Covid, Phase II. Commonsense is the order of the day. | Vital Football

Covid, Phase II. Commonsense is the order of the day.

Spursex

Alert Team
#1
Whilst I expect the vast majority to retain and use a modicum of commonsense, I fear a significant minority simply can't do it....

Anyway, for now, the lockdown is effectively over except for the most vulnerable amongst us - I thought that worthy of a new fresh Cornavirus thread:







CORONAVIRUS
Use common sense to prevent a second spike, Britons are urged

Lucy Fisher
Monday June 01 2020, 12.01am, The Times

It will take two to three weeks to know if lockdown has been eased too quickly
DOMINIC LIPINSKI/PA



The public have been told to play their part to avoid a second coronavirus spike after lockdown measures ease from today, because the “room for manoeuvre is quite limited”.
People from different households can now meet in groups of six, as long as they stay two metres apart.
The government is ready to impose local lockdowns if a rise in cases suddenly becomes apparent.

As Covid-19 continues to infect people across the globe, we track how the virus has spread from a few cases in China to thousands worldwide
Read the feature
Primary schools are set to reopen as are outdoor markets and car showrooms. More than two million vulnerable people who have been shielding since March will be allowed to spend time with other people outdoors.
Speaking at the daily Downing Street press conference yesterday Robert Jenrick, the housing secretary, said: “We’re reasonably confident that the steps we’ve taken and will be taking [today] are manageable but we have to all continue to play our part in that because the rate of infection remains somewhere between 0.7 and 0.9 and the room for manoeuvre is quite limited.


“We’ll obviously keep this under very close scrutiny as we move into this next phase and as we approach the next decision point on June 15.”
Dr Jenny Harries, the deputy chief medical officer for England, said that people should limit themselves to what was sensible rather than possible, and called for common sense to be deployed.
Some scientists suggested that the government was taking a risk by easing lockdown measures so soon. The Association of Directors of Public Health said that it was “not supported by the science” and that they were “increasingly concerned that the government is misjudging the balance of risk between more social interaction and the risk of a resurgence of the virus, and is easing too many restrictions too quickly”.
Peter Openshaw, an immunologist who sits on the government’s New and Emerging Respiratory Virus Threats Advisory Group, said “unlocking too fast carries a great risk”, and that the nation needed “to proceed with great, great care at this point”.
The impact of the government’s move to repeal restrictions today would only become visible in two to three weeks, he said.
“It’s going to be very patchy,” he told The Andrew Marr Show on BBC One. “It may be that actually easing lockdown is perfectly OK in areas like London which were hit early and hit hard, and where the epidemic seems to have been virtually passed in many parts of the community, with a few exceptions.
“But up north it’s still a very large number of cases. I think we need to be more subtle about the geography and we need to look at the particular areas where it may be appropriate to ease lockdown. Maybe there needs to be a bit more subtlety to the way in which lockdown is eased.”
Dominic Raab, the foreign secretary, acknowledged that “this is a sensitive moment”, but added: “We can’t just stay in lockdown for ever. We have got to transition.”
The government could not expect all scientists to agree on the right course of action in a pandemic situation, he said.
The latest lockdown easing is due to take place at a time when the nation is still at level four in the government’s Covid alert levels system, which represents an “epidemic in general circulation”, with transmission rates high or rising. At level three, the outbreak is deemed to be “in general circulation”.
Defending the decision to press ahead with lifting restrictions, Mr Raab told Sky News: “We’re transitioning from level four to level three. The R [virus reproduction] level is below one. The death rate, if you look at the trend data, is coming down,” he said.
He underlined the government’s resistance to reimposing a lockdown in England if there is a second rise in infections.
“What we really want to avoid is any re-entering of the lockdown,” he told the BBC. “If there’s any uptick in one particular locality or one particular setting, we’ve got the ability to take targeted measures.”
Daily coronavirus testing capacity reached 200,000 before the government’s deadline of the end of May, Matt Hancock, the health secretary, said.
A total of 205,634 tests were available on Saturday, including 40,000 antibody tests for NHS staff and care workers to determine whether they have had the virus, according to the Department for Health and Social Care.
It is unclear how many of the tests were actually carried out, however. Boris Johnson set the goal at the beginning of the month to double testing from 100,000 to 200,000 a day. Downing Street was accused of watering down the pledge after clarification that it referred to capacity rather than tests that were conducted.
What we can do from today
• Spend time outdoors, including in private gardens and other outdoor spaces, in groups of up to six people from different households, following social distancing guidelines.
• Visit car showrooms and outdoor markets.
• Send children to school or nursery if they are in early years, reception, year 1 or year 6, if your school is open.
• Professional athletes can also train and compete using the specified gyms, pools and sports facilities.
However, the public cannot:
• Visit friends and family inside their homes.
• Stay overnight away from your own home, except in a limited set of circumstances.
• Exercise in an indoor gym or go swimming in a public pool.
• Use an outdoor gym or playground.
• Gather outdoors in a group of more than six (excluding members of your own household).
 

