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Some covid SAQ NAFE and GP


dgul
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I'll start with this from today:

  11 hours ago, Pinkpanther said:

Thanks for that 

I have one question that has been bothering me and I was wondering if you could enlighten me or point me in the right direction.

If the immune system in the vaxxed is not controlling the virus. Then what stops the virus replicating? 

My limited knowledge of this area would lead me to conclude that the virus would replicate (because that what they do) until all the cells that it can replicate in have been used. Or in other words it would take over and kill you. But obviously not.

Expand  

The way the immune system responds to viral infections is rather complex, particularly for respiratory infections, and involves innate* antibodies, a variety of innate cellular responses some of which involve the creation of chemical responses and others that are directly cellular, adaptive cellular responses and adaptive system antibodies, most of which are used to signal cellular responses but some of which neutralise the virus.

[* innate means there anyway and not linked to a memory of a prior infection; adaptive means arising as a result of a prior infection]

Part of our problem here is the unfortunate way government 'education' has simplified this into 'antibodies! antibodies! antibodies!', mainly because the covid vaccines mainly work by priming the body to produce antibodies by the bucketful (a much stronger response than you'd get with natural infection) and don't do that much else (there is also a limited adaptive-cellular response, which appears to be a much smaller response than you'd find with a natural infection).  I don't understand why they've had this single-minded response to medically-responding to covid, other than 'if the only tool that'll make me money is a hammer, it is in my interest to make people think that all problems look like nails'.

Anyway...

When you get a respiratory tract infection your body responds with the innate immune system -- this allows the body to limit the spread of the infection and also produces the symptoms we're familiar with ('having a cold').  These symptoms can* last for some time, as these processes don't clear up the infection on their own.

[* I'll come back to this]

The adaptive immune system does clear up the infection, but takes a while to get up to speed.  In coronavirus infections this is 'about a week', which is why colds typically last as long as they do.  In the upper respiratory tract the main mechanism appears to be antibodies that bind to any viral proteins and signal the cellular immune system to act.

Note, signalling antibodies that don't neutralise the virus on their own.  There are also neutralising antibodies, that bind to 'important bits' of the viral proteins and stop it working.  For the covid vaccines this is the single target, which is strange because it appears to be the least important part of the immune responses to respiratory tract infections in general, including coronaviruses.

It is also interesting to note that the antibody response to coronaviruses (in general, as well as other upper respiratory tract infections) is rather short lived -- it is as if the body tries to get rid of the antibodies because they're not that helpful in the end.

So really your question should be 'what are the vaccines doing anyway?', or, perhaps, 'how do they work at all?'.

I think they're doing a number of things:

  • Neutralising antibodies in the upper respiratory tract do have some direct impact on controlling infection, but not much.  These do reduce viral load by some margin and will help stop infection in the first place.
  • However they also compete with the innate immune system, suppressing it and stopping it from working so well.  This will reduce 'cold like' symptoms (because it is the immune system that creates the symptoms, not the virus), but will also likely make the infection last longer.  Note that the virus is still there and replicating 'enough', so the individual will be infectious and able to transmit even without symptoms -- this is different from a normal infection where lack of symptoms generally means that the virus hasn't taken hold (hasn't stimulated the innate immune system to act).
  • If the virus moves from the lungs to the whole body (particularly the blood) then the neutralising antibodies that are floating around really do stop the infection (this is their forte) -- this then significantly reduces the risk of serious covid (which is a whole-body problem, not a respiratory problem).

This is exactly what we see as a result of vaccination:  reduction of risk of infection, strong reduction in mild symptomatic disease and highly significant reduction in serious disease.  

But the other consequences of this will also mean longer infectious periods in the vaccinated infected, and a higher level of asymptomatic transmission.

Note that this might result in a weird pattern in the response of the body to coronaviruses (in general, and perhaps other upper respiratory tract viruses).  When a naive individual gets 'a cold' they should clear it up in about a week.  If they're reinfected within a timescale of 'about a month' they should fight off the infection (primed innate and adaptive immunity).  If they're reinfected after about 6 months they should just have a 'normal cold' (normal innate immunity and no adaptive immunity).  But if they're reinfected in a time scale of about 6 weeks to 3 months they should get longer lived but very mild symptoms such as a 'not that annoying' persistent cough that just doesn't go away (primed adaptive immunity and suppressed innate immunity).

