Evidence now suggests herd immunity likely impossible without a vaccine

[rabas]

27 minutes ago, Heppinger said:

They also fail to stipulate the difference between covid-19 and coronavirus.   I guess if people knew that a coronavirus can include the common cold then they wouldn't be scared sh*tless and so keen to relinquish their freedoms.

Most common colds are not caused by coronavirus.  Coronaviruses that do cause colds do not bond to ACE2 receptors, except the very recent NL63, which not surprisingly causes more severe illness.

 

Severe, acute, respiratory syndrome SARS viruses do bond to ACE2 receptors. SARS-2 bonds to ACE2 exceptionally well causing its very high interactivity. 

 

So, it's OK to be scared enough to protect yourself and others. A bit silly listening to others telling you not to.

[Monomial]

3 hours ago, J Town said:

They're not even considered a living thing.

 

They are, however, considered organic. And unlike dirt, they evolve just as life evolves in a way that will maximize the strains that are most likely to survive. You can look at this as a form of rudimentary intelligence, albeit one easily explained by simple processes and mathematics and dependent on random fluctuations rather than specific intent.

 

So "dangerous dirt" is a bad analogy. Dirt doesn't change and react to your actions. A virus can.

[checkered flag]

1 hour ago, Jingthing said:

Very true. Also they are completely apolitical and don't have a concept of borders. 

The topic of this thread you started is about herd immunity. Has it evolved to something else or are you off topic?

[partington]

2 hours ago, Logosone said:

This.

 

And yes, of course we are on the way to herd immunity, how could it be otherwise?

 

It is possible the immunity will not last forever, but immunity is a fact.

 

Of course there are 5000 coronaviruses that were found in bats, the chances of future, more deadly viruses can not be discounted.

 

What are the odds, when the planet is vastly overpopulated with old and obese people that a virus appears that strikes down old and obese people? Michel Foucault when told of the AIDS virus refused to believe it, 'it's too perfect' he said. Same again now.

Michel Foucault knew Foucault about viruses.

Edited July 18, 2020 by partington

[rumak]

6 hours ago, rabas said:

Viruses definitely have memory in their genes, which is how they learn to infect new things and replicate more efficiently. It  decides what and how to infect based on past experience. Viruses  are particularly good at evolving because they easily change their encoded memory.

Change a few words and you have a fairly accurate description of how some genders can take

advantage of another gender.  From my observations that other gender does not appear able to

produce enough antibodies to reverse this process.

note:  a vaccine does not seem likely in the near future.  a slap in the head by a friend has been

shown to have minimal effect on the outcome

[rumak]

23 minutes ago, checkered flag said:

The topic of this thread you started is about herd immunity. Has it evolved to something else or are you off topic?

hahaha   calling him out on his own game !    good work

[partington]

6 hours ago, rabas said:

You don't need a human like brain for life, memory, or learning. Any replicating system with genetic codes can remember, evolve, and make strategic decisions. An amoeba has no brain yet searches for food, decides what to eat, avoids danger, and evolves to become a better amoeba.

 

Viruses definitely have memory in their genes, which is how they learn to infect new things and replicate more efficiently. It  decides what and how to infect based on past experience. Viruses  are particularly good at evolving because they easily change their encoded memory. IOW, they learn easily.

 

SARS2 seems to be rather smart. Just today:

Scientists identify six different types of coronavirus with increasing severity levels

 

This is nonsensically bad reporting by the way. Scientist have NOT identified six different types of coronavirus with increasing severity levels.

 

They have found that people infected with the same virus - SARS-CoV2 - show disease symptoms that can be grouped into six major groups according to type and severity. It is a classification of different physiological responses to the same virus.

 

There is no implcation or evidence whatsoever that these differences are caused by different types of virus: they are caused by different immune and related reponses within different individuals.

[rabas]

1 hour ago, partington said:

This is nonsensically bad reporting by the way. Scientist have NOT identified six different types of coronavirus with increasing severity levels.

 

They have found that people infected with the same virus - SARS-CoV2 - show disease symptoms that can be grouped into six major groups according to type and severity. It is a classification of different physiological responses to the same virus.

 

There is no implcation or evidence whatsoever that these differences are caused by different types of virus: they are caused by different immune and related reponses within different individuals.

Yes, it is nonsensically bad and you are 100% correct. What they meant was distinct types COVID-19 disease.

 

[cmarshall]

11 hours ago, ukrules said:

We do seem to be forgetting about something here, a very large percentage of the population don't get ill at all with this virus, and plenty appear to have a mild 'inconvenience' of an infection which passes quickly and easily.