Spursex

Alert Team
#3
Coronavirus May Be a Blood Vessel Disease, Which Explains Everything
Many of the infection’s bizarre symptoms have one thing in common

Part I


May 29 · 8 min read


In April, blood clots emerged as one of the many mysterious symptoms attributed to Covid-19, a disease that had initially been thought to largely affect the lungs in the form of pneumonia. Quickly after came reports of young people dying due to coronavirus-related strokes. Next it was Covid toes — painful red or purple digits.
What do all of these symptoms have in common? An impairment in blood circulation. Add in the fact that 40% of deaths from Covid-19 are related to cardiovascular complications, and the disease starts to look like a vascular infection instead of a purely respiratory one.
Months into the pandemic, there is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged.


“All these Covid-associated complications were a mystery. We see blood clotting, we see kidney damage, we see inflammation of the heart, we see stroke, we see encephalitis [swelling of the brain],” says William Li, MD, president of the Angiogenesis Foundation. “A whole myriad of seemingly unconnected phenomena that you do not normally see with SARS or H1N1 or, frankly, most infectious diseases.”
“If you start to put all of the data together that’s emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels],” says Mandeep Mehra, MD, medical director of the Brigham and Women’s Hospital Heart and Vascular Center.
In a paper published in April in the scientific journal The Lancet, Mehra and a team of scientists discovered that the SARS-CoV-2 virus can infect the endothelial cells that line the inside of blood vessels. Endothelial cells protect the cardiovascular system, and they release proteins that influence everything from blood clotting to the immune response. In the paper, the scientists showed damage to endothelial cells in the lungs, heart, kidneys, liver, and intestines in people with Covid-19.
“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” says Mehra.
A respiratory virus infecting blood cells and circulating through the body is virtually unheard of.​
A one-of-a-kind respiratory virus
SARS-CoV-2 is thought to enter the body through ACE2 receptors present on the surface of cells that line the respiratory tract in the nose and throat. Once in the lungs, the virus appears to move from the alveoli, the air sacs in the lung, into the blood vessels, which are also rich in ACE2 receptors.
“[The virus] enters the lung, it destroys the lung tissue, and people start coughing. The destruction of the lung tissue breaks open some blood vessels,” Mehra explains. “Then it starts to infect endothelial cell after endothelial cell, creates a local immune response, and inflames the endothelium.”
A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus, a sister coronavirus to the current infection, did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.


Benhur Lee, MD, a professor of microbiology at the Icahn School of Medicine at Mount Sinai, says the difference between SARS and SARS-CoV-2 likely stems from an extra protein each of the viruses requires to activate and spread. Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell. The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells.
“In SARS1, the protein that’s required to cleave it is likely present only in the lung environment, so that’s where it can replicate. To my knowledge, it doesn’t really go systemic,” Lee says. “[SARS-CoV-2] is cleaved by a protein called furin, and that’s a big danger because furin is present in all our cells, it’s ubiquitous.”
Endothelial damage could explain the virus’ weird symptoms
An infection of the blood vessels would explain many of the weird tendencies of the novel coronavirus, like the high rates of blood clots. Endothelial cells help regulate clot formation by sending out proteins that turn the coagulation system on or off. The cells also help ensure that blood flows smoothly and doesn’t get caught on any rough edges on the blood vessel walls.
“The endothelial cell layer is in part responsible for [clot] regulation, it inhibits clot formation through a variety of ways,” says Sanjum Sethi, MD, MPH, an interventional cardiologist at Columbia University Irving Medical Center. “If that’s disrupted, you could see why that may potentially promote clot formation.”
Endothelial damage might account for the high rates of cardiovascular damage and seemingly spontaneous heart attacks in people with Covid-19, too. Damage to endothelial cells causes inflammation in the blood vessels, and that can cause any plaque that’s accumulated to rupture, causing a heart attack. This means anyone who has plaque in their blood vessels that might normally have remained stable or been controlled with medication is suddenly at a much higher risk for a heart attack.
“Inflammation and endothelial dysfunction promote plaque rupture,” Sethi says. “Endothelial dysfunction is linked towards worse heart outcomes, in particular myocardial infarction or heart attack.”
Blood vessel damage could also explain why people with pre-existing conditions like high blood pressure, high cholesterol, diabetes, and heart disease are at a higher risk for severe complications from a virus that’s supposed to just infect the lungs. All of those diseases cause endothelial cell dysfunction, and the additional damage and inflammation in the blood vessels caused by the infection could push them over the edge and cause serious problems.


