That’s interesting. Big controversy here recently when one of the members of NPHET was extremely dismissive of LFTs (on sale at Lidl) because of concerns about exactly this happening. He got absolutely crucified on social media as a result. It’s so difficult to get the messaging right about this stuff. The concepts are super tricky for lay people. I’m qualified 20+ years and I still get myself confused about false negatives, false positives and the importance of prior predictive values!
SARS CoV-2 coronavirus / Covid-19 (No tin foil hat silliness please)
- Thread starter Don't Kill Bill
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I don't think the idea of it being 'man-made' is helpful and that's not what's being discussed. It's the possibility of a natural sample being studied at one of the Wuhan virology labs (which may or may not have been modified as part of their studies, or may or may not have mutated under lab conditions) escaping the lab via a biosecurity breach (such as a researcher or technician becoming infected).
KCL biosecurity researcher Filippa Lentzos is on record questioning the background and credentials of the WHO team as far as them being able to deem the possibility of a biosecurity failure as unlikely as they claimed.
Whatever the actual origin is, the way it just immediately became a political football is sickening. The same news sources who were describing the lab leak as a debunked fringe conspiracy theory last year are now saying the evidence could point either way as soon as Biden calls for a review of the origin.
A lab studying emerging diseases isn't any old sceincey lab though is it? Its the exact type of lab from which a new disease might escape.
Escaping disease from labs studying diseases have happened in the past and the discussion about control of these labs and their value has been ongoing inside the science community for decades.
If the Chinese govt hadn't lied to the WHO at the very start of this outbreak there might not have been an outbreak this big. If it is in the end an unjustified suspicion and just a coincidence that the outbreak was in the only city with this type of lab in China then that is unfortunately what happens when you get caught covering things up. It becomes more difficult to convince people that you are being honest.
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Looks like the Irish kids took one for the team after all!
Not really surprising is it? We've had the longest, hardest lockdown in Europe.
Probably the key summary from the analysis is about any predictions on death rates...
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Not sure if it's been mentioned yet, but this was in my Nature Briefing today:
Full scientific article: link
Some really good news.
(Assuming it's correct and some crazy variant doesn't ruin things.)
Full layman article: https://www.nature.com/articles/d41586-021-01442-9Nature Briefing Summary said:
Full scientific article: link
Some really good news.
(Assuming it's correct and some crazy variant doesn't ruin things.)For sure. Although it goes without saying that a mortality rate anywhere near the last one would represent a catastrophic failure. The tricky question now is what level of mortality is acceptable to press on with opening exactly as planned? Seeing lots of young people dead/dying in hospital would be terrible optics, even if the numbers are much lower than if it was elderly people bearing the brunt.
Agree on the optics, I think they'll still continue to press on. The % of deaths for those under 40 (with no under lying medical conditions) must be extremely low, assuming that they've not had their first dose of vaccine.
% tiny but absolute numbers could be very high if thousands (millions?) infected.
I've seen two very different analyses of the data today, and it's fair to say that everyone's watching the Bolton day on day data to see how it goes. As I'm in a mood for good news today, I'll pass on what the stats/epedemiology optimists are saying.
Bolton's local public health people reckon the case rates have plateaued and may be starting to fall again. They're anticipating a rise in hospital inpatients over the next two weeks, peaking around the 60 patients mark.
The belief is that the hospitalisation rates are actually demonstrating that the vaccines are doing a great job. They're looking at 5 fully vaccinated patients out of the 47 people currently in hospital. Given the typical hospital/age profile for covid and the very high vaccination take-up percentage in those age groups the vaccines are doing an extraordinarily good job against hospitalisation.
Bolton's local public health people reckon the case rates have plateaued and may be starting to fall again. They're anticipating a rise in hospital inpatients over the next two weeks, peaking around the 60 patients mark.
The belief is that the hospitalisation rates are actually demonstrating that the vaccines are doing a great job. They're looking at 5 fully vaccinated patients out of the 47 people currently in hospital. Given the typical hospital/age profile for covid and the very high vaccination take-up percentage in those age groups the vaccines are doing an extraordinarily good job against hospitalisation.
The below would tie in with what the local PH would be saying, it's 7 day per 100k rate has been declining for the last 4 days.
