DawgTalkers.net Forums DawgTalk Everything Else... Covid-19: It Continues

This is a good article on the topic:

https://www.statnews.com/2020/08/25/four-scenarios-on-how-we-might-develop-immunity-to-covid-19/

From what I've read, there's always been isolated cases of reinfections from any virus or pathogen in the past.

This is certainly possible, especially based on past coronavirus behavior, yet we need more data.

If 1% of people can get infected again within a year -- then that would possibly lead to tens of thousands of re-infections across America.

At the same time, it wouldn't be a significant issue in terms of eventually developing population level immunity, or in affecting how most people will respond to a vaccine.

Have you not met "Florida man" the super hero by internet search?

If you're going to start with
" I Categorize this as what the heck is wrong with people"
Followed by
Associated Press: Florida Man.

I literally stopped, Oh Florida Man, what have you done this time?

Like lol

You're one that knows a lot about this stuff. Is it not possible that his first positive test was incorrect to begin with, so his "second" infection was really his first?

Here is a good twitter thread on this from an expert:



Long-story short. It seems likely that the Chinese "reinfection" case was a false positive in the initial test. The US case had a number of pieces of supporting evidence, and is likely a true re-infection case.

Not quite.

"The researchers sequenced the RNA from both virus samples, and found they were two different strains, making it a true reinfection."


Different strain, so not *really* a true re-infection. It's just another infection. Which, again, is as many suspected it would be the case with apparent "re-infections".

So how do you propose a vaccine can be made while this virus keeps morphing into different strains? Seems very much like a flu shot. It protects you "if" they predicted the right strain hits you.

1. I don't
2. same as they do with the flu... they will outright guess which strain to produce for in any given year
3. There aren't that many strains right now. There are lots of mutations, but not a lot of strains (my information may well be old on that).

I believe "reinfection" is correct. At least the current state of medical knowledge indicates that the strains are similar enough that getting one form of the virus is supposed to provide immunity to the other.

There are likely millions of technically different "strains" of coronavirus. I believe an early sample of 2000 patients in mid-April found ~1500 different strains. Almost all of them are functionally identical, with mutations far from the spike-protein which are immaterial to virus identification or operation.

There is one potentially important mutation, the D614G mutation, which is a change of a single amino acid (Aspartic Acid to Glycene) which happens to occur very near the spike-protein. This branch occurred in January and is fairly distinct between Asian Sources (which mainly have coronavirus with D at position 614) and European/US (which are primarily G). The G variant is thought to spread somewhat more rapidly, but it is believed that immunity to one version should give you immunity to both.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7310631/


Here is a good paper that argues that D614G will not strongly impact vaccine design:

https://www.cell.com/cell/pdf/S0092-8674(20)30817-5.pdf

Please stop with your anti-science nonsense. Your argument for herd immunity, which has been shown to be near impossible, went up in flames a long time ago. Why you continue to cape for people to get covid, despite there being serious long lasting quality of life consequences, will forever escape me.

It’s okay to admit you’re wrong, Purp. For the sake of yourself and others, please listen to the science and doctors.

J/C

Covid-19 doesn't appear to mutate near as fast as the flu:

https://www.livescience.com/coronavirus-mutation-rate.html
https://medicalxpress.com/news/2020-06-sars-cov-mutating-slowly-good.html

j/c:

CDC says 94% of ALL Americans who have died of COVID-19 had at least one other underlying disease

https://www.dailymail.co.uk/health/artic...s.html#comments

__________________________________

I posted this in the other covid thread:

Here's the Shockingly Small Number of People Who Died From Only the Coronavirus

The Centers for Disease Control and Prevention (CDC) website disclosed the shockingly small number of people who died from only the Wuhan coronavirus, with no other cause of death mentioned. Hold on to your hat because here it is: out of the 161,392 deaths in the CDC data, just six percent, about 9,700 deaths, were attributed to the coronavirus alone. According to the CDC, the other 94 percent had an average of 2.6 additional conditions or causes of deaths, such as heart disease, diabetes, and sepsis.


