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Duda Jarek

Covid-19 vaccines thread

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2 hours ago, Delberty said:

What percentage of the UK's 68 million people were tested?  

The fact is that only sick people are or were being tested, the 90 percent who were infected like my entire family were not counted.  This is not like the flu where 100 percent of those infected have horrible symptoms for 1 to 3 weeks

I can't do that because I do not have a doctor

All doctors do is lie so that we get more tests

I saw the info on TV several times, one must remember that no one knows if the immunity is permanent or if not for how long it will last or will it apply to new strains.  Officially the government still wants everyone to be terrified of talking to a neighbor

There is a lot of false information there. 

-Without testing you do not know what you had. Making medical assumption based on gut feeling is really bad idea. 

-Influenza is not 100% symptomatic. Estimates are difficult (for obvious reasons). Longitudinal tests based on serological studies tend to estimate above 75% of asymptomatic cases (e.g. Hayward et al. Lancet 2014) . Note that influenza is much better investigated than COVID-19 and there are still a lot of unknowns and with influenza there are widely divergent estimates. The only thing we know with certainty is that your assertion is entirely unfounded.

-  Asserting that your feeling trumps actual data via testing is utterly ridiculous. Of course MDs should order tests. One might call it evidence-based medicine or just common sense. Acting on anything else is basically endangering oneself and others.

- The unknown regarding immunity is actually correct. We only have limited data suggesting that there may be immunity, but we need to collect more. Also serological testing (but not, say gut feeling) can provide additional evidence of duration of immunity.

 

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3 hours ago, Delberty said:

All doctors do is lie so that we get more tests

!

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Slurs or prejudice against any group of people (or person) are prohibited. You can do better than such generalizations.

 

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3 hours ago, Delberty said:

What percentage of the UK's 68 million people were tested?  

The fact is that only sick people are or were being tested, the 90 percent who were infected like my entire family were not counted.  This is not like the flu where 100 percent of those infected have horrible symptoms for 1 to 3 weeks

I can't do that because I do not have a doctor

All doctors do is lie so that we get more tests

I saw the info on TV several times, one must remember that no one knows if the immunity is permanent or if not for how long it will last or will it apply to new strains.  Officially the government still wants everyone to be terrified of talking to a neighbor

Why do you think this? (bolded part)

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42 minutes ago, StringJunky said:

Why do you think this? (bolded part)

 

!

Moderator Note

A question best answered elsewhere, lest this thread continue to get dragged off topic. 

 

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Are there any reasons to more or less hopeful of current expedited/heavily-funded/heavily-fast-tracked  COVID-19 vaccine projects (being efficacious) when the CDC reveals the following stats re: myriad flu vaccine efficacy in prev season/years:

US Flu VE Data for 2018-2019 (note relatively poor %total effectiveness, esp in +50 yo)

https://www.cdc.gov/flu/vaccines-work/2018-2019.html

https://www.cdc.gov/flu/vaccines-work/past-seasons-estimates.html

 

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There is little relation between these observations. For influenza a challenge is that there are numerous strains and the annual vaccines are designed around the modeling of which strains migh be dominant. There are years where the predictions fail or when something really unexpected happen. Now SARS-CoV-2, has a significantly lower mutation rate than influenza. While different variants have been detected to since the outbreak, the changes were fairly minor among the dominant variants. Most vaccines target conserved parts of the virus which so far did not seem to vary much. However, there are other challenges surrounding the development of a new vaccine, of course.

So to re-iterate, I do not see any information from influenza vaccines that we could meaningfully translate  to COVID-19.

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38 minutes ago, CharonY said:

There is little relation between these observations. For influenza a challenge is that there are numerous strains and the annual vaccines are designed around the modeling of which strains migh be dominant. There are years where the predictions fail or when something really unexpected happen. Now SARS-CoV-2, has a significantly lower mutation rate than influenza. While different variants have been detected to since the outbreak, the changes were fairly minor among the dominant variants. Most vaccines target conserved parts of the virus which so far did not seem to vary much. However, there are other challenges surrounding the development of a new vaccine, of course.

So to re-iterate, I do not see any information from influenza vaccines that we could meaningfully translate  to COVID-19.

Hmmm ... so both (influenza and corona), being RNA viruses, don't share too much wrt "recombination" ???

Let's say the current human-volunteer vaccine trials of COVID-19 do produce some positive results. Antibodies are isolated and a vaccine is developed. Are you suggesting this might be a treatment with, say,  >40% efficacy (which is about the avg for seasonal flu vacc).

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1 hour ago, invasive-feces said:

Hmmm ... so both (influenza and corona), being RNA viruses, don't share too much wrt "recombination" ???

Their genomes are quite different and critically, SARS-CoV-2 has a proof-reading enzyme that cuts down on replication errors and hence, mutation rate.