The theory could even solve the mystery of why ventilation often isn’t enough to help many Covid-19 patients breathe better. Moving air into the lungs, which ventilators help with, is only one part of the equation. The exchange of oxygen and carbon dioxide in the blood is just as important to provide the rest of the body with oxygen, and that process relies on functioning blood vessels in the lungs.
“If you have blood clots within the blood vessels that are required for complete oxygen exchange, even if you’re moving air in and out of the airways, [if] the circulation is blocked, the full benefits of mechanical ventilatory support are somewhat thwarted,” says Li.
A new paper published last week in the New England Journal of Medicine, on which Li is a co-author, found widespread evidence of blood clots and infection in the endothelial cells in the lungs of people who died from Covid-19. This was in stark contrast to people who died from H1N1, who had nine times fewer blood clots in the lungs. Even the structure of the blood vessels was different in the Covid-19 lungs, with many more new branches that likely formed after the original blood vessels were damaged.
“We saw blood clots everywhere,” Li says. “We were observing virus particles filling up the endothelial cell like filling up a gumball machine. The endothelial cell swells and the cell membrane starts to break down, and now you have a layer of injured endothelium.”
Finally, infection of the blood vessels may be how the virus travels through the body and infects other organs — something that’s atypical of respiratory infections.
“Endothelial cells connect the entire circulation [system], 60,000 miles worth of blood vessels throughout our body,” says Li. “Is this one way that Covid-19 can impact the brain, the heart, the Covid toe? Does SARS-CoV-2 traffic itself through the endothelial cells or get into the bloodstream this way? We don’t know the answer to that.”
In another paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival.​
If Covid-19 is a vascular disease, the best antiviral therapy might not be antiviral therapy
 

Spursex

Alert Team
#4
An alternative theory is that the blood clotting and symptoms in other organs are caused by inflammation in the body due to an over-reactive immune response — the so-called cytokine storm. This inflammatory reaction can occur in other respiratory illnesses and severe cases of pneumonia, which is why the initial reports of blood clots, heart complications, and neurological symptoms didn’t sound the alarm bells. However, the magnitude of the problems seen with Covid-19 appear to go beyond the inflammation experienced in other respiratory infections.
“There is some increased propensity, we think, of clotting happening with these [other] viruses. I think inflammation in general promotes that,” Sethi says. “Is this over and above or unique for SARS-CoV-2, or is that just because [the infection] is just that much more severe? I think those are all really good questions that unfortunately we don’t have the answer to yet.”
Anecdotally, Sethi says the number of requests he received as the director of the pulmonary embolism response team, which deals with blood clots in the lungs, in April 2020 was two to three times the number in April 2019. The question he’s now trying to answer is whether that’s because there were simply more patients at the hospital during that month, the peak of the pandemic, or if Covid-19 patients really do have a higher risk for blood clots.
“I suspect from what we see and what our preliminary data show is that this virus has an additional risk factor for blood clots, but I can’t prove that yet,” Sethi says.
The good news is that if Covid-19 is a vascular disease, there are existing drugs that can help protect against endothelial cell damage. In another New England Journal of Medicine paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival. Statins reduce the risk of heart attacks not only by lowering cholesterol or preventing plaque, they also stabilize existing plaque, meaning they’re less likely to rupture if someone is on the drugs.