Finally -- why does the body try so very hard to produce an immune response to coronaviruses (in general, 'colds'), but then 'forgets' all about it so rapidly?  I believe that this is a function of man's natural social habitat and issues with coronavirus antibodies.  Humans evolved in relatively small 'extended family' tribes -- when these were infected with a cold (maybe from casual contact with a person from a neighbouring tribe) it would rapidly move through the entire tribe but then run out of hosts as everyone would have had an infection and generated a level of protective immunity (by various mechanisms).  Thus immunity wouldn't need to last long -- only as long as it took for all potential hosts to become infected and to clear up the infection -- there would then be no virus in the community and no need for a protective immune response.  But why make the antibodies go away?  I see four possible 'reasons'*; because structural similarities between viral proteins and human proteins meant there was a risk of an autoimmune response (eg, the body creating blood clots) so it was best to get rid of them if they weren't being useful; because mutations in the viral proteins by the next time it came around (6-12 months) meant that there was a risk of the antibodies to the first variant actually assisting the viral variant that comes around next (eg, ADE); because having those antibodies hanging around at the time of next infection introduces selective pressure for the virus to mutate 'at important bits', increasing the risk that it will mutate to get around the immunity and, because of original antigenic sin, the body would struggle to produce antibodies to this new form in the future; increasing the risk that it will mutate to get around the immunity and happen upon a more virulent form.

I don't know if this is true or which of those potential mechanisms might be important -- but very kindly the world's politicians have just designed an experiment to find out. 

[* this means 'selective pressure for humans to evolve to have a different immune response to some viruses, where they don't produce a long lived antibody response']

I'll add that there are more explanations for antibody decline -- the most important one is 'it is just that way and there's no reason' -- this always has to be considered.  And there's also 'the virus has evolved to trick the immune system into lowering defences so that it can reinfect more easily' -- this is certainly plausible; immunity is a merry dance between the body building defences and pathogens evolving to get around the defences.

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Mental Floss

Ooooh can I have one! There appears to be an implied superiority of vaccination protection vs infection acquired immunity.

Is there any scientific rationale for this? 

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8 minutes ago, Mental Floss said:

Ooooh can I have one! There appears to be an implied superiority of vaccination protection vs infection acquired immunity.

Is there any scientific rationale for this? 

Yes.

Vaccination offers very high levels of neutralising antibodies, either circulating in the body or produced by B cells on infection.  These are highly protective and significantly reduce the impact of infection.  

Except in upper respiratory tract infections, where innate and cellular immunity is more important.

Covid vaccines are very good at producing neutralising antibodies to the very specific proteins that are in the vaccine.  These antibodies are also very long lived, compared with antibodies created in response to natural infection.  But they're rather poor at producing a cellular response (other than B cells creating new antibodies).  Thus the actual protective impact of the vaccines will be inferior to natural infection.  Any protective effect from the antibodies is also time-limited because high vaccination levels create immense selective pressure for the virus to evolve vaccine escape, making the fact that the antibodies are still circulating a moot point.  In addition, Original Antigenic Sin will make the immune response to future infections biased towards the original (vaccine) spike protein and thus suppress the ability of the immune system to respond adequately.

I find it rather concerning that the pharma companies have negotiated that in future, clinical trials of vaccine candidates will only have to show an immune (antibody) response, rather than having to go to the effort of showing protective impact on the population.  I find this extraordinarily short-sighted and liable to result in significant problems.

 

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  • 1 month later...

@dgul So something that not even they can spin as COVID is causing a high incidence of deaths in 45-64 year olds?

Edited by Loki
i can't words
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Posted (edited)
1 minute ago, Loki said:

@dgul So something that not even they can spin as COVID is causing a high incidence of deaths in 45-64 year olds?

Looks like it.

I imagine they'll try harder to spin it as covid.  Perhaps it is related to covid (some sort of delayed reaction specific to Delta).

Or it might be the vaccines.