I don’t think anyone denies that the vaccines are doing a great job against this variant. Which is a huge fecking relief. The worry is that if it’s massively more contagious the absolute numbers of people infected could put far too many of them in hospital if only a small % of those who are vaccinated make up that number.
Any trends towards plateauing of cases is music to my ears. I wonder what’s driving that though? Are people in the affected areas winding back on their socialising? What happens when pubs and indoor dining get back into full swing?
I guess the most optimistic interpretation of a short spike that levels off rapidly would be an influx of people bringing the new variant from abroad then running out of close contacts to infect. We would just have to hope that they don’t travel around the country (or over to Ireland, thanks very much!) and the outbreak burns itself out in those worst affected areas. Although there are a lot of affected areas.
Certainly there's a massive risk that the opening decision is being driven by boredom - lockdown fatigue, Tory MPs and media who want to "get on with it", Boris's attention span etc. I've also seen it suggested that we're now heading into the herd immunity (by infection) for the under 25s phase of the pandemic.
If you look at antibody (vaccine and/or infection acquired stats by age you get a profile something like:
Which, assuming the good news about vaccines is confirmed, gives them quite a bit of NHS capacity buffer to complete the first dose rollout for all over 18s, and the over 40 second doses, before the whole thing collapses.
I suspect Bolton has become a test case for the new version of "local measures". More tests, more vaccine centres, more community workers helping people fill in the paperwork to get extra money when they have to self isolate etc. If it works it'll be a lot better than the fiasco of Bolton spending most of last year in the top local lockdown category and still having some of the worst case numbers in the country.
Wow. Those prior infection % are amazing. Especially 15-24. One in three of them have had covid. Bonkers. Although also blows the claims of zero covid goons about “1 in 10” get long covid right out of the water.Certainly there's a massive risk that the opening decision is being driven by boredom - lockdown fatigue, Tory MPs and media who want to "get on with it", Boris's attention span etc. I've also seen it suggested that we're now heading into the herd immunity (by infection) for the under 25s phase of the pandemic.
If you look at antibody (vaccine and/or infection acquired stats by age you get a profile something like:
Which, assuming the good news about vaccines is confirmed, gives them quite a bit of NHS capacity buffer to complete the first dose rollout for all over 18s, and the over 40 second doses, before the whole thing collapses.
I suspect Bolton has become a test case for the new version of "local measures". More tests, more vaccine centres, more community workers helping people fill in the paperwork to get extra money when they have to self isolate etc. If it works it'll be a lot better than the fiasco of Bolton spending most of last year in the top local lockdown category and still having some of the worst case numbers in the country.
This article is excellent, I think it makes a fair argument that what we know this accidental lab release better than natural transmission. I hope you'll read it but I'll quote the best parts:
-The wet market connection, the major point of similarity with the SARS1 and MERS epidemics, was soon broken: Chinese researchers found earlier cases in Wuhan with no link to the wet market. (meaning patient zero came from elsewhere)
-It later turned out that the Lancet letter had been organized and drafted by Peter Daszak, president of the EcoHealth Alliance of New York. Daszak’s organization funded coronavirus research at the Wuhan Institute of Virology. If the SARS2 virus had indeed escaped from research he funded, Daszak would be potentially culpable. This acute conflict of interest was not declared to the Lancet’s readers. To the contrary, the letter concluded, “We declare no competing interests.”
-
A second statement that had enormous influence in shaping public attitudes was a letter (in other words an opinion piece, not a scientific article) published on 17 March 2020 in the journal Nature Medicine. Its authors were a group of virologists led by Kristian G. Andersen of the Scripps Research Institute. “Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus,” the five virologists declared in the second paragraph of their letter.
Unfortunately, this was another case of poor science, in the sense defined above. True, some older methods of cutting and pasting viral genomes retain tell-tale signs of manipulation. But newer methods, called “no-see-um” or “seamless” approaches, leave no defining marks. Nor do other methods for manipulating viruses such as serial passage, the repeated transfer of viruses from one culture of cells to another. If a virus has been manipulated, whether with a seamless method or by serial passage, there is no way of knowing that this is the case. Andersen and his colleagues were assuring their readers of something they could not know.