“It turns out that both statins and ACE inhibitors are extremely protective on vascular dysfunction,” Mehra says. “Most of their benefit in the continuum of cardiovascular illness — be it high blood pressure, be it stroke, be it heart attack, be it arrhythmia, be it heart failure — in any situation the mechanism by which they protect the cardiovascular system starts with their ability to stabilize the endothelial cells.”
Mehra continues, “What we’re saying is that maybe the best antiviral therapy is not actually an antiviral therapy. The best therapy might actually be a drug that stabilizes the vascular endothelial. We’re building a drastically different concept.”
 

Harry-Kari

Vital Squad Member
#5
That’s in
An alternative theory is that the blood clotting and symptoms in other organs are caused by inflammation in the body due to an over-reactive immune response — the so-called cytokine storm. This inflammatory reaction can occur in other respiratory illnesses and severe cases of pneumonia, which is why the initial reports of blood clots, heart complications, and neurological symptoms didn’t sound the alarm bells. However, the magnitude of the problems seen with Covid-19 appear to go beyond the inflammation experienced in other respiratory infections.
“There is some increased propensity, we think, of clotting happening with these [other] viruses. I think inflammation in general promotes that,” Sethi says. “Is this over and above or unique for SARS-CoV-2, or is that just because [the infection] is just that much more severe? I think those are all really good questions that unfortunately we don’t have the answer to yet.”
Anecdotally, Sethi says the number of requests he received as the director of the pulmonary embolism response team, which deals with blood clots in the lungs, in April 2020 was two to three times the number in April 2019. The question he’s now trying to answer is whether that’s because there were simply more patients at the hospital during that month, the peak of the pandemic, or if Covid-19 patients really do have a higher risk for blood clots.
“I suspect from what we see and what our preliminary data show is that this virus has an additional risk factor for blood clots, but I can’t prove that yet,” Sethi says.
The good news is that if Covid-19 is a vascular disease, there are existing drugs that can help protect against endothelial cell damage. In another New England Journal of Medicine paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival. Statins reduce the risk of heart attacks not only by lowering cholesterol or preventing plaque, they also stabilize existing plaque, meaning they’re less likely to rupture if someone is on the drugs.
“It turns out that both statins and ACE inhibitors are extremely protective on vascular dysfunction,” Mehra says. “Most of their benefit in the continuum of cardiovascular illness — be it high blood pressure, be it stroke, be it heart attack, be it arrhythmia, be it heart failure — in any situation the mechanism by which they protect the cardiovascular system starts with their ability to stabilize the endothelial cells.”
Mehra continues, “What we’re saying is that maybe the best antiviral therapy is not actually an antiviral therapy. The best therapy might actually be a drug that stabilizes the vascular endothelial. We’re building a drastically different concept.”
That’s interesting maybe affects the current vaccine developments, but doesn’t explain why so many people are asymptomatic or only have mild illnesses, which is what the Cambridge scientists are currently exploring.
 

Harry-Kari

Vital Squad Member
#6
Also, if true, to my non-scientific brain it suggests the possibility of an engineered virus rather than a natural one, which would have explosive repercussions.
 

Pompey Yid

Vital Youth Team
#7
I am happy today, though I have kept my worries quiet, my missus, who is top of the tree vunerable, has been more unwell for about a week, so we were worrying she may have got you know what, god know's from where though, but hey ho this morning we got a call from her Doctor telling her all was ok and that her problem was an afverse effect brought on by the latest meds she had been prescribed and was to stop taking them immediately, new stuff was on way, so all smiles again, phew.
 

Spursex

Alert Team
#8
Also, if true, to my non-scientific brain it suggests the possibility of an engineered virus rather than a natural one, which would have explosive repercussions.
The engineered hypothesis has been widely explored, and no matter what corner of the World you're from the scientific community have widely dismissed it - apparently there would be specific tell - tale signs, and there aren't, it would suit the rest of the World if they could prove it one suspects, as it really would be the catalyst to go to stage 2 of punishing the chinese.
 

Spursex

Alert Team
#9
(Fusion Medical Animation/Unsplash)

HEALTH
Scientists Are Tired of Explaining Why The COVID-19 Virus Was Not Made in a Lab

JACINTA BOWLER
20 APRIL 2020

It's a rumour that just won't die. When asked whether the COVID-19 virus was genetically engineered in a lab, scientists have already said "no" rather firmly, but the matter of the new coronavirus' origin is unlikely to be put to rest so easily.

