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Posted (edited)
4 hours ago, Brewster67 said:

Even the chief professor of epidemiology at Oxford University has come out and said the figures are alarmingly massaged, her and dozens of doctors and scientists in the virology field are all saying the same... the figures are being falsified.

These kinds of arguments are ridiculous. You write as if the scientific community are all supporting your argument. There are plenty of epidemiologists who are wrestling with the issues caused by this virus because there are so many unknowns. The oxford University paper I assume you are referencing was not peer reviewed and many epidemiologists disagreed with it. What figures do you think were falsified?

Edited by chessman
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4 hours ago, Brewster67 said:

That's the sort of thing idiots post when they have absolutely no argument that holds up to scrutiny.

Here is some research on the COVID-19 virus itself. There are more than 1 type of test based around this very virus, it isn't a scam and people who claim so are not just wrong, but promoting dangerous disinformation during a pandemic. 

 

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies and biochemical experiments SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides, which additionally led to the predicted acquisition of three O-linked glycans around the site.

 

1. Mutations in the receptor-binding domain of SARS-CoV-2

The receptor-binding domain (RBD) in the spike protein is the most variable part of the coronavirus genome, Six RBD amino acids have been shown to be critical for binding to ACE2 receptors and for determining the host range of SARS-CoV-like viruses. With coordinates based on SARS-CoV, they are Y442, L472, N479, D480, T487 and Y4911, which correspond to L455, F486, Q493, S494, N501 and Y505 in SARS-CoV-2. Five of these six residues differ between SARS-CoV-2 and SARS-CoV. On the basis of structural studies and biochemical experiments, SARS-CoV-2 seems to have an RBD that binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology.

 

While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

 

2. Polybasic furin cleavage site and O-linked glycans

The second notable feature of SARS-CoV-2 is a polybasic cleavage site (RRAR) at the junction of S1 and S2, the two subunits of the spike. This allows effective cleavage by furin and other proteases and has a role in determining viral infectivity and host range. In addition, a leading proline is also inserted at this site in SARS-CoV-2; thus, the inserted sequence is PRRA. The turn created by the proline is predicted to result in the addition of O-linked glycans to S673, T678 and S686, which flank the cleavage site and are unique to SARS-CoV-2. Polybasic cleavage sites have not been observed in related ‘lineage B’ betacoronaviruses, although other human betacoronaviruses, including HKU1 (lineage A), have those sites and predicted O-linked glycans. Given the level of genetic variation in the spike, it is likely that SARS-CoV-2-like viruses with partial or full polybasic cleavage sites will be discovered in other species.

 

The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown, and it will be important to determine its impact on transmissibility and pathogenesis in animal models. Experiments with SARS-CoV have shown that insertion of a furin cleavage site at the S1–S2 junction enhances cell–cell fusion without affecting viral entry. In addition, efficient cleavage of the MERS-CoV spike enables MERS-like coronaviruses from bats to infect human cells. In avian influenza viruses, rapid replication and transmission in highly dense chicken populations selects for the acquisition of polybasic cleavage sites in the hemagglutinin (HA) protein which serves a function similar to that of the coronavirus spike protein. Acquisition of polybasic cleavage sites in HA, by insertion or recombination, converts low-pathogenicity avian influenza viruses into highly pathogenic forms. The acquisition of polybasic cleavage sites by HA has also been observed after repeated passage in cell culture or through animals.

 

The function of the predicted O-linked glycans is unclear, but they could create a ‘mucin-like domain’ that shields epitopes or key residues on the SARS-CoV-2 spike protein. Several viruses utilize mucin-like domains as glycan shields involved immunoevasion. Although prediction of O-linked glycosylation is robust, experimental studies are needed to determine if these sites are used in SARS-CoV-2

 

Conclusions

In the midst of the global COVID-19 public-health emergency, it is reasonable to wonder why the origins of the pandemic matter. Detailed understanding of how an animal virus jumped species boundaries to infect humans so productively will help in the prevention of future zoonotic events. For example, if SARS-CoV-2 pre-adapted in another animal species, then there is the risk of future re-emergence events. In contrast, if the adaptive process occurred in humans, then even if repeated zoonotic transfers occur, they are unlikely to take off without the same series of mutations. In addition, identifying the closest viral relatives of SARS-CoV-2 circulating in animals will greatly assist studies of viral function. Indeed, the availability of the RaTG13 bat sequence helped reveal key RBD mutations and the polybasic cleavage site.

 

The genomic features described here may explain in part the infectiousness and transmissibility of SARS-CoV-2 in humans. Although the evidence shows that SARS-CoV-2 is not a purposefully manipulated virus, it is currently impossible to prove or disprove the other theories of its origin described here. However, since we observed all notable SARS-CoV-2 features, including the optimized RBD and polybasic cleavage site, in related coronaviruses in nature, we do not believe that any type of laboratory-based scenario is plausible.

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The odd thing to me is after 9-11, after Hurricane Katrina in the U.S. we saw families crying, people who lost loved ones interviewed, all sorts of personal stories of loss. 

9-11 killed about 2900.  Covid 19 has killed over 8,000 in the USA and no news stories I can find online or see on TV has shown grieving families, loved ones.  No stories?  What is up with that?

If you want to ensure that people stay at home, show personal stories, interview those that have had their lives devastated after losing a loved one, show mothers with children crying over the loss of their husband/father to the virus. That will let people know this is serious.  Numbers on a board just dont always sink in

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It's a bit silly arguing over this graph, that graph, this report, that report..... 