 

This is already immunity in a large percentage of the population, the question is what causes it, do we have this immunity already and if not, how to get it?

 

Looking back into history we know that immunity can and does happen from 'similar' viruses, a major example being that of cowpox and smallpox. The mild generally non lethal cowpox was found to prevent the much more lethal smallpox - it stopped it dead and that was back in the 1700's.

 

Whatever immune response happened when someone caught cowpox, often dairy farmers when it was first noticed, protected against a subsequent smallpox infection, they simply didn't get it.

 

This means they had an acquired immunity.

 

Something similar is going on with COVID, we're already on the way to herd immunity as there are a lot of what they call 'asymptomatics' being found when contact trace tests are being done. Technically they're infected as they breathed it in but the test is almost certainly detecting the rna from the dead virus particles that are left behind after the immediate immune response destroyed it. This leaves them without an illness but with a positive test.

 

The PCR test was never designed to be a diagnostic and the Nobel prize winning inventor warned against this at the time.

 

I'm sure there are plenty of scientists out there looking for the virus which does what cowpox did for smallpox - induce immunity. Something that induces immunity can be thought of as a natural vaccine - like cowpox.

 

We know about the previous 4 coronarivus colds but that doesn't mean there's not plenty more of them, after all 2 of them were only found recently. There is speculation that there could be plenty more coronaviruses doing the rounds for centuries and we would never really know about them as they're so harmless.

 

Here's a recent link for some light reading : https://www.technologynetworks.com/immunology/news/common-cold-coronaviruses-could-help-produce-anti-sars-cov-2-immune-cells-337504

 

 

You fail to understand some basic concepts.  It's true that a large number of people who are infected with Covid-19 do not develop symptoms.  Being asymptomatic, however, is quite different from "being immune."  Asymptomatics are definitely not immune, because they are infected and can transmit the virus to other people not all of whom will themselves be asymptomatic.

 

As I have pointed out there is research that suggests that infection with Covid-19 does not result in long-lasting immunity which is consistent with what is known about other coronaviruses.  If there is no individual immunity then there is no herd immunity.  While some scientist like Dr. Haseltine accept this as a fact, there is no consensus yet in the scientific community as a whole.  But what is clear is that the possibility of herd immunity for Covid-10 has never been scientifically established making criminally negligent the policies of the British and Swedish governments which committed to a high death rate in pursuit of herd immunity.  My own view is that, because of what is known about the family of coronaviruses, lasting immunity or herd immunity is unlikely and should not be assumed.

 

The article cited describes research that points out that Covid infection produces T cells.  It's not known if those T cells responsive to the Covid virus persist, but in any case while T cells play a role in immune response they do not prevent reinfection and so do not provide immunity.  If they do persist, T cells might reduce the severity of the infection.  It's not at all surprising the Covid infection produces a T cell response, but the critical issue remains, does that T cell response persist and, if so, how long?

 

The antibodies that are responsible for immunity against subsequent infection are neutralizing antibodies.  Here is the abstract from a paper by British researchers that suggests that the neutralizing antibodies from Covid are "transient," i.e. do not last long, which they point out is just like other coronaviruses.

 

Antibody (Ab) responses to SARS-CoV-2 can be detected in most infected individuals 10-15
30 days following the onset of COVID-19 symptoms. However, due to the recent emergence of
31 this virus in the human population it is not yet known how long these Ab responses will be
32 maintained or whether they will provide protection from re-infection. Using sequential serum
33 samples collected up to 94 days post onset of symptoms (POS) from 65 RT-qPCR confirmed
34 SARS-CoV-2-infected individuals, we show seroconversion in >95% of cases and neutralizing
35 antibody (nAb) responses when sampled beyond 8 days POS. We demonstrate that the
36 magnitude of the nAb response is dependent upon the disease severity, but this does not
37 affect the kinetics of the nAb response. Declining nAb titres were observed during the follow
38 up period. Whilst some individuals with high peak ID50 (>10,000) maintained titres >1,000 at
39 >60 days POS, some with lower peak ID50 had titres approaching baseline within the follow
40 up period. A similar decline in nAb titres was also observed in a cohort of seropositive
41 healthcare workers from Guy’s and St Thomas’ Hospitals. We suggest that this transient nAb
42 response is a feature shared by both a SARS-CoV-2 infection that causes low disease severity
43 and the circulating seasonal coronaviruses that are associated with common colds. This study
44 has important implications when considering widespread serological testing, Ab protection
45 against re-infection with SARS-CoV-2 and the durability of vaccine protection.
 

https://www.medrxiv.org/content/10.1101/2020.07.09.20148429v1.full.pdf

 

 

[cmarshall]

Dr. Haseltine has a new article out in Forbes Magazine and on his blog.  This article focuses on why developing a vaccine against Sars-Cov-2 will be exceptionally difficult (or impossible.)  Here is an excerpt:

 

There are hints that coronaviruses, SARS-CoV-2 included, may employ several immune evasion techniques. We already know that SARS-CoV-2 does produce one or more proteins that actively interfere with immune function. The orf-3b gene product specifically interferes with precisely those signals impotent for initiating the production of anti-viral antibodies and T-cells. The orf3b protein down-regulates the production of interferon-gamma and IL-2, both necessary for initiating the production of anti-viral antibodies and T-cells.