https://townhall.com/tipsheet/bronsonsto...avirus-n2575306

US citizens are notoriously overweight and lazy. Most US citizens over 55 have list of diagnosis already.
How many people that I’ve cared for over the past 15 years in hospice died of one thing? A VERY VERY small number. As we get older we rack up a list of diagnosis like a criminal with a rap sheet. So on our death beds were dying of multi-system failures typically. Ultimately heart failure kills us all. Our hearts stop, we die. But only one diagnosis gets placed as the ‘cause of death’.
How many US citizens over 55 have no diagnosis in their list... diabetes, history of cancer, heart disease, COPD, CKD, etc?
How many of the people that died ‘of COVID’ would still be alive, living with their diabetes, history of cancer, heart disease, COPD, etc if it weren’t for catching COVID? My guess is many. So while COVID maybe didn’t technically kill them it certainly drove their body over the edge.

Look around at your families and peer groups. How many are over weight? Have diabetes? Have COPD? CHF?... I know in my family it’s my mom and most of my aunts and uncles. If they catch it they’re in a higher mortality bracket.
So yes, most people that die of it have comorbidities. Of course. So do most of my aging family members. I’m not so flippant as to write off the disease because of it.

And as I said in the other thread, people don't die from AIDS. People die from complications due to AIDS. Very rarely does anyone die because of a single virus; people die from complications that arise due to viruses.

Please take the doctors and scientists seriously.

I'll read that later. My understanding of the terminology was that there are mutations and then there are strains, and the difference being that a strain is when there is a mutation that changes the behavior whereas a mere mutation is simply a benign difference in the RNA.

So, when I use the term "strain", that's what I was referring to. There are TONS of mutations out there, but - and again, I admit that my information is likely far out of date - I was under the impression there were actually only two strains, currently.

I'm not anti-science. My interpretation of the science just goes against what you want to shove down everyone's throat. That's all.

Not anti-science in any way. I AM absolutely anti-whatever-the-Hell you're pushing, though.

Like button pushed.

Most Americans, period, have comorbidities while walking around every day. Our society is to where this is quite probably the norm and that we have more people - in all age groups - with them than without.

We are an EXCEPTIONALLY unhealthy society, and it has absolutely nothing at all to do with our healthcare system and absolutely everything to do with our culture, our education, and our near-inherent laziness.

I think that is fairly close (and i'm not an expert here). I think mutations just refer to any change in a virus RNA, while strains correspond to the viruses themselves after the mutations. Different viral strains can be do to a point mutation (D614G is a simple point mutation, with exactly one amino acid changed). The thing that makes this mutation different than the thousands of other ones, is that it is at an active site of the virus, rather than in an inactive region.

My point above, though -- is that if you have been infected with either strain of Coronavirus, then it is very likely that you are immune to both strains that are circulating. While there are some viruses (like the flu) that mutate a lot, such that you are not generally immune to the flu next year -- the coronavirus mutation is relatively small, and is unlikely to affect immunity.

As a more extreme example - Cowpox and Smallpox are two entirely different viruses at this point (cowpox in fact has 40,000 more base-pairs than smallpox). However, they are similar enough in key regions of RNA that exposure to cowpox tends to give people significant immunity to smallpox.

Exactly. So to act as though the virus isn’t so bad because it’s only killed 9000+ people on its own is absurd when damn near everyone we know is a walking comorbidity list.

but, clearly not an absolute, if the so-called re-infections are real.

In short, if both are close enough to being the same that making one vaccine to handle them both isn't really an issue, then that also means that the vaccine is just as unlikely to work as recovering from an infection and generating your own antibodies the natural way.

What do people think they're going to do... get quarterly or monthly booster shots? Hell no; nobody is going to accept that... well, not nobody, there are plenty of fools out there that would sign up for that.

In either case, based simply on the incredibly low prevalence, I would definitely classify re-infection as a complete and total outlier and not something you have to game plan for at this stage. Yes, it appears it is possible, but it is also mathematically highly unlikely at this point. If it were anything other than that, especially given the short timespan this reinfection occurred within, we would have had thousands - or at the very least hundreds - of confirmed reports of this by now, just in the US. We do not. Possibility, not a probability.

I would wager that if you compare the DNA of the people that get reinfected, there will be a common trait in there relating to how this virus behaves, or in the way it triggers immune responses for creating antibodies.

I think I agree with most of that. At the moment, it seems like reinfection (at least within ~6 months) is very rare.