-First, they say that the spike protein of SARS2 binds very well to its target, the human ACE2 receptor, but does so in a different way from that which physical calculations suggest would be the best fit. Therefore the virus must have arisen by natural selection, not manipulation. If this argument seems hard to grasp, it’s because it’s so strained. The authors’ basic assumption, not spelt out, is that anyone trying to make a bat virus bind to human cells could do so in only one way. First they would calculate the strongest possible fit between the human ACE2 receptor and the spike protein with which the virus latches onto it. They would then design the spike protein accordingly (by selecting the right string of amino acid units that compose it). Since the SARS2 spike protein is not of this calculated best design, the Andersen paper says, therefore it can’t have been manipulated. But this ignores the way that virologists do in fact get spike proteins to bind to chosen targets, which is not by calculation but by splicing in spike protein genes from other viruses or by serial passage.
-The authors’ second argument against manipulation is even more contrived. Although most living things use DNA as their hereditary material, a number of viruses use RNA, DNA’s close chemical cousin. But RNA is difficult to manipulate, so researchers working on coronaviruses, which are RNA-based, will first convert the RNA genome to DNA. They manipulate the DNA version, whether by adding or altering genes, and then arrange for the manipulated DNA genome to be converted back into infectious RNA. Only a certain number of these DNA backbones have been described in the scientific literature. Anyone manipulating the SARS2 virus “would probably” have used one of these known backbones, the Andersen group writes, and since SARS2 is not derived from any of them, therefore it was not manipulated. But the argument is conspicuously inconclusive. DNA backbones are quite easy to make, so it’s obviously possible that SARS2 was manipulated using an unpublished DNA backbone. And that’s it. These are the two arguments made by the Andersen group in support of their declaration that the SARS2 virus was clearly not manipulated.
-The Chinese had no evidence to offer the commission in support of the natural emergence theory. This was surprising because both the SARS1 and MERS viruses had left copious traces in the environment. The intermediary host species of SARS1 was identified within four months of the epidemic’s outbreak, and the host of MERS within nine months. Yet some 15 months after the SARS2 pandemic began, and after a presumably intensive search, Chinese researchers had failed to find either the original bat population, or the intermediate species to which SARS2 might have jumped, or any serological evidence that any Chinese population, including that of Wuhan, had ever been exposed to the virus prior to December 2019.
-(Head bat coronaviruses researcher) Shi returned to her lab at the Wuhan Institute of Virology and resumed the work she had started on genetically engineering coronaviruses to attack human cells. How can we be so sure? Because, by a strange twist in the story, her work was funded by the National Institute of Allergy and Infectious Diseases (NIAID), a part of the US National Institutes of Health (NIH). And grant proposals that funded her work, which are a matter of public record, specify exactly what she planned to do with the money. The grants were assigned to the prime contractor, Daszak of the EcoHealth Alliance, who subcontracted them to Shi. Here are extracts from the grants:
-What this means, in non-technical language, is that Shi set out to create novel coronaviruses with the highest possible infectivity for human cells. Her plan was to take genes that coded for spike proteins possessing a variety of measured affinities for human cells, ranging from high to low. She would insert these spike genes one by one into the backbone of a number of viral genomes (“reverse genetics” and “infectious clone technology”), creating a series of chimeric viruses. These chimeric viruses would then be tested for their ability to attack human cell cultures (“in vitro”) and humanized mice (“in vivo”). And this information would help predict the likelihood of “spillover,” the jump of a coronavirus from bats to people. The methodical approach was designed to find the best combination of coronavirus backbone and spike protein for infecting human cells. The approach could have generated SARS2-like viruses, and indeed may have created the SARS2 virus itself with the right combination of virus backbone and spike protein.
-It cannot yet be stated that Shi did or did not generate SARS2 in her lab because her records have been sealed, but it seems she was certainly on the right track to have done so. “It is clear that the Wuhan Institute of Virology was systematically constructing novel chimeric coronaviruses and was assessing their ability to infect human cells and human-ACE2-expressing mice,” says Richard H. Ebright, a molecular biologist at Rutgers University and leading expert on biosafety.
“It is also clear,” Ebright said, “that, depending on the constant genomic contexts chosen for analysis, this work could have produced SARS-CoV-2 or a proximal progenitor of SARS-CoV-2.” “Genomic context” refers to the particular viral backbone used as the testbed for the spike protein.