The ability of orf3b to interfere with immune activation is very likely the tip of a very large iceberg when it comes to altering the immune response. At least 9 SARS virus proteins and 6 MERS virus proteins are known to interfere with the host immune response. It is very likely that SARS-CoV-2 also carries a full complement of similar genes that collectively may help explain three usual features of infection, antibody-negative convalescents, rapidly fading antibody levels, and re-infection.

 

If the suggestion turns out to be true then it would mean that unlike the flu virus which mutates to get around the body's immune response from the last flu infection, Sars-Cov-2 may disable the immune response making mutations unnecessary and immunity impossible.  If that is true then we can look forward either to annual lethal Sars-Cov-2 pandemics in places like Thailand which have successfully managed this year's outbreak or, in countries like the US which have spectacularly failed to do so, the virus will become endemic, i.e. it never goes away.

 

https://www.forbes.com/sites/williamhaseltine/2020/07/16/what-does-disappearing-immunity-to-covid-19-mean-for-a-vaccine/#21d45df49ed8

 

[GroveHillWanderer]

14 hours ago, Heppinger said:

They also fail to stipulate the difference between covid-19 and coronavirus.   I guess if people knew that a coronavirus can include the common cold then they wouldn't be scared sh*tless and so keen to relinquish their freedoms.

That's a ridiculous argument. It's like saying that if people knew that the Reston virus belongs to the same family of viruses as Ebola (filoviruses) but does not cause any serious illness in humans, then they needn't be afraid of contracting the Ebola virus. Just because one member of a virus family is relatively non-lethal, doesn't have any bearing on how lethal the others are.

Edited July 19, 2020 by GroveHillWanderer

[simple1]

On 7/16/2020 at 2:03 PM, Jingthing said:

A couple of related points including some good news. 

 

For the crowd that is still cheerleading for natural herd immunity super hot infection zones like Florida may provide some cause for celebration. 

 

While personally I think exponential infection zones are tragic, there is a bright side. 

 

When live population testing begins on promising vaccines that process can be sped up alot by doing the tests in the hot infection zones. 

 

Also if such testing can be done on US populations the tricky politics of exporting such testing colonial style to third world countries can be avoided. 

 

Also there is always the x factor of mutations. Viruses main impetus is to keep infecting as many people as people. That's best done with a less lethal virus because if a virus kills people right away the host isn't helping perpetuate new infections. The point being that although mutations can be towards more or less lethality my sources say less lethal is more likely. 

So although mass infections may not bring about natural herd immunity they might result in a dominant mutation more like a cold. Of course this would totally depend on dumb luck to happen. 

Trump Administration Aims to Block New Funding for Testing and Tracing

 

https://www.nytimes.com/2020/07/18/world/coronavirus-news.html

[ukrules]

13 hours ago, cmarshall said:

Asymptomatics are definitely not immune, because they are infected and can transmit the virus to other people not all of whom will themselves be asymptomatic.

That's a giant leap of faith there and includes a lot of assumptions.

 

The fools in the medical profession who've been pushing this 'asymptomatic transmission' narrative will one day be mocked and ridiculed for their naivete.

 

Like I mentioned in my post anyone who breathes it in will have cells that become infected, this process is being 'nipped in the bud' by the immune system in a lot of people so it doesn't get to the symptom stage of infection.

 

Those 'asymptomatic spreaders' are a myth, they have detectable covid particles left over since the immune system destroyed them and test positive, the rest is hysteria.

 

Looking at investigations of clusters of infections from various countries, she said that where an asymptomatic case had been followed up it was "very rare" to find secondary infections among their contacts.

 

That's because it doesn't generally happen and when it does the person may have had very mild symptoms (as in they didn't even notice it) before beating the disease.