We don't yet know if reinfection will also be rare on multi-year timescales.

We also don't know whether reinfection will lead to serious or mild illness.

These facts will be related to the effectiveness of the vaccine, so there is a lot we won't know about the long term effectiveness of the vaccine either.

and the vaccine's effectiveness will only be as good and valuable as the antibody responses triggered, at best.

Tons we simply cannot know because we haven't gone through it, yet, but I think it is safe to say for now that - so far- worries of mass or frequent re-infection isn't anything a rational mind should trouble themselves with right now, nor will the rates of it be an issue in any way. And, just to poke the bear... it will NOT prevent or inhibit achieving herd immunity in any way whatsoever. It simply doesn't happen enough to matter. Any suggestion to the contrary is a blatant rebuke of what the data incontrovertibly shows. Recovery rates will easily swamp reinfections and we will easily achieve herd immunity.

I mean - we could get to herd immunity, but about a million people will die first.... I feel like that shouldn't be the goal.

I've done napkin math elsewhere on here that attempts to guess where we are right now based on best guesses at "true" infection rates versus confirmed cases. The best estimates I've seen say that there are anywhere from 6 to 20+ people that have had covid for every confirmed case of it.

The US has had 6.2 million confirmed cases (and one reinfection).
On the low end of the scale, yes, that means only 37 million so far; we're sitting at only about 12% of our population. In that scenario, yes, the extrapolation would have us seeing about 1.5 million deaths.
On the upper end of the range, that estimate puts us over 120 million and sitting nicely at 37.5%, in which case we're over halfway there.

If I had to randomly choose a number to guess where we are, I'd guess 10-12 cases for every confirmed, or 62-74 million people, or 21-25%.
We're six months in and stand a very good chance of being 1/3rd of the way there. It is highly likely, especially with cold & flu season in the on-deck box, that we end up getting there before any vaccine is even ready - and definitely before it is ready on a sufficient scale - and in that event, these are deaths that are going to happen anyway.

If nothing else changes between now and whenever, then we're looking at about 525,000-650,000.


Those are still pretty big numbers, and they could easily go way higher or way lower depending on nothing more than Who gets infected.

It is overly simplified napkin math, for sure, but one thing is pretty clear: we are well into this now, and by the end of winter, we will very likely be in the home stretch.

Not sure if been posted before...

A Supercomputer Analyzed Covid-19 — and an Interesting New Theory Has Emerged
A closer look at the Bradykinin hypothesis

Thomas Smith
2 days ago·8 min read

3d rendering of multiple coronavirus.

Earlier this summer, the Summit supercomputer at Oak Ridge National Lab in Tennessee set about crunching data on more than 40,000 genes from 17,000 genetic samples in an effort to better understand Covid-19. Summit is the second-fastest computer in the world, but the process — which involved analyzing 2.5 billion genetic combinations — still took more than a week.

When Summit was done, researchers analyzed the results. It was, in the words of Dr. Daniel Jacobson, lead researcher and chief scientist for computational systems biology at Oak Ridge, a “eureka moment.” The computer had revealed a new theory about how Covid-19 impacts the body: the bradykinin hypothesis. The hypothesis provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms. It also suggests 10-plus potential treatments, many of which are already FDA approved. Jacobson’s group published their results in a paper in the journal eLife in early July.

According to the team’s findings, a Covid-19 infection generally begins when the virus enters the body through ACE2 receptors in the nose, (The receptors, which the virus is known to target, are abundant there.) The virus then proceeds through the body, entering cells in other places where ACE2 is also present: the intestines, kidneys, and heart. This likely accounts for at least some of the disease’s cardiac and GI symptoms.

