about the immune system.

That system may be vexingly complex, but it is also both efficient and resilient in a way that our society could take lessons from. It prepares in advance, and learns from its past. It has many redundancies in case any one defense fails. It acts fast, but has checks and balances to prevent overreactions. And, in the main, it just works. Despite the multitude of infectious threats that constantly surround us, most people spend most of the time not being sick.

“It’s a complicated system,” Iwasaki says. “I think it’s beautiful.”

https://www.theatlantic.com/health/archive/2020/08/covid-19-immunity-is-the-pandemics-central-mystery/614956/

 

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Winter is coming: Why America’s window of opportunity to beat back Covid-19 is closing

By HELEN BRANSWELL | AUGUST 10, 2020

The good news: The United States has a window of opportunity to beat back Covid-19 before things get much, much worse.

The bad news: That window is rapidly closing. And the country seems unwilling or unable to seize the moment.

Winter is coming. Winter means cold and flu season, which is all but sure to complicate the task of figuring out who is sick with Covid-19 and who is suffering from a less threatening respiratory tract infection. It also means that cherished outdoor freedoms that link us to pre-Covid life — pop-up restaurant patios, picnics in parks, trips to the beach — will soon be out of reach, at least in northern parts of the country.

Unless Americans use the dwindling weeks between now and the onset of “indoor weather” to tamp down transmission in the country, this winter could be Dickensianly bleak, public health experts warn.

“I think November, December, January, February are going to be tough months in this country without a vaccine,” said Michael Osterholm, director of the Center for Infectious Diseases Research and Policy at the University of Minnesota.

It is possible, of course, that some vaccines could be approved by then, thanks to historically rapid scientific work. But there is little prospect that vast numbers of Americans will be vaccinated in time to forestall the grim winter Osterholm and others foresee.

Human coronaviruses, the distant cold-causing cousins of the virus that causes Covid-19, circulate year-round. Now is typically the low season for transmission. But in this summer of America’s failed Covid-19 response, the SARS-CoV-2 virus is widespread across the country, and pandemic-weary Americans seem more interested in resuming pre-Covid lifestyles than in suppressing the virus to the point where schools can be reopened, and stay open, and restaurants, movie theaters, and gyms can function with some restrictions.

“We should be aiming for no transmission before we open the schools and we put kids in harm’s way — kids and teachers and their caregivers. And so, if that means no gym, no movie theaters, so be it,” said Caroline Buckee, associate director of the Center for Communicable Disease Dynamics at Harvard’s T.H. Chan School of Public Health.

“We seem to be choosing leisure activities now over children’s safety in a month’s time. And I cannot understand that tradeoff.”

While many countries managed to suppress spread of SARS-CoV-2, the United States has failed miserably. Countries in Europe and Asia are worrying about a second wave. Here, the first wave rages on, engulfing rural as well as urban parts of the country. Though there’s been a slight decline in cases in the past couple of weeks, more than 50,000 Americans a day are being diagnosed with Covid-19. And those are just the confirmed cases.

To put that in perspective, at this rate the U.S. is racking up more cases in a week than Britain has accumulated since the start of the pandemic.

Public health officials had hoped transmission of the virus would abate with the warm temperatures of summer and the tendency — heightened this year — of people to take their recreational activities outdoors. Experts do believe people are less likely to transmit the virus outside, especially if they are wearing face coverings and keeping a safe distance apart.

But in some places, people have been throwing Covid cautions to the wind, flouting public health orders in the process. Kristen Ehresmann, director of infectious disease epidemiology, prevention, and control for the Minnesota Department of Health, points to a large, three-day rodeo that was held recently in her state. Organizers knew they were supposed to limit the number of attendees to 250 but refused; thousands attended. In Sturgis, S.D., an estimated quarter of a million motorcyclists were expected to descend on the city this past weekend for an annual rally that spans 10 days.

Even on smaller scales, public health authorities know some people are letting down their guard. Others have never embraced the need to try to prevent spread of the virus. Ehresmann’s father was recently invited to visit some friends; he went, she said, but wore his mask, elbow bumping instead of shaking proffered hands. “And the people kind of acted like, … ‘Oh, you drank that Kool-Aid,’ rather than, ‘We all need to be doing this.'”

Ehresmann and others in public health are flummoxed by the phenomenon of people refusing to acknowledge the risk the virus poses.

“Just this idea of, ‘I just don’t want to believe it so therefore it’s not going to be true’ — honestly, I have not really dealt with that as it relates to disease before,” she said.

Buckee, the Harvard expert, wonders if the magical thinking that seems to have infected swaths of the country is due to the fact many of the people who have died were elderly. For many Americans, she said, the disease has not yet touched their lives — but the movement restrictions and other response measures have.

“I think if children were dying, this would be … a different situation, quite honestly,” she said.