 

Quote from : https://www.bbc.com/news/health-52977940

[Oliver Holzerfilled]

14 hours ago, cmarshall said:

Dr. Haseltine has a new article out in Forbes Magazine and on his blog.  This article focuses on why developing a vaccine against Sars-Cov-2 will be exceptionally difficult (or impossible.)  Here is an excerpt:

 

There are hints that coronaviruses, SARS-CoV-2 included, may employ several immune evasion techniques. We already know that SARS-CoV-2 does produce one or more proteins that actively interfere with immune function. The orf-3b gene product specifically interferes with precisely those signals impotent for initiating the production of anti-viral antibodies and T-cells. The orf3b protein down-regulates the production of interferon-gamma and IL-2, both necessary for initiating the production of anti-viral antibodies and T-cells.

The ability of orf3b to interfere with immune activation is very likely the tip of a very large iceberg when it comes to altering the immune response. At least 9 SARS virus proteins and 6 MERS virus proteins are known to interfere with the host immune response. It is very likely that SARS-CoV-2 also carries a full complement of similar genes that collectively may help explain three usual features of infection, antibody-negative convalescents, rapidly fading antibody levels, and re-infection.

 

If the suggestion turns out to be true then it would mean that unlike the flu virus which mutates to get around the body's immune response from the last flu infection, Sars-Cov-2 may disable the immune response making mutations unnecessary and immunity impossible.  If that is true then we can look forward either to annual lethal Sars-Cov-2 pandemics in places like Thailand which have successfully managed this year's outbreak or, in countries like the US which have spectacularly failed to do so, the virus will become endemic, i.e. it never goes away.

 

https://www.forbes.com/sites/williamhaseltine/2020/07/16/what-does-disappearing-immunity-to-covid-19-mean-for-a-vaccine/#21d45df49ed8

 

You've inserted the word "impossible" twice into your own analysis. Where in the article does he suggest vaccine induced immunity is impossible? 

[Logosone]

16 hours ago, cmarshall said:

You fail to understand some basic concepts.  It's true that a large number of people who are infected with Covid-19 do not develop symptoms.  Being asymptomatic, however, is quite different from "being immune."  Asymptomatics are definitely not immune, because they are infected and can transmit the virus to other people not all of whom will themselves be asymptomatic.

 

 

You fail to understand some basic concepts. Firstly, you can not get "infected with Covid19".

 

You get infected with the virus, SARS Cov2. Then there is the illness Covid19.

 

Those who get the virus and are asymptomatic are most definitely immune, namely from the illness Covid19. Immunity refers to an illness.

 

Asymptomatic transmission has been shown to occur in 0-2.3% of cases. It's minute.

Edited July 19, 2020 by Logosone

[partington]

15 hours ago, cmarshall said:

Dr. Haseltine has a new article out in Forbes Magazine and on his blog.  This article focuses on why developing a vaccine against Sars-Cov-2 will be exceptionally difficult (or impossible.)  Here is an excerpt:

 

There are hints that coronaviruses, SARS-CoV-2 included, may employ several immune evasion techniques. We already know that SARS-CoV-2 does produce one or more proteins that actively interfere with immune function. The orf-3b gene product specifically interferes with precisely those signals impotent for initiating the production of anti-viral antibodies and T-cells. The orf3b protein down-regulates the production of interferon-gamma and IL-2, both necessary for initiating the production of anti-viral antibodies and T-cells.

The ability of orf3b to interfere with immune activation is very likely the tip of a very large iceberg when it comes to altering the immune response. At least 9 SARS virus proteins and 6 MERS virus proteins are known to interfere with the host immune response. It is very likely that SARS-CoV-2 also carries a full complement of similar genes that collectively may help explain three usual features of infection, antibody-negative convalescents, rapidly fading antibody levels, and re-infection.

 

If the suggestion turns out to be true then it would mean that unlike the flu virus which mutates to get around the body's immune response from the last flu infection, Sars-Cov-2 may disable the immune response making mutations unnecessary and immunity impossible.  If that is true then we can look forward either to annual lethal Sars-Cov-2 pandemics in places like Thailand which have successfully managed this year's outbreak or, in countries like the US which have spectacularly failed to do so, the virus will become endemic, i.e. it never goes away.

 

https://www.forbes.com/sites/williamhaseltine/2020/07/16/what-does-disappearing-immunity-to-covid-19-mean-for-a-vaccine/#21d45df49ed8

 

I have no idea who the Haseltine you quote is, and have not bothered to look him up, but the whole premise seems logically flawed. It doesn't matter if during an infection the virus triggers synthesis of proteins that can inhibit or slow down the immune response, because a vaccine doesn't.

 

The whole point of a vaccine is that it is NOT an infection. When you inject a vaccine that consists, for example, of the spike protein of SARS-Cov2, it is intended to trigger a vigorous immune response that produces both a rising neutralising antibody titre, and a set of T-cells which will attack  virus-infected cells, and which will be stored as memory T-cells in lymph nodes, to undergo rapid replication in a subsequent infection.