The disease has not changed, but scientific understanding has evolved dramatically
elemental.medium.com

But once Covid-19 has established itself in the body, things start to get really interesting. According to Jacobson’s group, the data Summit analyzed shows that Covid-19 isn’t content to simply infect cells that already express lots of ACE2 receptors. Instead, it actively hijacks the body’s own systems, tricking it into upregulating ACE2 receptors in places where they’re usually expressed at low or medium levels, including the lungs.
In this sense, Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house. Once inside, though, they don’t just take your stuff — they also throw open all your doors and windows so their accomplices can rush in and help pillage more efficiently.
The renin–angiotensin system (RAS) controls many aspects of the circulatory system, including the body’s levels of a chemical called bradykinin, which normally helps to regulate blood pressure. According to the team’s analysis, when the virus tweaks the RAS, it causes the body’s mechanisms for regulating bradykinin to go haywire. Bradykinin receptors are resensitized, and the body also stops effectively breaking down bradykinin. (ACE normally degrades bradykinin, but when the virus downregulates it, it can’t do this as effectively.)
The end result, the researchers say, is to release a bradykinin storm — a massive, runaway buildup of bradykinin in the body. According to the bradykinin hypothesis, it’s this storm that is ultimately responsible for many of Covid-19’s deadly effects. Jacobson’s team says in their paper that “the pathology of Covid-19 is likely the result of Bradykinin Storms rather than cytokine storms,” which had been previously identified in Covid-19 patients, but that “the two may be intricately linked.” Other papers had previously identified bradykinin storms as a possible cause of Covid-19’s pathologies.
Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house.

As bradykinin builds up in the body, it dramatically increases vascular permeability. In short, it makes your blood vessels leaky. This aligns with recent clinical data, which increasingly views Covid-19 primarily as a vascular disease, rather than a respiratory one. But Covid-19 still has a massive effect on the lungs. As blood vessels start to leak due to a bradykinin storm, the researchers say, the lungs can fill with fluid. Immune cells also leak out into the lungs, Jacobson’s team found, causing inflammation.

Coronavirus May Be a Blood Vessel Disease, Which Explains Everything
Many of the infection’s bizarre symptoms have one thing in common
elemental.medium.com

And Covid-19 has another especially insidious trick. Through another pathway, the team’s data shows, it increases production of hyaluronic acid (HLA) in the lungs. HLA is often used in soaps and lotions for its ability to absorb more than 1,000 times its weight in fluid. When it combines with fluid leaking into the lungs, the results are disastrous: It forms a hydrogel, which can fill the lungs in some patients. According to Jacobson, once this happens, “it’s like trying to breathe through Jell-O.”
This may explain why ventilators have proven less effective in treating advanced Covid-19 than doctors originally expected, based on experiences with other viruses. “It reaches a point where regardless of how much oxygen you pump in, it doesn’t matter, because the alveoli in the lungs are filled with this hydrogel,” Jacobson says. “The lungs become like a water balloon.” Patients can suffocate even while receiving full breathing support.

The bradykinin hypothesis also extends to many of Covid-19’s effects on the heart. About one in five hospitalized Covid-19 patients have damage to their hearts, even if they never had cardiac issues before. Some of this is likely due to the virus infecting the heart directly through its ACE2 receptors. But the RAS also controls aspects of cardiac contractions and blood pressure. According to the researchers, bradykinin storms could create arrhythmias and low blood pressure, which are often seen in Covid-19 patients.

The bradykinin hypothesis also accounts for Covid-19’s neurological effects, which are some of the most surprising and concerning elements of the disease. These symptoms (which include dizziness, seizures, delirium, and stroke) are present in as many as half of hospitalized Covid-19 patients. According to Jacobson and his team, MRI studies in France revealed that many Covid-19 patients have evidence of leaky blood vessels in their brains.

Bradykinin — especially at high doses — can also lead to a breakdown of the blood-brain barrier. Under normal circumstances, this barrier acts as a filter between your brain and the rest of your circulatory system. It lets in the nutrients and small molecules that the brain needs to function, while keeping out toxins and pathogens and keeping the brain’s internal environment tightly regulated.
If bradykinin storms cause the blood-brain barrier to break down, this could allow harmful cells and compounds into the brain, leading to inflammation, potential brain damage, and many of the neurological symptoms Covid-19 patients experience. Jacobson told me, “It is a reasonable hypothesis that many of the neurological symptoms in Covid-19 could be due to an excess of bradykinin. It has been reported that bradykinin would indeed be likely to increase the permeability of the blood-brain barrier. In addition, similar neurological symptoms have been observed in other diseases that result from an excess of bradykinin.”