-Even if the grant required the work plan described above, how can we be sure that the plan was in fact carried out? For that we can rely on the word of Daszak, who has been much protesting for the last 15 months that lab escape was a ludicrous conspiracy theory invented by China-bashers.
On December 9, 2019, before the outbreak of the pandemic became generally known, Daszak gave an interview in which he talked in glowing terms of how researchers at the Wuhan Institute of Virology had been reprogramming the spike protein and generating chimeric coronaviruses capable of infecting humanized mice: "And we have now found, you know, after 6 or 7 years of doing this, over 100 new SARS-related coronaviruses, very close to SARS,” Daszak says around minute 28 of the interview. “Some of them get into human cells in the lab, some of them can cause SARS disease in humanized mice models and are untreatable with therapeutic monoclonals and you can’t vaccinate against them with a vaccine."
-“Interviewer: You say these are diverse coronaviruses and you can’t vaccinate against them, and no anti-virals — so what do we do?
“Daszak: Well I think…coronaviruses — you can manipulate them in the lab pretty easily. Spike protein drives a lot of what happen with coronavirus, in zoonotic risk. So you can get the sequence, you can build the protein, and we work a lot with Ralph Baric at UNC to do this. Insert into the backbone of another virus and do some work in the lab. So you can get more predictive when you find a sequence. You’ve got this diversity. Now the logical progression for vaccines is, if you are going to develop a vaccine for SARS, people are going to use pandemic SARS, but let’s insert some of these other things and get a better vaccine.”
(They're not building a bioweapon, it's for vaccine work, the theory is escape)
-Much of Shi’s work on gain-of-function in coronaviruses was performed at the BSL2 safety level, as is stated in her publications and other documents. She has said in an interview with Science magazine that “[t]he coronavirus research in our laboratory is conducted in BSL-2 or BSL-3 laboratories. It is clear that some or all of this work was being performed using a biosafety standard — biosafety level 2, the biosafety level of a standard US dentist’s office — that would pose an unacceptably high risk of infection of laboratory staff upon contact with a virus having the transmission properties of SARS-CoV-2,” Ebright says. "It also is clear,” he adds, “that this work never should have been funded and never should have been performed.”
(BSL-2 is the level of your dentist)
This is getting too long ago in going to post a second set of quotes but here's the article, sourced by the Washington Post for their recent article
https://thebulletin.org/2021/05/the...RLE8HbzcWVCfVU0qH_GL7V48wh1P98NUxCx5M5OTFnmeY
Continued from article:
A couple have some technical detail, but these are among the most persuasive for those who may care to follow the argument.
1) The place of origin. Start with geography. The two closest known relatives of the SARS2 virus were collected from bats living in caves in Yunnan, a province of southern China. If the SARS2 virus had first infected people living around the Yunnan caves, that would strongly support the idea that the virus had spilled over to people naturally. But this isn’t what happened. The pandemic broke out 1,500 kilometers away, in Wuhan.
Beta-coronaviruses, the family of bat viruses to which SARS2 belongs, infect the horseshoe bat Rhinolophus affinis, which ranges across southern China. The bats’ range is 50 kilometers, so it’s unlikely that any made it to Wuhan. In any case, the first cases of the COVID-19 pandemic probably occurred in September, when temperatures in Hubei province are already cold enough to send bats into hibernation.
What if the bat viruses infected some intermediate host first? You would need a longstanding population of bats in frequent proximity with an intermediate host, which in turn must often cross paths with people. All these exchanges of virus must take place somewhere outside Wuhan, a busy metropolis which so far as is known is not a natural habitat of Rhinolophus bat colonies. The infected person (or animal) carrying this highly transmissible virus must have traveled to Wuhan without infecting anyone else. No one in his or her family got sick. If the person jumped on a train to Wuhan, no fellow passengers fell ill.
It’s a stretch, in other words, to get the pandemic to break out naturally outside Wuhan and then, without leaving any trace, to make its first appearance there.
For the lab escape scenario, a Wuhan origin for the virus is a no-brainer. Wuhan is home to China’s leading center of coronavirus research where, as noted above, researchers were genetically engineering bat coronaviruses to attack human cells. They were doing so under the minimal safety conditions of a BSL2 lab. If a virus with the unexpected infectiousness of SARS2 had been generated there, its escape would be no surprise.