Discussions around this subject have become even more pertinent since US government intelligence officials are reportedly investigating the potential source of the pandemic, focussing on theories that it may have originated in a laboratory, despite all evidence pointing to SARS-CoV-2 not being human-made.
"All evidence so far points to the fact the COVID-19 virus is naturally derived and not man-made," explains immunologist Nigel McMillan from the Menzies Health Institute Queensland.
"If you were going to design it in a lab the sequence changes make no sense as all previous evidence would tell you it would make the virus worse. No system exists in the lab to make some of the changes found."
Back in late March, we covered a study published in Nature Medicine, in which the researchers investigated the genomic data of SARS-CoV-2 - particularly the receptor-binding domain (RBD) sections of the virus - to try and discover how it mutated into the virulent and deadly version we're currently struggling to contain.
As a by-product of their research, they were able to determine that SARS-CoV-2 was not genetically manipulated.

"By comparing the available genome sequence data for known coronavirus strains, we can firmly determine that SARS-CoV-2 originated through natural processes," one of the researchers, Scripps Research immunologist Kristian Andersen, said at the time.
"Two features of the virus, the mutations in the RBD portion of the spike protein and its distinct backbone, rules out laboratory manipulation as a potential origin for SARS-CoV-2."
Although it is clear the virus was not created in the lab, there have been ongoing concerns it may have 'escaped' a research facility, with most of the speculation - understandably - focussed on the Wuhan Institute of Virology (WIV). However, it remains just speculation. The Washington Post recently reported that US embassy officials had safety concerns about the lab back in 2018, and the institute did keep a closely related bat virus - but even that's far from a smoking gun.
"The closest known relative of SARS-CoV-2 is a bat virus named RaTG13, which was kept at the WIV. There is some unfounded speculation that this virus was the origin of SARS-CoV-2," explains University of Sydney evolutionary virologist, Edward Holmes.

"However, RaTG13 was sampled from a different province of China (Yunnan) to where COVID-19 first appeared and the level of genome sequence divergence between SARS-CoV-2 and RaTG13 is equivalent to an average of 50 years (and at least 20 years) of evolutionary change."
Now, it is important to note that viruses can mutate naturally anywhere - in animal hosts, in humans, or even in laboratory cell cultures. Unfortunately, it's difficult to determine where and how the new coronavirus acquired its mutations, although most researchers think the process involved an animal host.
Additionally, researchers are still investigating if the necessary mutations for causing the new disease occurred before or after SARS-CoV-2 made the jump to humans.
The institute at the centre of the controversy has repeatedly denied accusations of being the source of the pandemic. Back in March, head of bat coronavirus research at WIV, Shi Zhengli, explained that when she first received samples from early COVID-19 patients, she immediately did a thorough investigation at her department, finding no match between the viruses her lab had been working on, and COVID-19 patients.
"That really took a load off my mind," she told Scientific American. "I had not slept a wink for days."
What experts do agree on is that a pandemic like this is no surprise. Scientists have been warning governments for years that a new disease was on the horizon, and that many countries were woefully under-prepared.
For example, the director of the US National Institute of Allergy and Infectious Diseases, Anthony Fauci, told the incoming US government administration in January 2017 about the inevitability of a "surprise outbreak", urging them to make preparations.
"We've been aware for some time that another coronavirus, like SARS and MERS before it, could cause a pandemic, and so in many ways, the emergence of a new coronavirus with pandemic potential is not a surprise," explains La Trobe University epidemiologist Hassan Vally.
"We have to be careful to not aid those irresponsibly using this global crisis for political point-scoring by giving any oxygen to these and other rumours."
 

Nick Real Deal

Vital Football Legend
#10
Is there any possibility the virus could have been cultured in a lab by only using animal victims. ? So fine tuning and worsening by natural process. A concentrated attempt to find a virulent strain may be easier and quicker in a lab than in the wild left to chance.
 
#12
Is there any possibility the virus could have been cultured in a lab by only using animal victims. ? So fine tuning and worsening by natural process. A concentrated attempt to find a virulent strain may be easier and quicker in a lab than in the wild left to chance.
You should apply the law of Parsimony, or as some prefer it, Occam's Razor.
 