 

Neither of these immune responses to the vaccine can or will be inhibited by the orf-3b or any other viral proteins, because they are simply not there, and not produced. 

 

In the absence of the viral proteins that may inhibit and shorten an immune response, a vaccine can, and is likely to, produce a much more robust immune response than a real infection would. So the response to a vaccine is NOT the same as the response to a viral infection.

 

 

[cmarshall]

 

7 hours ago, partington said:

I have no idea who the Haseltine you quote is, and have not bothered to look him up, but the whole premise seems logically flawed. It doesn't matter if during an infection the virus triggers synthesis of proteins that can inhibit or slow down the immune response, because a vaccine doesn't.

 

The whole point of a vaccine is that it is NOT an infection. When you inject a vaccine that consists, for example, of the spike protein of SARS-Cov2, it is intended to trigger a vigorous immune response that produces both a rising neutralising antibody titre, and a set of T-cells which will attack  virus-infected cells, and which will be stored as memory T-cells in lymph nodes, to undergo rapid replication in a subsequent infection.

 

Neither of these immune responses to the vaccine can or will be inhibited by the orf-3b or any other viral proteins, because they are simply not there, and not produced. 

 

In the absence of the viral proteins that may inhibit and shorten an immune response, a vaccine can, and is likely to, produce a much more robust immune response than a real infection would. So the response to a vaccine is NOT the same as the response to a viral infection.

 

 

This is a good question.

 

The discussion of orf-3b in particular is just an example of how one viral protein in Sars-Cov2 can defeat the production of neutralizing antibodies and does not comprise the whole of the immunosuppressant capabilities of the virus.  As Hazeltine speculates:

 

The ability of orf3b to interfere with immune activation is very likely the tip of a very large iceberg when it comes to altering the immune response. At least 9 SARS virus proteins and 6 MERS virus proteins are known to interfere with the host immune response. It is very likely that SARS-CoV-2 also carries a full complement of similar genes that collectively may help explain three usual features of infection, antibody-negative convalescents, rapidly fading antibody levels, and re-infection.

 

So the problem for the vaccine designer is to use a variant of some protein from Sars-Cov2 that effectively stimulates the desired immune response without also enabling some mechanism to defeat it, if possible.  There may be some way to achieve this, but they were not able to do so for coronaviruses SARS, MERS, or the four coronaviruses that produces colds all of which exhibit the same immunosuppressant effects.  The cold-producing coronaviruses apparently account for 30% of seasonal colds, so we can conclude the failure to develop a vaccine against them is not from lack of economic incentive.

[checkered flag]

18 minutes ago, cmarshall said:

 

This is a good question.

 

The discussion of orf-3b in particular is just an example of how one viral protein in Sars-Cov2 can defeat the production of neutralizing antibodies and does not comprise the whole of the immunosuppressant capabilities of the virus.  As Hazeltine speculates:

 

The ability of orf3b to interfere with immune activation is very likely the tip of a very large iceberg when it comes to altering the immune response. At least 9 SARS virus proteins and 6 MERS virus proteins are known to interfere with the host immune response. It is very likely that SARS-CoV-2 also carries a full complement of similar genes that collectively may help explain three usual features of infection, antibody-negative convalescents, rapidly fading antibody levels, and re-infection.

 

So the problem for the vaccine designer is to use a variant of some protein from Sars-Cov2 that effectively stimulates the desired immune response without also enabling some mechanism to defeat it, if possible.  There may be some way to achieve this, but they were not able to do so for coronaviruses SARS, MERS, or the four coronaviruses that produces colds all of which exhibit the same immunosuppressant effects.  The cold-producing coronaviruses apparently account for 30% of seasonal colds, so we can conclude the failure to develop a vaccine against them is not from lack of economic incentive.

Is this guy Hazeltine related to CMarshal or something. Relying on one source is not responsible reporting. If he's only speculating (as stated) it needs reliable confirmation.

[partington]

1 hour ago, cmarshall said:

 

This is a good question.

 

The discussion of orf-3b in particular is just an example of how one viral protein in Sars-Cov2 can defeat the production of neutralizing antibodies and does not comprise the whole of the immunosuppressant capabilities of the virus.  As Hazeltine speculates:

 

The ability of orf3b to interfere with immune activation is very likely the tip of a very large iceberg when it comes to altering the immune response. At least 9 SARS virus proteins and 6 MERS virus proteins are known to interfere with the host immune response. It is very likely that SARS-CoV-2 also carries a full complement of similar genes that collectively may help explain three usual features of infection, antibody-negative convalescents, rapidly fading antibody levels, and re-infection.