Edited by dgul
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Long time lurking

 

2 hours ago, dgul said:

Ignore the yellow bit at the end -- the graph always falls away like that for the provisional (most recent) data.  The important data point is the last point before the yellow zone -- week 29, which is 19-25th July -- getting above the dotted red line which marks the threshold for a 'substantial increase' in deaths.

Was that not around the time (week 29) or shortly after that the guy involved with the Oxford vaccine ,came out and said booster shoots were worthless an the vaccines are never going to achieve herd immunity ?

My money is on he has access to data that the public are likely never to see 

Is this the reason for the U turn ?

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Bornagain
6 hours ago, dgul said:

I note that England (not the other countries in the UK yet) has now got a signal for a 'substantial increase' in deaths, according to Euromomo (https://www.euromomo.eu/graphs-and-maps)

This is today's update:

euromomo-deaths.png.7fc4c0f81151e078f42aab6ec6f4ea48.png

Ignore the yellow bit at the end -- the graph always falls away like that for the provisional (most recent) data.  The important data point is the last point before the yellow zone -- week 29, which is 19-25th July -- getting above the dotted red line which marks the threshold for a 'substantial increase' in deaths.

The graph above is for 'all ages', but the signal for 'substantial increase is seen in 15-44 years, 45-64 years, 75-84 years,  not quite for 65-74 years and not for 0-14 or 85+.  The biggest signal is seen in 45-64 years.

I should point out that the graph above is for 'z-score', which is a measure of 'how unusual it is' given the normal variability in the data, rather than a simple count of excess deaths.   So, you might have the same number of deaths 'per million' because of 'whatever cause', but in the 85+ group it would be masked by the death rate in that group being rather high because of the usual causes of death in the elderly (ie, 'not unusual').  But the same deaths 'per million' might be a 'substantial increase' for 15-44 years, who don't have a high background rate of deaths to mask it.   If you go to the Euromomo website you can play with the data -- it should be apparent that 'substantial increase' is rather unusual; outside covid times 15-44 years haven't seen a substantial increase back to 2016, and the 45-64 years data only shows one substantial increase, during the influenza spike of winter 2017-2018, which was the worst UK excess deaths since 1975 (apparently).  

As the highest increase is seen in 45-64 it might be considered that 'whatever cause' is hitting them worse (as they've got the highest z-score, so 'unusual increase' and they've got higher background death rates that might have masked it). 

Or, perhaps the 45-64 age group has the highest incidence of 'whatever it is' that is making them more susceptible to death...

And, whatever it is, doesn't seem to be affecting the 0-14 age group, for whatever reason.

Now, we have just been through a covid wave, so perhaps they're all dying of covid.  But we have the covid deaths data. 

covid-deaths.thumb.png.a65690ccf57f219acb20a9dd6b59d9c7.png

Note that the 'all ages' excess deaths data (top graph) has a similar 'substantial increase' for week 29 2021 as for weeks 45-50 2020 (most of Nov and first half of Dec).  But the data above shows late Nov early Dec to have had about 400-450 covid deaths per day, whereas the data for week 29 (end July) shows about 80 deaths per day (it isn't quite as simple as this, as the z-score includes a seasonality adjustment, but it is going to be close enough).

Now, the NHS/Gov is very careful to ensure that every single covid death is counted as a covid death (and then some); it is unlikely that there are any 'missing' covid deaths.  So the excess deaths data can't simply be reflecting covid deaths.

So, according to the Euromomo data we've had during late July something near 300-350 'excess' deaths per day* not due to covid (the exact range of non-covid excess deaths is harder to quantify -- there are a rather a few factors to consider -- but even with the 'unknowns' the excess deaths appears to be real and substantial).

This is a very early signal, but the Euromomo data is fairly robust.  Something rather significant appears to be going on here.   I guess we'll find out more in the coming weeks.

I must add that the Euromomo data seems to be subject to revision on occasion -- so this might 'disappear' at some point -- but this is the current data 'hot off the press'.

[* ie, the z-score suggests 400-450 deaths per day (assuming that the only cause of excess deaths last autumn was covid) but we're only seeing 80ish deaths per day of covid -- so, there's 320-370 unaccounted for -- I rounded this down to 300-350]

If this is true and the vaccines are genuinely to blame, then either the government cover it up, or sooner or later the shit is going to really hit the fan.