Epidemiologist Michael Mina despairs that an important chance to wrestle the virus under control is being lost, as Americans ignore the realities of the pandemic in favor of trying to resume pre-Covid life.

“We just continue to squander every bit of opportunity we get with this epidemic to get it under control,’’ said Mina, an assistant professor in Harvard’s T.H. Chan School of Public Health and associate medical director of clinical microbiology at Boston’s Brigham and Women’s Hospital.

“The best time to squash a pandemic is when the environmental characteristics slow transmission. It’s your one opportunity in the year, really, to leverage that extra assistance and get transmission under control,” he said, his frustration audible.

Driving back transmission would require people to continue to make sacrifices, to accept the fact that life post-Covid cannot proceed as normal, not while so many people remain vulnerable to the virus. Instead, people are giddily throwing off the shackles of coronavirus suppression efforts, seemingly convinced that a few weeks of sacrifice during the spring was a one-time solution.

Osterholm has for months warned that people were being misled about how long the restrictions on daily life would need to be in place. He now thinks the time has come for another lockdown. “What we did before and more,” he said.

The country has fallen into a dangerous pattern, Osterholm said, where a spike in cases in a location leads to some temporary restraint from people who eventually become alarmed enough to start to take precautions. But as soon as cases start to plateau or decline a little, victory over the virus is declared and people think it’s safe to resume normal life.

“It’s like an all or nothing phenomenon, right?” said Anthony Fauci, director of the National Institute for Allergy and Infectious Diseases. “You all locked down or you get so discouraged with being in lockdown that you decide you’re going to be in crowded bars … you can have indoor parties with no masks. You can do all the things that are going to get you in trouble.”

Osterholm said with the K-12 school year resuming in some parts of the country or set to start — along with universities — in a few weeks, transmission will take off and cases will start to climb again. He predicted the next peaks will “exceed by far the peak we have just experienced. Winter is only going to reinforce that. Indoor air,” he said.

Buckee thinks that if the country doesn’t alter the trajectory it is on, more shutdowns are inevitable. “I can’t see a way that we’re going to have restaurants and bars open in the winter, frankly. We’ll have resurgence. Everything will get shut down again.”

Fauci favors a reset of the reopening measures, with a strong messaging component aimed at explaining to people why driving down transmission now will pay off later. Young people in particular need to understand that even if they are less likely to die from Covid-19, statistically speaking, transmission among 20-somethings will eventually lead to infections among their parents and grandparents, where the risk of severe infections and fatal outcomes is higher. (Young people can also develop long-term health problems as a result of the virus.)

“It’s not them alone in a vacuum,” Fauci said. “They are spreading it to the people who are going to wind up in the hospital.”

Everyone has to work together to get cases down to more manageable levels, if the country hopes to avoid “a disastrous winter,” he said.

“I think we can get it under much better control, between now and the mid-to-late fall when we get influenza or we get whatever it is we get in the fall and the winter. I’m not giving up,” said Fauci.

But without an all-in effort “the cases are not going to come down,” he warned. “They’re not. They’re just not.”

https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing

 

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SkyMan

 

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Headshot

The pandemic is more real than most people know. From the credible sources I'm reading, the pandemic is just getting started and has a long way to go before it runs its course. With more infectious strains (mutations) now being discovered, the fact that it has now been established that antibodies disappear in short order, and that the disease creates its own comorbidities to weaken people if they are reinfected, it is inevitable that this virus will continue to sweep through the human population.

It is the reactions of most governments of countries and the actions of official agencies around the world that are BS. Everybody is blindly following the lead of those who do not have (and never have had) people's best interests at heart. People need to figure out for themselves why this virus was created, why it was released into the human population, and what the desired outcome was before we can truly get the true source of the virus under control. The virus, itself, will likely never be under control.

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Ricbak

May I ask Headshot,

 

People need to figure out for themselves why this virus was created, What Headshot is your view?

 

'why it was released into the human population.' Who was it that released the virus?

'and what the desired outcome was before we can truly get the true source of the virus under control.' By whom?

The virus, itself, will likely never be under control. ........Well it will probably die down mutate into less "dangerous" forms.

 

Thanks, Ricbak

 

 

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19 hours ago, Headshot said:

The pandemic is more real than most people know. From the credible sources I'm reading, the pandemic is just getting started and has a long way to go before it runs its course. With more infectious strains (mutations) now being discovered, the fact that it has now been established that antibodies disappear in short order, and that the disease creates its own comorbidities to weaken people if they are reinfected, it is inevitable that this virus will continue to sweep through the human population.

It is the reactions of most governments of countries and the actions of official agencies around the world that are BS. Everybody is blindly following the lead of those who do not have (and never have had) people's best interests at heart. People need to figure out for themselves why this virus was created, why it was released into the human population, and what the desired outcome was before we can truly get the true source of the virus under control. The virus, itself, will likely never be under control.