Quote

Are you suggesting this might be a treatment with, say,  >40% efficacy (which is about the avg for seasonal flu vacc).

It is utterly unknown. Could be between 0-100%.

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Good day to all...

What is the proper word for a single 'cell', 'protein', 'virus', 'microbe', 'molecule', microorganism', 'nucleus', ... of the covid19 ?

If one and only one single covid19 'protein' is placed in a healthy person; comparing the effects of someone else infected with hundreds or thousands from a 'massive sneeze' exposure.

Is the infection expected to be different in magnitude, requiering much less treatment, medications, and posing less death risks for the single exposure ?   Or the single virus 'protein' will self replicate/multiply to a certain count in order to take over the host ?

If infection by one single virus count is not lethal and can be treated/managed with much less fatality;  and can be singled/separated (as by microscope) to inoculate a person, would that be a sort of vaccine ?

Does the virus stops multiplying by some reason (like being a powerful enough force to kill now, no more needed🙄) in the infected person ? 

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7 hours ago, Externet said:

What is the proper word for a single 'cell', 'protein', 'virus', 'microbe', 'molecule', microorganism', 'nucleus', ... of the covid19 ?

A single virus particles is called a virion.

Yes, the number of virions you are exposed to (the "viral load") affects the risk, and possibly the severity, of infection. But I'll leave someone more knowledgable to answer those questions.

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Thanks for educating me. It smelled like it had to have a name.

Then one single virion particle infecting a healthy person compared to a multitude of virions infecting another person.   Repeating the previous post, then,

Is the infection expected to be different in magnitude, requiering much less treatment, medications, and posing less death risks for the single virion exposure ?   Or the single virion will self replicate/multiply to a certain count in order to take over the host ?

If infection by one single virion is not lethal and can be treated/managed with much less fatality;  and can be singled/separated (as by microscope) to inoculate a person, would that be a sort of vaccine ?

Does the virion stops multiplying by some reason (like being a powerful enough force to kill now, no more needed🙄) in the infected person ? 

 

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Infections are to some degree stochastic, but there is the concept of the minimum infective dose, which indicates the minimum dose required to infect someone. However, it is actually a fair bit more compicated as folks rarely quantify individual virus particles, which is difficult. In practice, many virology labs use a tissue-based quatification system which cell destruction using dilutions of a a virus dilution. The dilution at which 50% of the tissue show damages or other cytopathic effects are then defined as the TCID50. I.e. the actual particle count is often not actually known.

However, a single particle is highly unlikely to elicit any kind of meaning full effect, you need quite a few more than that. How many, depends a lot on virus and host factors. I seem to recall that I found an estimate of as low as ~200 virus particles in the cases of some coronaviruses, but frankly I do not recall it very well and may be mistaken.

That being said, there is support for for single-hit models, in e.g. noroviruses. They are more theoretical and assume that the virus slip through all defensive barriers and reach their target fully functional. Effectively more than than one particle are needed for exposure, but this model have some what different dose response models compared to the more simple one which only looks at exposure and outcome.

If the question is whether the mere exposure to a single virus is sufficient to create immunity, the answer is no. Acquired immunity requires sensing of a significant amount of antigens through a process called seroconversion. So it would only work if the virus in your body replicates sufficiently trigger first the primary infection (which is not associated with immune responses) and then persist enough to lead to to the buildup of immunological memory.

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Posted (edited)
17 minutes ago, CharonY said:

Infections are to some degree stochastic, but there is the concept of the minimum infective dose, which indicates the minimum dose required to infect someone. However, it is actually a fair bit more compicated as folks rarely quantify individual virus particles, which is difficult. In practice, many virology labs use a tissue-based quatification system which cell destruction using dilutions of a a virus dilution. The dilution at which 50% of the tissue show damages or other cytopathic effects are then defined as the TCID50. I.e. the actual particle count is often not actually known.

However, a single particle is highly unlikely to elicit any kind of meaning full effect, you need quite a few more than that. How many, depends a lot on virus and host factors. I seem to recall that I found an estimate of as low as ~200 virus particles in the cases of some coronaviruses, but frankly I do not recall it very well and may be mistaken.

That being said, there is support for for single-hit models, in e.g. noroviruses. They are more theoretical and assume that the virus slip through all defensive barriers and reach their target fully functional. Effectively more than than one particle are needed for exposure, but this model have some what different dose response models compared to the more simple one which only looks at exposure and outcome.

If the question is whether the mere exposure to a single virus is sufficient to create immunity, the answer is no. Acquired immunity requires sensing of a significant amount of antigens through a process called seroconversion. So it would only work if the virus in your body replicates sufficiently trigger first the primary infection (which is not associated with immune responses) and then persist enough to lead to to the buildup of immunological memory.

Is 'virulence' the term used for a pathogen's relative ability to infect? Less pathogens needed to cause infection = more virulent.