 

So the problem for the vaccine designer is to use a variant of some protein from Sars-Cov2 that effectively stimulates the desired immune response without also enabling some mechanism to defeat it, if possible.  There may be some way to achieve this, but they were not able to do so for coronaviruses SARS, MERS, or the four coronaviruses that produces colds all of which exhibit the same immunosuppressant effects.  The cold-producing coronaviruses apparently account for 30% of seasonal colds, so we can conclude the failure to develop a vaccine against them is not from lack of economic incentive.

You seem to be ignoring the logical point that the proteins responsible for the immunosuppressant effects are simply not present in a vaccine, and there is no way for a vaccine to produce them. Therefore an immune response to a vaccine will just not be suppressed in this way. It's not tricky or difficult-the proteins he mentions , and any others that potentially have the same effect just aren't  there, so the vaccine simply cannot enable this mechanism to defeat it . The immune response is caused by the vaccine and is not suppressed.

 

 

 SARS and MERS vaccine research largely stopped because these infections stopped, not because vaccines were tried and failed, so this point also doesn't actually tell you anything at all about how successful  any vaccines to these diseases might be. In fact there is a current MERS vaccine in development that does show a robust immune response in human trials.

 

 

Most colds are not coronavirus induced,  and  there are at least four different very common coronaviruses that cause colds as well as several other less common ones  that also cause colds. There is limited incentive for development of vaccines against  only 30% of colds, each of which may have to raise immune responses against 5 to 6 different coronaviruses, and a very difficult prospect.

 

 

 

Edited July 20, 2020 by partington

[rabas]

26 minutes ago, partington said:

You seem to be ignoring the logical point that the proteins responsible for the immunosuppressant effects are simply not present in a vaccine, and there is no way for a vaccine to produce them. Therefore an immune response to a vaccine will just not be suppressed in this way. It's not tricky or difficult-the proteins he mentions , and any others that potentially have the same effect just aren't  there, so the vaccine simply cannot enable this mechanism to defeat it . The immune response is caused by the vaccine and is not suppressed.

Thank you for clear explanations. Speaking of viral proteins triggering  immunosuppressant effects, can you comment on this report and paper? I am not a viral person but it seems to say that SARS-2 oddly lacks one set of extra-cellular immunosuppressant mechanisms that most all viruses have. How would this impact immunity, etc?

 

Summary article in Stat

https://www.statnews.com/2020/05/21/coronavirus-hijacks-cells-in-unique-ways/

Original paper in Cell.

https://www.cell.com/cell/fulltext/S0092-8674(20)30489-X

 

[cmarshall]

24 minutes ago, partington said:

You seem to be ignoring the logical point that the proteins responsible for the immunosuppressant effects are simply not present in a vaccine, and there is no way for a vaccine to produce them. Therefore an immune response to a vaccine will just not be suppressed in this way. It's not tricky or difficult-the proteins he mentions , and any others that potentially have the same effect just aren't  there, so the vaccine simply cannot enable this mechanism to defeat it . The immune response is caused by the vaccine and is not suppressed.

 

 

 SARS and MERS vaccine research largely stopped because these infections stopped, not because vaccines were tried and failed, so this point also doesn't actually tell you anything at all about how successful  any vaccines to these diseases might be. In fact there is a current MERS vaccine in development that does show a robust immune response in human trials.

 

 

Most colds are not coronavirus induced,  and  there are at least four different very common coronaviruses that cause colds as well as several other less common ones  that also cause colds. There is limited incentive for development of vaccines against  only 30% of colds, each of which may have to raise immune responses against 5 to 6 different coronaviruses, and a very difficult prospect.

 

 

 

You are assuming that without the immunosuppressive proteins attached to sabotage the result, there is some other Sars-Cov2 protein that, when delivered in a vaccine, will stimulate a lasting immune response. But how do we know that?  We only know they haven't found one yet.

 

The SARS pandemic began on Nov. 16, 2002 with the last new cases reported in May, 2004, a total of 17 months compared to the probably 8 months so far of Sars-Cov2 and that was 16 years ago.  The SARS virus has not been eradicated and could still break out again.  If work on a MERS virus has continued after its suppression, work may also have continued against SARS which killed many more people, but we don't hear of any success.  The history of vaccine efforts against coronaviruses is not dispositive, but neither is it encouraging.