People are dying and more will die, that's a fact.

More people will die from suicides, murders and malnutrition by the time the governments let everyone out to play again though... That's an opinion 🙄

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12 hours ago, Brewster67 said:

The MSM keeps publishing FAKE NEWS... Look how often they use the term 'tested positive for Covid-19'.... 

 

The tests are NOT showing Covid-19, they are showing 'coronavirus'.... Cold and flu will also show coronavirus present.

 

the Covid-19 testing requires a pathology lab examination of the sample and they are NOT being done.

 

My niece works in the path lab in a Colchester, UK Hospital, and she says they are not even testing fellow staff let alone the public.

 

The vast amount of deaths being blamed on Covid-19 are just not true, the overwhelming majority of deaths are very old people who have 2,3 or 4 health conditions and their immune systems are shot to bits and they were always going to die the next time they caught a cold or flu.

 

Even the chief professor of epidemiology at Oxford University has come out and said the figures are alarmingly massaged, her and dozens of doctors and scientists in the virology field are all saying the same... the figures are being falsified.

 

IT'S ALL A SCAM..... WAKE UP!

No basis for US suing China for 20 trillion then. Let me ask for you to be called in as a key witness for defense.

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14 hours ago, CanadaSam said:

So, 1 guy out of 1 hundred will die.  And in fact, the old and sick.  Do we really need to worry all that much about it?

Tell that to widow of the 30 year old male

Mother and father of the 13 year old boy and several others around the world with no underlying health issues under the age 50

The numbers who contracted MERS was much smaller than those currently infected with this virus

MERS Monthly Summary, November 2019 At the end of November 2019, a total of 2494 laboratory-confirmed cases of Middle East respiratory syndrome (MERS), including 858 associated deaths (case-fatality rate: 34.4%) were reported globally; the majority of these cases were reported from Saudi Arabia (2102 cases, including 780 related deaths with a case-fatality rate of 37.1%).

https://www.who.int/emergencies/mers-cov/en/

 

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1 minute ago, PatOngo said:

Please send my regards to your parents!

 

Do you know his folks ?? Small world hey...

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Posted (edited)
8 hours ago, chessman said:

Even the chief professor of epidemiology at Oxford University has come out and said the figures are alarmingly massaged, her and dozens of doctors and scientists in the virology field are all saying the same... the figures are being falsified.

This the actual wording:

The same weekend Johnson did his volte face, an Oxford University team led by Sunetra Gupta, a professor of theoretical epidemiology, pointed out that figures on the morbidity of Covid-19 were virtually meaningless in the absence of testing. They suggested that half the population could have had already it mildly, which, if true, would imply the death rate was far lower than thought. Were that the case, it might seem more sensible to throw resources at the NHS and merely encourage people to avoid crowds rather than shut down the economy.

 

https://www.theguardian.com/commentisfree/2020/apr/02/wrong-coronavirus-world-scientists-optimism-experts

 

Edited by RJRS1301
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Posted (edited)
18 minutes ago, RJRS1301 said:

This the actual wording:

The same weekend Johnson did his volte face, an Oxford University team led by Sunetra Gupta, a professor of theoretical epidemiology, pointed out that figures on the morbidity of Covid-19 were virtually meaningless in the absence of testing. They suggested that half the population could have had already it mildly, which, if true, would imply the death rate was far lower than thought. Were that the case, it might seem more sensible to throw resources at the NHS and merely encourage people to avoid crowds rather than shut down the economy.

 

https://www.theguardian.com/commentisfree/2020/apr/02/wrong-coronavirus-world-scientists-optimism-experts

 

Then by all means if a correct assumption on the part of this doctor, and that is an assumption, and you know what happens when you assume....you make an ass-out-of u-and-me., Let the mass testing begin.....Sorry, but my post it towards the statements and not the poster himself

Edited by ThailandRyan

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Posted (edited)
11 minutes ago, ThailandRyan said:

Then by all means if a correct assumption on his part, and that is an assumption, and you know what happens when you assume....you make an ass-out-of u-and-me., Let the mass testing begin.....

Please read the post I was atempting  to correct incorrect information stated:

 

Even the chief professor of epidemiology at Oxford University has come out and said the figures are alarmingly massaged, her and dozens of doctors and scientists in the virology field are all saying the same... the figures are being falsified.

 

I was not supporting any theory/hypothosis what so ever

Edited by RJRS1301
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Posted (edited)
16 minutes ago, RJRS1301 said:

This the actual wording:

The same weekend Johnson did his volte face, an Oxford University team led by Sunetra Gupta, a professor of theoretical epidemiology, pointed out that figures on the morbidity of Covid-19 were virtually meaningless in the absence of testing. They suggested that half the population could have had already it mildly, which, if true, would imply the death rate was far lower than thought. Were that the case, it might seem more sensible to throw resources at the NHS and merely encourage people to avoid crowds rather than shut down the economy.

 

https://www.theguardian.com/commentisfree/2020/apr/02/wrong-coronavirus-world-scientists-optimism-experts

 

So much for experts talking to MSM. This is a nonsensical statement because if half of the population already had it, then the total case curves would look vastly different. Go look at prediction curves at the half way point. The rising exponentials we do see are characteristic of early stages.

Edited by rabas
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