-Mutation — a change in one of its RNA units — causes a different amino acid unit to be incorporated into its spike protein and makes the spike protein better able to attack the cells of some other species.
Through several more such mutation-driven adjustments, the virus adapts to its new host, say some animal with which bats are in frequent contact. The whole process then resumes as the virus moves from this intermediate host to people.
In the case of SARS1, researchers have documented the successive changes in its spike protein as the virus evolved step by step into a dangerous pathogen. After it had gotten from bats into civets, there were six further changes in its spike protein before it became a mild pathogen in people. After a further 14 changes, the virus was much better adapted to humans, and with a further four, the epidemic took off.
But when you look for the fingerprints of a similar transition in SARS2, a strange surprise awaits. The virus has changed hardly at all, at least until recently. From its very first appearance, it was well adapted to human cells. Researchers led by Alina Chan of the Broad Institute compared SARS2 with late stage SARS1, which by then was well adapted to human cells, and found that the two viruses were similarly well adapted. “By the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV,” they wrote.
Even those who think lab origin unlikely agree that SARS2 genomes are remarkably uniform. Baric writes that “early strains identified in Wuhan, China, showed limited genetic diversity, which suggests that the virus may have been introduced from a single source.”
A single source would of course be compatible with lab escape, less so with the massive variation and selection which is evolution’s hallmark way of doing business.
The uniform structure of SARS2 genomes gives no hint of any passage through an intermediate animal host, and no such host has been identified in nature.
- The furin cleavage site. The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first, called S1, recognizes the virus’s target, a protein called angiotensin converting enzyme-2 (or ACE2) which studs the surface of cells lining the human airways. The second, S2, helps the virus, once anchored to the cell, to fuse with the cell’s membrane. After the virus’s outer membrane has coalesced with that of the stricken cell, the viral genome is injected into the cell, hijacks its protein-making machinery and forces it to generate new viruses.
But this invasion cannot begin until the S1 and S2 subunits have been cut apart. And there, right at the S1/S2 junction, is the furin cleavage site that ensures the spike protein will be cleaved in exactly the right place.
The virus, a model of economic design, does not carry its own cleaver. It relies on the cell to do the cleaving for it. Human cells have a protein cutting tool on their surface known as furin. Furin will cut any protein chain that carries its signature target cutting site. This is the sequence of amino acid units proline-arginine-arginine-alanine, or PRRA in the code that refers to each amino acid by a letter of the alphabet. PRRA is the amino acid sequence at the core of SARS2’s furin cleavage site.
Viruses have all kinds of clever tricks, so why does the furin cleavage site stand out? Because of all known SARS-related beta-coronaviruses, only SARS2 possesses a furin cleavage site. All the other viruses have their S2 unit cleaved at a different site and by a different mechanism.
How then did SARS2 acquire its furin cleavage site? Either the site evolved naturally, or it was inserted by researchers at the S1/S2 junction in a gain-of-function experiment.
Consider natural origin first. Two ways viruses evolve are by mutation and by recombination. Mutation is the process of random change in DNA (or RNA for coronaviruses) that usually results in one amino acid in a protein chain being switched for another. Many of these changes harm the virus but natural selection retains the few that do something useful. Mutation is the process by which the SARS1 spike protein gradually switched its preferred target cells from those of bats to civets, and then to humans.
Mutation seems a less likely way for SARS2’s furin cleavage site to be generated, even though it can’t completely be ruled out. The site’s four amino acid units are all together, and all at just the right place in the S1/S2 junction. Mutation is a random process triggered by copying errors (when new viral genomes are being generated) or by chemical decay of genomic units. So it typically affects single amino acids at different spots in a protein chain. A string of amino acids like that of the furin cleavage site is much more likely to be acquired all together through a quite different process known as recombination.
Recombination is an inadvertent swapping of genomic material that occurs when two viruses happen to invade the same cell, and their progeny are assembled with bits and pieces of RNA belonging to the other. Beta-coronaviruses will only combine with other beta-coronaviruses but can acquire, by recombination, almost any genetic element present in the collective genomic pool. What they cannot acquire is an element the pool does not possess. And no known SARS-related beta-coronavirus, the class to which SARS2 belongs, possesses a furin cleavage site.