The pandemic is real, but lets not pretend as if this is some doom virus that will wipe out humanity.
If you look at the response from certain governments, it certainly makes it seem like we are dealing with something the likes of the bubonic plague, the knee jerk reactions, economic suicide causing 45% unemployment (2008 crisis and great depression are rookie numbers compared to this), borderline martial law, you name it.


The world has been dealing with much more serious illnesses, and none of them caused the wide spread panic and chaos that covid did.
Dengue has a 20% mortality rate, yet apart from a few posters here and there, there isn't much being done about it.
Then there is tuberculosis which is a much more serious and deadly virus, sure there is a vaccine but the Philippines currently has over 1 million active infected (source: WHO https://www.who.int/philippines/news/commentaries/detail/it-s-time-to-end-tb-in-the-philippines ).

I'd take covid over TB or dengue any day of the week.

Edited by Dutch
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Mangoshake

All this fuzz for some flue.

Sweden didn’t do any lockdown whatsoever  and have the Swedish extinct? 

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Salty Dog

If you guys want to discuss political ramifications, please take it to the CR.

There is a thread there to discuss such things and their relationships to COVID-19. 

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Headshot

 

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cookie47

From an on line Senior's website which I'm a Member 

https://www.yourlifechoices.com.au/health/covid19/glasses-cut-covid-infections-study?

This although not conclusive I found interesting as I've worn glasses since 10 years old ..(myopic)

Researchers in China have found that people who wear glasses appear to be at lower risk of catching COVID-19. The authors of the study, published in JAMA Ophthalmology, noticed that since the coronavirus outbreak in Wuhan in December 2019, few patients with spectacles were admitted to hospital suffering from COVID-19. To investigate further, they collected data on the wearing of glasses from all patients with COVID-19 as part of their medical history.

Their small study found that only 16 (5.8 per cent) of the 276 patients admitted with COVID-19 wore glasses for more than eight hours a day. As they determined that all these patients were short-sighted, they next looked up the proportion of people with myopia (short-sightedness) in Hubei Province, where the hospital is located. They found this to be much larger (31.5 per cent), indicating that the proportion of short-sighted COVID-19 hospital admissions was over five times lower than might be expected from that population.

This is a fascinating observation, but as with all single studies the results must be treated with caution. While eye protection has always been an important component of personal protective equipment (PPE), the magnitude of difference reported by this study raises suspicion. This is not to say that the results may not be real, but rather that we shouldn’t start advising large-scale behavioural changes (such as wearing goggles alongside our face masks) until they have been independently confirmed.

Are eyes a window for the virus?
One of the key steps for any viral infection is the initial entry into the body. While most of our body is covered with protective skin, which is very effective at preventing viruses or bacteria crossing into our body, far thinner ‘membranes’ cover our airways, digestive system and eyes. The role of these thinner membranes is to allow external things such as oxygen, food, and in the case of eyes, light, into our bodies. Unfortunately, viruses have learnt to take advantage of these entry points.

This is the reason PPE is designed to protect these entry points, through the use of face masks, goggles and protective clothing. However, whereas we might imagine that the main attack on these regions comes from viral particles transmitted through the air as aerosols, the main way that viral particles get to these weak points is actually via our hands. Hence the COVID-19 advice to wash our hands often, for 20 seconds or more, and avoid touching our faces.

It therefore makes sense that covering our eyes with glasses may offer extra protection, both from the virus that may be carried in other people’s breath, but also in preventing wearers from touching their eyes. Indeed, as far back as February there were reports of people catching COVID-19 by not suitably protecting their eyes in healthcare settings. It is also known that similar points of entry into the body (ACE-2 receptors) favoured by the coronavirus are also present in the eyes.

Should we start wearing goggles?
A critical part of interpreting any evidence coming from observational studies is remembering that correlation (two things happening together) does not necessarily mean causation (one thing causes the other). To test for causation, a controlled trial or test is now needed.

Ideally, this would follow two carefully matched groups of people – some wearing glasses and some not wearing glasses – to see which group gets infected more often. Evidence from such a controlled trial will always be far stronger than evidence from an observational study such as that in the recent paper.

We must also note that the authors of this study listed a number of weaknesses. It was a very small study at a single site. The researchers’ data for the general population came from a much earlier study on a sample that was not exactly matched (in terms of age, demography and other factors) to their sample admitted to hospital with COVID-19. And they couldn’t guarantee that all the people with short-sightedness in the general population also wore glasses for more than eight hours a day.

So, although this new study is very interesting, there are plenty of reasons to be cautious about this result. We certainly need more data before any advice can be given about wearing goggles alongside our face masks.

Simon Kolstoe, Senior Lecturer in Evidence Based Healthcare and University Ethics Advisor, University of Portsmouth

This article is republished from The Conversation under a Creative Commons licence. Read the original article.

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