Increased bradykinin levels could also account for other common Covid-19 symptoms. ACE inhibitors — a class of drugs used to treat high blood pressure — have a similar effect on the RAS system as Covid-19, increasing bradykinin levels. In fact, Jacobson and his team note in their paper that “the virus… acts pharmacologically as an ACE inhibitor” — almost directly mirroring the actions of these drugs.
Medium Coronavirus Blog

By acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs. ACE inhibitors are known to cause a dry cough and fatigue, two textbook symptoms of Covid-19. And they can potentially increase blood potassium levels, which has also been observed in Covid-19 patients. The similarities between ACE inhibitor side effects and Covid-19 symptoms strengthen the bradykinin hypothesis, the researchers say.

ACE inhibitors are also known to cause a loss of taste and smell. Jacobson stresses, though, that this symptom is more likely due to the virus “affecting the cells surrounding olfactory nerve cells” than the direct effects of bradykinin.

Though still an emerging theory, the bradykinin hypothesis explains several other of Covid-19’s seemingly bizarre symptoms. Jacobson and his team speculate that leaky vasculature caused by bradykinin storms could be responsible for “Covid toes,” a condition involving swollen, bruised toes that some Covid-19 patients experience. Bradykinin can also mess with the thyroid gland, which could produce the thyroid symptoms recently observed in some patients.

The bradykinin hypothesis could also explain some of the broader demographic patterns of the disease’s spread. The researchers note that some aspects of the RAS system are sex-linked, with proteins for several receptors (such as one called TMSB4X) located on the X chromosome. This means that “women… would have twice the levels of this protein than men,” a result borne out by the researchers’ data. In their paper, Jacobson’s team concludes that this “could explain the lower incidence of Covid-19 induced mortality in women.” A genetic quirk of the RAS could be giving women extra protection against the disease.

The bradykinin hypothesis provides a model that “contributes to a better understanding of Covid-19” and “adds novelty to the existing literature,” according to scientists Frank van de Veerdonk, Jos WM van der Meer, and Roger Little, who peer-reviewed the team’s paper. It predicts nearly all the disease’s symptoms, even ones (like bruises on the toes) that at first appear random, and further suggests new treatments for the disease.
As Jacobson and team point out, several drugs target aspects of the RAS and are already FDA approved to treat other conditions. They could arguably be applied to treating Covid-19 as well. Several, like danazol, stanozolol, and ecallantide, reduce bradykinin production and could potentially stop a deadly bradykinin storm. Others, like icatibant, reduce bradykinin signaling and could blunt its effects once it’s already in the body.

Interestingly, Jacobson’s team also suggests vitamin D as a potentially useful Covid-19 drug. The vitamin is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN. Again, this could stop potentially deadly bradykinin storms from forming. The researchers note that vitamin D has already been shown to help those with Covid-19. The vitamin is readily available over the counter, and around 20% of the population is deficient. If indeed the vitamin proves effective at reducing the severity of bradykinin storms, it could be an easy, relatively safe way to reduce the severity of the virus.
Other compounds could treat symptoms associated with bradykinin storms. Hymecromone, for example, could reduce hyaluronic acid levels, potentially stopping deadly hydrogels from forming in the lungs. And timbetasin could mimic the mechanism that the researchers believe protects women from more severe Covid-19 infections. All of these potential treatments are speculative, of course, and would need to be studied in a rigorous, controlled environment before their effectiveness could be determined and they could be used more broadly.

Covid-19 stands out for both the scale of its global impact and the apparent randomness of its many symptoms. Physicians have struggled to understand the disease and come up with a unified theory for how it works. Though as of yet unproven, the bradykinin hypothesis provides such a theory. And like all good hypotheses, it also provides specific, testable predictions — in this case, actual drugs that could provide relief to real patients.

The researchers are quick to point out that “the testing of any of these pharmaceutical interventions should be done in well-designed clinical trials.” As to the next step in the process, Jacobson is clear: “We have to get this message out.” His team’s finding won’t cure Covid-19. But if the treatments it points to pan out in the clinic, interventions guided by the bradykinin hypothesis could greatly reduce patients’ suffering — and potentially save lives.

https://elemental.medium.com/a-supercomp...ed-31cb8eba9d63

I read this the other day. Kink of correlates with the B10 finding cardiomegaly in 30-35% of the athletes that tested positive. Asymptomatic or not.
This is more than just a respiratory illness.