 

 

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On 15/07/2021 at 13:05, dgul said:

I'll break my own rules about no chitchat because it is my thread and I can do what I like.

But looking at the text I just posted I'm reminded of Cgnao -- he was far more sensible than me and would have distilled the above into:

447 
WTPZ31 KNHC 150851
TCPEP1

BULLETIN
SARS-COV-2 Advisory Number   5   

EP062021 200 AM PDT Thu Jul 15 2021

+++BIOLOGICAL EMERGENCY UPDATE+++

+++IMMINENT LOWERING IN CASES WILL MASK SUBSTANTIAL INFECTIOUS PRESSURE+++

+++LOSS OF IMMUNITY FOR SARS-COV-2 VACCINATED+++

+++MASS ASYMPTOMATIC INFECTION AND TRANSMISSION+++

+++INVOKE EMERGENCY PREPARATIVE PLANS NOW+++

+++SIGNIFICANT WAVE EXPECTED NOVEMBER+++

+++MESSAGE ENDS+++

Muhahahaha

100% guaranteed.

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geordie_lurch

Thanks for mentioning this thread you created @dgul in the other ones I follow and especially that possible excess deaths spot at the end of July :Beer: I tend to only track a few threads I'm interested in due to time constraints as well as not wanting to hold too much of anything in my head at once but will be following this one now too :Geek:

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1 hour ago, Bornagain said:

If this is true and the vaccines are genuinely to blame, then either the government cover it up, or sooner or later the shit is going to really hit the fan.

 

 

It can't be long before birth defects start to appear, whether vaxxified or not. Some will make a connection and go ape/post on Mumsnet.

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A tremendous # on the lung

And / or the impact of lockdowns, a barely functioning health service, and patient reluctance to go to a GP/hospital.

Is there any granular info re: cause of death?

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stop_the_craziness

So, if we take the normal DOSBODS news/MSM timeline, I would expect this information to start becoming "news" around Christmas time.

Which is nice.

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9 hours ago, dgul said:

I note that England (not the other countries in the UK yet) has now got a signal for a 'substantial increase' in deaths, according to Euromomo (https://www.euromomo.eu/graphs-and-maps)

 

Co-infections might be worth looking at.  There's been lots of talk about flu and mentions of others like RSV (specifically for the young in that case IIRC), possibly could even be reactions of the vaccinated in particular to other infections.

Another possibility - deaths have been substantially under trend for months now - that may be because of above trend taking out the weak in the period before but could also mean an uptick is response to that trend. Seasonal change - very warm weather followed by significant cold (ish) period may also have affected the figures.

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18 minutes ago, onlyme said:

Another possibility - deaths have been substantially under trend for months now - that may be because of above trend taking out the weak in the period before but could also mean an uptick is response to that trend. Seasonal change - very warm weather followed by significant cold (ish) period may also have affected the figures.

Deaths for those 45-64 years hasn't really fallen below baseline all year.

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7 minutes ago, dgul said:

Deaths for those 45-64 years hasn't really fallen below baseline all year.

Sorry, stand corrected, didn't see how to drill down far enough, so took guidance from the overall death rate for the UK from the Euro momo stats.

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  • 3 weeks later...

Latent infection. @dgul

I've been thinking a about this recently and how mass vaccination appears to precede mass cases.

Could there be a mechanism whereby a virus could infect asymptomatically, lay dormant and become activated via jab? The jab reduces your immune system for a couple of weeks, does it not?

Edited by Reck B
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26 minutes ago, Reck B said:

Could there be a mechanism whereby a virus could infect asymptomatically, lay dormant and become activated via jab? The jab reduces your immune system for a couple of weeks, does it not?

Yes.

There is a suggestion that the viral infection hangs around in monocytes, but the supporting evidence is rather sparse (because few people have looked).

 

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On 08/09/2021 at 22:46, dgul said:

I am fascinated by the Hope-Simpson model of viral transmission (super-spreader) and what we're seeing in New Zealand. 

New Zealand is particularly interesting because they've had very few cases to date, and thus will have very little in the way of natural immunity, but they've also vaccinated a fair proportion of the population.