 

The first successful vaccine against any coronavirus will establish proof of concept.  Until then there is no scientific basis to expect a successful vaccine against Sars-Cov2.  Certainly not enough to base current public policy on it.  If every disease were susceptible to a vaccine, we wouldn't have to worrry about HIV, malaria, and dengue among other diseases without vaccines that have large affected populations with the concomitant economic incentives.

 

[checkered flag]

50 minutes ago, cmarshall said:

You are assuming that without the immunosuppressive proteins attached to sabotage the result, there is some other Sars-Cov2 protein that, when delivered in a vaccine, will stimulate a lasting immune response. But how do we know that?  We only know they haven't found one yet.

 

The SARS pandemic began on Nov. 16, 2002 with the last new cases reported in May, 2004, a total of 17 months compared to the probably 8 months so far of Sars-Cov2 and that was 16 years ago.  The SARS virus has not been eradicated and could still break out again.  If work on a MERS virus has continued after its suppression, work may also have continued against SARS which killed many more people, but we don't hear of any success.  The history of vaccine efforts against coronaviruses is not dispositive, but neither is it encouraging.

 

The first successful vaccine against any coronavirus will establish proof of concept.  Until then there is no scientific basis to expect a successful vaccine against Sars-Cov2.  Certainly not enough to base current public policy on it.  If every disease were susceptible to a vaccine, we wouldn't have to worrry about HIV, malaria, and dengue among other diseases without vaccines that have large affected populations with the concomitant economic incentives.

 

Malaria is a protozoan disease and is quite different from viral diseases. People do develop partial immunity (with P. falciparum) if they maintain a latent infection. Given a radical cure the immunity is quickly lost. This was observed in Africa when WHO campaigned to eliminate malaria.

Dr Haseltine has written a lot and was part of a Chinese/American group looking at Covid19 (Feb 2020) at a time China refused to let CDC officials into China. So something isn't adding up. Additionally he didn't dispute the notion or Herd immunity but said it would take a long time with many deaths. That said what happened in China that they could reopen very soon, is a big question. Lastly, because Dr Haseltine writes so much, I think CMarshall cherry picks what agrees with his preconceived points and ignores the rest.

As I said before confirmation by recognized unbiased experts is needed. 

[Jingthing]

Here is some new positive evidence that there will be long term immunity even though antibodies quickly go away after being infected the the novel Coronavirus --

 

 

 

[checkered flag]

2 hours ago, Jingthing said:

Here is some new positive evidence that there will be long term immunity even though antibodies quickly go away after being infected the the novel Coronavirus --

 

 

 

So you are now in the U turn lane regarding herd immunity or are you simply retrolling this subject?

[GroveHillWanderer]

23 hours ago, cmarshall said:

You are assuming that without the immunosuppressive proteins attached to sabotage the result, there is some other Sars-Cov2 protein that, when delivered in a vaccine, will stimulate a lasting immune response. But how do we know that?  We only know they haven't found one yet.

 

The SARS pandemic began on Nov. 16, 2002 with the last new cases reported in May, 2004, a total of 17 months compared to the probably 8 months so far of Sars-Cov2 and that was 16 years ago.  The SARS virus has not been eradicated and could still break out again.  If work on a MERS virus has continued after its suppression, work may also have continued against SARS which killed many more people, but we don't hear of any success.  The history of vaccine efforts against coronaviruses is not dispositive, but neither is it encouraging.

 

The first successful vaccine against any coronavirus will establish proof of concept.  Until then there is no scientific basis to expect a successful vaccine against Sars-Cov2.  Certainly not enough to base current public policy on it.  If every disease were susceptible to a vaccine, we wouldn't have to worrry about HIV, malaria, and dengue among other diseases without vaccines that have large affected populations with the concomitant economic incentives.

 

It's true we don't know whether a SARS-CoV-2 vaccine can produce a long-lasting immune response, simply because not enough time has elapsed since human trials of them started but we do know a vaccine can elicit a very powerful immune response - the published results from Pfizer's candidate vaccine showed it can induce the production of neutralising antibodies at a level up to 46 times higher than that found in convalescent plasma.
 
I'm not sure what you mean by MERS being suppressed - after an initial spike in the first year it emerged, it's still killing people at the same rate now, as it has been doing for the last 7 years. And although it hasn't been licensed yet, there is a MERS vaccine currently undergoing phase 1 human trials in Saudi Arabia, which has shown promising results in all phases of its development so far. In fact it was developed by Oxford University and their current candidate vaccine for CoVid-19 is essentially identical, with just a slight change where they inserted the genetic code for the SARS-Cov-2 spike protein in place of the one for MERS.  
 
So as the Oxford team says, there are very good reasons to be hopeful that their CoViD-19 vaccine will succeed (although of course it's not guaranteed) based on their experience with the MERS vaccine.
 