Key model predicts 400,000 coronavirus deaths in US by January

A key forecasting model often cited by experts and used by the White House has revised its prediction of COVID-19 deaths in the U.S., now estimating a peak of 410,451 by January 1.

The model created by the Institute for Health Metrics and Evaluation (IHME) at the University of Washington posted an update Friday predicting an additional 224,000 Americans will die by the beginning of next year.

The model says that as many as 122,000 of those deaths could be avoided with safety measures, including near-universal mask use, but it warns that easing restrictions could cause the death toll to be more than 620,000.

“We all must learn from those leaders of nations where the virus has been contained, or where second waves of infections have occurred, and where swift action has been taken to prevent loss of life,” IHME Director Christopher Murray said in a statement.

Murray warned about governments pursuing herd immunity as a way to expedite the reopening economies.

“This first global forecast represents an opportunity to underscore the problem with herd immunity, which, essentially, ignores science and ethics, and allows millions of avoidable deaths,” Murray said. “It is, quite simply, reprehensible.”

The IHME model is more aggressive in its predictions than some other models. Their update comes just one day after the Centers for Disease Control and Prevention established a new forecast predicting 211,000 U.S. deaths from COVID-19 by September 26.

https://thehill.com/policy/healthcare/51...n-us-by-january

My youngest brother has multiple symptoms and was tested Monday. He will get his results sometime today. He seems to be doing alright right now, and says he feels a little better this morning. His 44th birthday was yesterday.

Ohio college students test positive for coronavirus, throw party
NEWS
by: Haley Townsend and Nexstar Media Wire
Posted: Sep 11, 2020 / 09:33 PM EDT / Updated: Sep 11, 2020 / 09:33 PM EDT


OXFORD, Ohio (NewsNation Now) — A college student house held a party over the Labor Day weekend that included people who had recently tested positive for the coronavirus, according to police body camera footage obtained by NewsNationNow.com.

Oxford police cited six men at a house near Miami University on Saturday for violating the state’s mass gathering and quarantine ordinance.


Bodycam footage shows an officer arriving at a home near the campus and finding men without masks on the porch drinking and listening to music. The incident reports states the officer heard the music playing from over 25 feet away and saw seven people standing on the porch or in the front yard.

One of the men tells police that about 20 people have gathered at the house, twice the amount of people allowed to congregate in Ohio. The officer asks the group to disperse while he runs the ID of one of the residents.

“I’ve never seen this before,” the officer is heard saying to the student after running his ID. “There’s an input on the computer that you tested positive for COVID?”


“Yes,” the student answers. He goes on to disclose that he tested positive a week before and that every single person at the party has COVID-19, including two people from the house across the street.

“Oh, God. This is what we’re trying to prevent,” the officer responds. “We want to keep this town open.”

The officer questioned why the students weren’t practicing a self-imposed quarantine for 14 days, as recommended by state and federal health officials. The student responds that the guests were just passing by.

According to the Oxford Police incident report, one of the residents of the home later stopped by the police department and expressed a desire to press trespassing charges against everyone at the house who was not a resident, and denied participating in any mass gatherings. Another resident who was cited emailed the department stating he too would like to press charges for trespass and said he was sick in bed and did not respond to the porch until he was asked to by the officer.

Gov. Mike DeWine said in a briefing Thursday that cases at Miami are the reason why Butler County remains at a level 3 on the state’s public health advisory system.

The university still plans to start in-person classes on Sept. 21. But school officials have warned that students who refuse to take a test will be denied access to campus services and will have to return to remote learning.

I spoke with him yesterday, but he was still waiting. He was feeling about the same or a little better and doesn't seem to have the severe symptoms, so I think he's going to be alright either way right now. Thanks for asking.

Spain can’t stop partying: Late night discos and sauna socials pushing Covid rate to soar further
The Telegraph
James Badcock
,The Telegraph•September 12, 2020

Spain is pleading with young people to stop socialising at illegal parties as the country's monunting Covid caseload continues to lead the way in Europe's impending second wave of infections.

In spite of the warnings from authorities to rein in expansive social behaviour, in the early hours of Thursday Madrid police caught and fined 73 people who had sidestepped a ban on late-night discotheques by partying in a basement sauna in the capital’s main business district. No one was wearing a face mask.