Nick Real Deal

Vital Football Legend
#13
You should apply the law of Parsimony, or as some prefer it, Occam's Razor.
The simplistic explanation is often the right one !! By not humanly interfering with the mutation they are in the clear. But constant breeding and nurturing of animals with the disease could throw up new strains. Inter breeding of dogs with physical traits can cause illness and deformities.
 
#14
The simplistic explanation is often the right one !! By not humanly interfering with the mutation they are in the clear. But constant breeding and nurturing of animals with the disease could throw up new strains. Inter breeding of dogs with physical traits can cause illness and deformities.
You've missed the point: why 'help' build a virus that is has no inbuilt prejudice?

You'd be nuts to do it, and the Chinese are pragmatists above all else, it's been one of their gudiing principles for the past 40 years and it's served them well; creating anything that fucked up their 100 year anniversary plan, just wouldn't be on their agenda, even if they were mad enough to not care what they created.
 

Nick Real Deal

Vital Football Legend
#16
You've missed the point: why 'help' build a virus that is has no inbuilt prejudice?

You'd be nuts to do it, and the Chinese are pragmatists above all else, it's been one of their gudiing principles for the past 40 years and it's served them well; creating anything that fucked up their 100 year anniversary plan, just wouldn't be on their agenda, even if they were mad enough to not care what they created.
It depends what inbuilt prejudice means. The virus targets certain groups. In comparison very few have died in China compared to other Countries especially with large populations. China it seems were ready for it.
It depends on the definition of Nuts also. The regime operates with suppression of it's people. Look what's happening in Hong Kong.
 
#17
Ethical guidelines for infecting COVID-19 vaccine trial volunteers

  • Richards AD
  • J Med Ethics
  • 27 May 2020


An article published in the Journal of Medical Ethics sets out ethical guidelines for human trials of candidate COVID-19 vaccine.

Dr Adair Richards, an Associate Professor at the University of Warwick, said it is now incumbent on regulators, researchers and ethicists to work together quickly to consider whether or not it is ethically acceptable to conduct human challenge experiments with COVID-19, and if so, how best to do it.

He argues that deliberately infecting an individual with SARS-CoV-2 is necessary to speed up the process of vaccine development and potentially save many lives. And, he says, this can be done ethically.

“Deliberately infecting volunteers with a disease as dangerous as COVID-19 has previously been considered to be unethical by the research community. However I believe that the current global situation is so different to those previously faced, that it is ethical in this case,” said Dr Richards.

The research analyses each of the common arguments against these types of experiments including the risk of harm to volunteers; the risk of non-useable vaccine; the validity of a volunteer’s informed consent; the reputational risk to research; and that this could be a slippery slope to increasingly unethical research.

Dr Richards demonstrates that these arguments can be overcome. We do not need to lower our ethical standards to permit these types of experiment if sufficient ethical safeguards are put in place.

“Not to consider these issues now would be a dereliction of our moral responsibility to society,” he said.
 

Greavswasthegreatest

Vital Football Legend
#18
Finally got response to my test.....so scompleted it and sent it back,...got results
it came back negative...withloads of caveat so what does tht tell me...I aint got it at this precise moment in time of the test ...have I had it...not part of the test...what doies that tell me sweet FA
 
#19
Finally got response to my test.....so scompleted it and sent it back,...got results
it came back negative...withloads of caveat so what does tht tell me...I aint got it at this precise moment in time of the test ...have I had it...not part of the test...what doies that tell me sweet FA
Just means you haven't got it - be grateful for that and keep calm and carry on!
 

Harry-Kari

Vital Squad Member
#20
The engineered hypothesis has been widely explored, and no matter what corner of the World you're from the scientific community have widely dismissed it - apparently there would be specific tell - tale signs, and there aren't, it would suit the rest of the World if they could prove it one suspects, as it really would be the catalyst to go to stage 2 of punishing the chinese.
I understand that is the widespread opinion but wonder if that is based upon work done prior to the discovery that the protein used by Covid-19 to access the body is furin which is contained in every endothelial cell as opposed to previous Corona viruses which use a protein found almost exclusively in the lungs...natural evolution maybe or not?