Incidentally, there's not been a single trace of the SARS virus for 16 years now, so although there are some samples still kept in laboratories, it's a pretty safe bet that it has been eradicated for all practical purposes. As an article in MedicalXpress puts it:
 
"It is clear that our response to SARS-CoV-1 led to the extinction of that lineage of viruses in humans."
 
 

 

[checkered flag]

On 7/21/2020 at 8:42 AM, GroveHillWanderer said:

It's true we don't know whether a SARS-CoV-2 vaccine can produce a long-lasting immune response, simply because not enough time has elapsed since human trials of them started but we do know a vaccine can elicit a very powerful immune response - the published results from Pfizer's candidate vaccine showed it can induce the production of neutralising antibodies at a level up to 46 times higher than that found in convalescent plasma.
 
I'm not sure what you mean by MERS being suppressed - after an initial spike in the first year it emerged, it's still killing people at the same rate now, as it has been doing for the last 7 years. And although it hasn't been licensed yet, there is a MERS vaccine currently undergoing phase 1 human trials in Saudi Arabia, which has shown promising results in all phases of its development so far. In fact it was developed by Oxford University and their current candidate vaccine for CoVid-19 is essentially identical, with just a slight change where they inserted the genetic code for the SARS-Cov-2 spike protein in place of the one for MERS.  
 
So as the Oxford team says, there are very good reasons to be hopeful that their CoViD-19 vaccine will succeed (although of course it's not guaranteed) based on their experience with the MERS vaccine.
 
Incidentally, there's not been a single trace of the SARS virus for 16 years now, so although there are some samples still kept in laboratories, it's a pretty safe bet that it has been eradicated for all practical purposes. As an article in MedicalXpress puts it:
 
"It is clear that our response to SARS-CoV-1 led to the extinction of that lineage of viruses in humans."
 
 

 

The T cells response is the key to long term immunity. The T cells store the antibody information that's released if re-exposed. This is pretty basic in immunology.

[GroveHillWanderer]

2 hours ago, checkered flag said:

The T cells response is the key to long term immunity. The T cells store the antibody information that's released if re-exposed. This is pretty basic in immunology.

Yes, that's why it's encouraging that both the Oxford and CanSino vaccines that announced results this week, elicited a powerful T cell response, as well as neutralising antibodies.

[Rancid]

On 7/16/2020 at 8:42 AM, thaibeachlovers said:

That was just the first wave. They are set to do far, far better in the second, third etc waves to come having got further down the herd immunity track.

Every country that locked down has a population with very little immunity. Vaccine for 8 billion- dream on.

Exactly, lock downs never claimed to save lives, they just relieve pressure from the health system. What they do though is spread the virus out over a much longer period, death toll will be the same.

 

As such Sweden should see most of the damage already done, with a relatively intact economy. Those that locked down will see ongoing infections and deaths for months to come, but with shattered economies.

 

With no vaccine the virus has to run out of hosts to end, herd immunity. In locked down countries still plenty to infect. Lets also bear in mind flu vaccines are generally not anywhere near  100% effective, and no one has ever made a successful corona vaccine. Why pining for a vaccine is the rational of an imbecile.

[farang51]

8 minutes ago, Rancid said:

Exactly, lock downs never claimed to save lives, they just relieve pressure from the health system. What they do though is spread the virus out over a much longer period, death toll will be the same.

Even if you are right (which I don't think you are) then you are wrong about the death toll. We have better treatments now and will have even better treatments later, and we now know a lot more about how to protect the vulnerable. In Sweden, they will have had a lot of people that didn't need to die.

[GroveHillWanderer]

1 hour ago, Rancid said:

Lets also bear in mind flu vaccines are generally not anywhere near  100% effective, and no one has ever made a successful corona vaccine. Why pining for a vaccine is the rational of an imbecile.

How successful flu vaccines are, has no influence on how successful a SARS-CoV-2 vaccine might be. Different virus types and different vaccine development parameters.

 

As to nobody having made a successful coronavirus vaccine previously, that's a bit of a red herring. There has never been a high enough level of medical necessity or financial resources going into the development of a coronavirus vaccine before. The common cold coronaviruses are not lethal enough, SARS died out (and the funding dried up) before a vaccine could be finalised and MERS remains limited in both geographical spread and number of fatalities (less than 200 per year on average) so again, not a massive, massive priority in global terms. Despite that, a MERS vaccine which has come through all its previous development steps with flying colours, is currently undergoing testing in Saudi Arabia and may eventually prove successful.

Edited July 22, 2020 by GroveHillWanderer