Edited by StringJunky

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1 hour ago, Externet said:

If infection by one single virion🙄 is not lethal and can be treated/managed with much less fatality;  and can be singled/separated (as by microscope) to inoculate a person, would that be a sort of vaccine ?)

The outcome of some viral diseases might be affected by the exposure viral load, and indeed, lower exposure viral load could lead to milder symptoms. But even if you deal with such a disease, you cannot use limited viral exposure as a form of vaccination. The important quality of vaccine is that it creates immunity, but does not create spreadable disease.... In your case, however, such 'vaccinated' persons would spread the disease and your method might make things worse.

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6 hours ago, CharonY said:

 

However, a single particle is highly unlikely to elicit any kind of meaning full effect, you need quite a few more than that. How many, depends a lot on virus and host factors. I seem to recall that I found an estimate of as low as ~200 virus particles in the cases of some coronaviruses, but frankly I do not recall it very well and may be mistaken.

 

I think  I may have seen  something like that  estimated figure too.

The only time I have read of  instances of single virus particles was when  a sample  on a surface had died out  in hours or days with presumably one virion being the last to die.

Well, there was also theoretical  talk of how small a sample could be to infect the entire human population if each person was allocated one virion apiece.(extremely small) 

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4 minutes ago, geordief said:

I think  I may have seen  something like that  estimated figure too.

The only time I have read of  instances of single virus particles was when  a sample  on a surface had died out  in hours or days with presumably one virion being the last to die.

Well, there was also theoretical  talk of how small a sample could be to infect the entire human population if each person was allocated one virion apiece.(extremely small) 

What does the term "die" mean in relation to a virus. Does that mean 'no longer able to infect' or something similar? How is that state of a virus determined? 

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1 hour ago, zapatos said:

What does the term "die" mean in relation to a virus. Does that mean 'no longer able to infect' or something similar? How is that state of a virus determined? 

Yes ,I realized after I posted that "die"   might be the wrong word.

 

I think  that you put it right,it is when it's reproductive /infective mechanism is sufficiently degraded (as far as I know,anyway)

 

No idea how they might determine that but I think they they  say that soap destroys its lipid exterior structure ,so it might be something similar that  which occurs when a virus is left in an inhospitable  (for it) environment.

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11 hours ago, StringJunky said:

Is 'virulence' the term used for a pathogen's relative ability to infect? Less pathogens needed to cause infection = more virulent.

In certain contexts it might be though I think most folk would actually state whether it is more or less infectious. Virulence refers the relative degree of disease caused by an organism. More commonly it could refer to e.g. severity or extent of infection (but I can see contexts where it might be used to minimal infective doses too). 

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3 hours ago, geordief said:

No idea how they might determine that but I think they they  say that soap destroys its lipid exterior structure ,so it might be something similar that  which occurs when a virus is left in an inhospitable  (for it) environment.

Typically you take the sample and apply it to a cell culture and see how many are getting infected compared to the reference.

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The Moderna vaccine mentioned earlier is almost done with phase I but preliminary results already indicate that some participants developed antibodies. This bodes well for the efficacy test.

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Is there a problem with this https://en.wikipedia.org/wiki/Molecular_clamp - that proteins in virus have higher energy required for fusion?

Just putting mRNA into a cell, shouldn't it produce the lowest energy protein?

If so, are these two configurations essentially different from anti-body perspective? Would such immune system attack infected cells and/or virus itself?

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1 hour ago, Duda Jarek said:

Is there a problem with this https://en.wikipedia.org/wiki/Molecular_clamp - that proteins in virus have higher energy required for fusion?

Just putting mRNA into a cell, shouldn't it produce the lowest energy protein?

If so, are these two configurations essentially different from anti-body perspective? Would such immune system attack infected cells and/or virus itself?

So while the issue with pre-/post-fusion proteins is an issue, I would like to note that in many cases one would frame it more about the conformation of the protein rather than overall energetics. There are several ways to stabilize a particular structure, independent on whether protein is ever part of a virus, or involved in membrane fusion or not. I.e. it is helpful when we think in terms of the dynamics and mechanisms of viral actions (as it needs to be performed within an energy gradient) but it may be less useful when we talk about other things, such as in this case recognition of structures.

Specifically, a particular structure is formed in dependence on its milieu, its amino sequence as well as other elements such as chaperones that help in folding the protein a specific way. Perhaps more importantly, recognition of the molecule by the immune system is only dependent on a fairly small part- the epitope. Moving on to RNA vaccines, in other viruses it already has been shown that antibodies raised just by simply introducing the primary sequence has resulted in antibodies that are able to bind pre- as well as post-fusion protein structures. They also stabilized the pre-fusion structure by introducing additional sequences (not dissimilar to the wiki article linked above) but the overall titer did not shift much.

This is not to say that this is not an issue with SARS-CoV-2, but it does not seem to be a fundamental issue, at least.

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