Last weekend, a few blocks away, 75 people were caught in an unlicensed premises operating as a bar and brothel, openly defying Spanish government orders to close down bordellos.

The city is one of the worst-hit places in Spain, with hospitals recording an alarming rise in admissions.

The government launched a campaign this week to deter youngsters from underplaying the danger of Covid. Hashtagged #EstoNoEsUnJuego (#ThisIsNotAGame), the black-and-white video juxtaposes young people gathering to drink in the street with images of people in hospital, ending with a less-than-subtle coffin on a gurney.

Customers sit at tables outside a bar on the Barceloneta promenade in Barcelona, Spain - Bloomberg
Customers sit at tables outside a bar on the Barceloneta promenade in Barcelona, Spain - Bloomberg
Fernando Simón, the head of the health ministry’s Covid-19 department, has pleaded with young people to ditch parties, saying “there are alternative ways to have fun without putting anyone at risk”, while also appealing to social network influencers to reach out to the young and convince them to follow the rules.

After Europe’s strictest lockdown was lifted on June 21 just as warm summer weather arrived, Spain’s younger generation returned to the streets, bars and clubs as all establishments were initially allowed to open, albeit with restrictions on the use of dance floors and the requirement to wear as face mask – except when drinking.

Spain’s Covid-19 caseload is now rising more rapidly than in any of its European neighbours, with more than half a million total known positives and the transmission rate now standing at 235 confirmed cases in the past 14 days per 100,000 inhabitants. This compares to 126 in France, the UK’s 37 and just 29 in Italy.

The explosion of Spanish nightlife has been targeted by Spanish authorities as one of key causes of the uptick in coronavirus cases through July and August, leading to a national agreement between the central and regional governments to shutter all bars no later than 1am, with last orders at midnight.

But the party is often not in a regular establishment in Spain, where huge numbers of young people tend to gather for outdoor drinking gatherings known as ‘botellones’ or raves in the open air.


On the last weekend in August police broke up a party of more than 100 people on Valdevaqueros beach near Tarifa, 300 saw their botellón interrupted in the town of Benimaclet, while 160 were caught enjoying a rave in a warehouse in Barcelona’s port area.

“It’s true that we have more interactive social behaviour than other countries. Almost nothing can be celebrated in Spain unless it is in a large group,” says Ildefonso Hernández, a professor in public health from Miguel Hernández University in Alicante.

“The number of meetings people have is very high, family life is very active, and we are seeing that a large number of outbreaks are caused by family occasions.”

Social gatherings, including family events, have been limited by several regions, including Madrid and Catalonia, to 10 people, while Murcia is the strictest with a maximum of six people.

Spanish health ministry figures show that around 25 per cent of new cases are being found in people aged 15-29, part of the reason, as well as higher detection levels, that the mortality rate is as low as 0.6 per cent, with less than five per cent requiring hospital treatment.


https://www.yahoo.com/news/spain-t-stop-partying-night-131157338.html

Israel is about to enter a second nationwide lockdown after its COVID-19 cases saw a major surge since reopening in May
Katie Canales 20 hours ago

Officials made the decision on Thursday to implement a strict two-week shutdown starting next week, per Bloomberg. After that, stringent limitations will be set for everyday activities for another two weeks. Other countries have reimposed partial safety measures following spikes in cases, but Israel is the first to implement a strict, second nationwide lockdown during the pandemic, per The Times.

The move comes as Israel has attempted to grapple with a resurgence in coronavirus cases. Israel came out of its first shutdown in May, at which time the total case count was about 17,000. The lockdown had successfully helped in stemming the spread of the disease in the country, but its case count has ballooned past 145,000 after what some say was a premature reopening. Some new daily tallies are sitting at about 4,000, and there are a reported 1,100 deaths in the nation.

Citizens have criticized Israel Prime Minister Benjamin Netanyahu and the government's response to the outbreak in the nation, with many participating in demonstrations protesting for an improvement in economic aid.

https://www.businessinsider.com/israel-shutdown-again-covid-19-coronavirus-2020-9

Just got word that my little brothers test was positive and he is quarantined with mild symptoms at this point. He started feeling symptoms last Sunday night late, so he is a week into this now.

Saying a prayer for him bro.