Proponents of natural emergence say SARS2 could have picked up the site from some as yet unknown beta-coronavirus. But bat SARS-related beta-coronaviruses evidently don’t need a furin cleavage site to infect bat cells, so there’s no great likelihood that any in fact possesses one, and indeed none has been found so far.
The proponents’ next argument is that SARS2 acquired its furin cleavage site from people. A predecessor of SARS2 could have been circulating in the human population for months or years until at some point it acquired a furin cleavage site from human cells. It would then have been ready to break out as a pandemic.
If this is what happened, there should be traces in hospital surveillance records of the people infected by the slowly evolving virus. But none has so far come to light. According to the WHO report on the origins of the virus, the sentinel hospitals in Hubei province, home of Wuhan, routinely monitor influenza-like illnesses and “no evidence to suggest substantial SARSCoV-2 transmission in the months preceding the outbreak in December was observed.”
So it’s hard to explain how the SARS2 virus picked up its furin cleavage site naturally, whether by mutation or recombination.
That leaves a gain-of-function experiment. For those who think SARS2 may have escaped from a lab, explaining the furin cleavage site is no problem at all. “Since 1992 the virology community has known that the one sure way to make a virus deadlier is to give it a furin cleavage site at the S1/S2 junction in the laboratory,” writes Steven Quay, a biotech entrepreneur interested in the origins of SARS2. “At least 11 gain-of-function experiments, adding a furin site to make a virus more infective, are published in the open literature, including [by] Dr. Zhengli Shi, head of coronavirus research at the Wuhan Institute of Virology.”
-For the lab escape scenario, the double CGG codon is no surprise. The human-preferred codon is routinely used in labs. So anyone who wanted to insert a furin cleavage site into the virus’s genome would synthesize the PRRA-making sequence in the lab and would be likely to use CGG codons to do so.
“When I first saw the furin cleavage site in the viral sequence, with its arginine codons, I said to my wife it was the smoking gun for the origin of the virus,” said David Baltimore, an eminent virologist and former president of CalTech. “These features make a powerful challenge to the idea of a natural origin for SARS2,” he said. [1]
In another article some Harvard expert said they were dismayed to learn some of the work was done as BSL-2, I'll see if I can find it.
But there's no proof for either theory at this point.
The geographical argument is utter rubbish. Humans get evolved bat viruses primarily through intermediate hosts.
Much of the rest seems to be reverse engineered to fit an agenda. For example, the idea that a furin cleveage site is a sure sign of lab involvement is nonsense - MERS has one.
https://www.sciencedirect.com/science/article/pii/S1873506120304165
Much of the rest seems to be reverse engineered to fit an agenda. For example, the idea that a furin cleveage site is a sure sign of lab involvement is nonsense - MERS has one.
https://www.sciencedirect.com/science/article/pii/S1873506120304165
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This is why I keep emphasizing the importance of the gold standard PCR test in this thread. Despite its convenience, LFTs have many inherent disadvantages and they can only be used as an adjunct to PCR.
Today is the first time for months that the UK has more new cases than Italy. Italy's are steadily falling of course, and have eventually reached UK levels.
It's encouraging for Italy, as the vaccine programme was very slow at first but is now going along well.
It's encouraging for Italy, as the vaccine programme was very slow at first but is now going along well.
All the far right commentators pushing the false narrative that suicides were were up massively this year, truth is it was down 20% on previous years, they have attributed it to the we are all in it together mentality.
Another month till the pubs reopen, we are doing that COVID passport which should see some of the polish anti vaccers at work get it hopefully, anyone know when 30 to 40s groups will be able to register in Ireland
Another month till the pubs reopen, we are doing that COVID passport which should see some of the polish anti vaccers at work get it hopefully, anyone know when 30 to 40s groups will be able to register in Ireland
I saw that Italy is opening up the jab for all over 16s, they must be in overdrive
45-49 registration opened up 10 days ago. 40-45 supposed to be open next week.
Surely it makes sense to delay the June 21st opening even more now with the clear increase in cases and hospitalisations going up too.
I think so. 4 weeks to ensure all over 50s have had two doses is what I’d do.
Seems like a no-brainer. You’ll be so close to fully opened up by then anyway the economic impact of a short delay should be trivial.
Feels inevitable to me, I think it will be pushed back to early July (think that's actually logical to study more on how pilots for sports and music events in middle of June go). And of course trying to get up to 50m vaccinated which should be possible for early July with pace of rollout. You're talking of well over 90% take up which is better than many predicted.
I never really expected anything to just end on June 21st anyway, did anyone really think compulsory mask wearing was just going to end there and then so have no issue with these restrictions stretching on for another few weeks while they monitor hospital admissions as there's still plenty you can do in day to day life compared to this time last year.
Here about 40% of symptomatic cases (not just hospitalisations) still had symptoms after 2 months. However, asymptomatic cases don't seem to be suffering from long covid, which isn't surprising. Of course we haven't had mass infection so we haven't had the same mass of young asymptomatic cases so symptomatic cases are a higher % overall here.
The Murdoch press was hammering that narrative during Melbournes lockdown.
Just made the Dan Andrews even more popular in the electorate.
Yes, but only in some regions. It depends where you live in Italy. Our region hasn't got there yet - my friend here had her first jab this week and she's 57.
It's a national vaccination plan, but the regions have a lot of leeway to tweak things.
Another protest in London today. 
They're down to over 30s with the vaccines now so you'd think it'd be safer to just delay the remaining easing a bit and encourage outdoor activity now the weather is (sort of) accepting that winter was meant to end 3 months ago. I don't think people will accept facing tougher restrictions again which is what they risk as the other alternative...although with this government that's probably exactly what will happen.
I think ideally you open up fully after eveyrone has at least been offered a vaccine and anyone in the over 50 group who chose to has had the first and second dose, but that might just be a little too far off on the horizon. I don't think there's anything trivial about any delay economically at this point unfortunately. A lot of jobs are hanging by a thread as it is...although the easing of restrictions we've already had should go some way to helping that hopefully.
Was going to start a thread on this.Another protest in London today.
I'm very pro rights/protesting when it's needed, but I know people that go to these and its literally just become an excuse to go out at this point because the festival/gig they wanted to go to can't happen. They pay lip service to the cause or whether protesting about it actually makes any sense, but as soon as you engage them in any debate it becomes clear they know feck all about it, never mind believe in it enough to be at a protest. I mean if you go to a protest about not being allowed to protest, and no one stops you from protesting, what are you actually protesting about? All you're going to do is piss everyone off and end up actually getting protests banned or restricted. No one I've spoken to who went to the "kill the bill" protest, had actually read the bill they were protesting about.
Extinction Rebellion already made this into a problem when they decided that protesting didn't have to make any sense or have a logical point anymore, and could literally just be about pissing as many people off as possible. Now these covid generation idiots are just going to make it very easy for the government/police to interpret the bill originally intended to stop stupid people glueing themselves to a bridge/train/airport, as a "beat up protesters whenever you want" licence. On top of that they've probably managed to kill a lot of people over the past year with their infection spreading.
Honestly one of the main things the past year has exposed is just how much stupid there is on BOTH sides of the fence.
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Late reaction but I was shocked to see how few people wore a mask in the Brentford vs Swansea game, and most of those who wore had worn it wrongly.
I think we're nearing the end of mask wearing now. I was in a small supermarket and half the people inside didn't have one on. Not even symbolically on their chin. Certainly none of the cahiers or store workers. The guard at the door wore one but wasn't stopping anyone else from entering without one.
a number of supermarkets in the UK have just had plastic barrier around the cashier, I suppose it does keep them safe from direct germ contact but I don't know how effective it is against the airborn component.
In any case with falling cases and more people being vaccinated, fewer people are going to bother with masks. Many weren't bothering at the height of the pandemic.
Bars a being forced to close now in Manchester because of covid cases. What is the point in the most vulnerable having thier jab and being protected if we are going to shut up shop every time this happens?
I thought they were closing because of positive cases in staff members, that led to the other staff getting instructions to self-isolate?
Has there been any research on whether the summer heat affects the spread of covid? Last summer here in Norway we basically went 3-4 months with almost no restrictions(apart from international travel and 1 meter distancing in bars etc). We had new reported covid cases every day, but things never really spiralled out of control. I wonder why that is?
If the heat does matter, then why has things gotten so out of control in India? Is it because of the mutations? Higher population density?
If the heat does matter, then why has things gotten so out of control in India? Is it because of the mutations? Higher population density?