This is the current situation:

daily_cases-2021-09-08.png.5dc95e624b1ada0c52b8531c2cdc6110.png

[It is worth noting that AFAIKT there are only two sets of home-grown infections in the above graph -- one in early 2020 the other last month.  All the noise in between appears to be imported cases that were quarantined]

The recent wave appears to have dissipated to near zero now.  It has been very short and sharp, with a total duration of about 15 days and a peak of about 60-70 cases per day.  The current rate of about 20 per day could be the limited number of normal community transmission infections, which will fizzle out as community transmission of covid has (according to the superspreader model) an R0 of about 0.2 (I think, according to rough calculations).  

I wonder if this is what a single super-spreader event looks like; a single person become highly contagious (for whatever reason) and spreads the disease (by whatever mechanism) for around a fortnight and then 'sorts out their infection' (by whatever means).  As the majority of people aren't superspreaders the people they spread covid to mostly don't go on to spread the disease to others, and so if there is no new superspreader the disease fizzles out.

Looking at the graph above, it looks to me like the spread of disease in early 2020 was comprised of two peaks close together, and about twice the duration of the recent peak -- was this two superspreaders?

So, what does this mean?  Well, the big difference between this year and last year is that NZ now has lots of vaccinated folk.  The question is, what does vaccination do to the risks of becoming superspreaders?

There are two main theories about where superspreaders get their disease:

  • Latent infection.  In this hypothesis a person remains infected but at a low level for several months until something comes along to suppress their innate immune system.  Hope-Simpson suggested vitD levels, and this certainly matches what we see with seasonality.  However, in the case of New Zealand they've not had cases recently to create a stock of latent-infected.  So, if this hypothesis is true we should see the next covid wave in NZ in about 3-4 months (as this appears to be the normal inter-wave period).
  • Immune system suppression.  In this hypothesis a person will only become a superspreader if they have a certain quality suppressed in their immune system.  It seems easy to say 'innate immune system' here, but it could be to do with specific (perhaps enhancing) antibody types that are generated only occasionally following infection.  If this hypothesis is true we should see the next covid wave in NZ as soon as those infected have a chance to turn into superspreaders -- and if it is to do with antibodies this should be in about 2-3 weeks.
  • There is another point, though.  We saw from the early 2020 wave that the sorts of infected numbers that occurred then wasn't enough to create new superspreaders (although note seasonality -- they were coming out of summer and so had robust vitD levels)  -- so the presumption is that superspreaders comprise less than about 0.2% of the population -- this seems tiny, but does sort-of account for some of the patterns we see (but not others, which really need them to be at 1%-5%).  So, if this is still the case then the next wave (either in 3-4 months or 2-3 weeks) should be at a similar scale to the current wave.  However, if vaccination increases susceptibility to becoming a superspreader, then we should see the next covid wave magnified by this increase in susceptibility.
  • Alternatively, if vaccination reduces susceptibility to turn into a superspreader, then we shouldn't see any wave as directly following this latest one (although, of course, a brand new covid wave could form).

So, that's here's my guess for NZ's future.  I think that the immune system suppression coupled with 'dodgy antibodies' idea looks sound, and that vaccination increases superspreader numbers.  If this is the case we'll see a sudden and dramatic rise in cases in NZ at around the end of Sept, with the peak of the wave at a multiple of this recent peak (only 60-70 per day) and duration of about 6-8 weeks (as seen with other covid waves).

I'd note that the latest wave was pretty much only Auckland (as it 'was only one person'), but that NZ's biocontrol measures aren't very effective (it being an island is what's effective) and the next wave will see outbreaks in every city.

I'd be content to be proven wrong -- the superspreader model has lots of parameters and I'd be happy to populate some of them even if it goes against my current thinking -- and, of course, the superspreader model could be incorrect (but it does explain 'what we see' better than the 'measles' model of disease progression, as used in the Imperial covid models).  But that's my current thinking -- over to you, NZ superspreaders.

I've gone through the data  from other countries and got a range of 'the most plausible' times for the superspreader theory (essentially a 90% probability) for a new superspreader to be formed.  Min 1.5 weeks or so, max about 3.5 weeks from the peak of the first superspreader's cases.  I still think this looks short, but that's what the stats show.

So we might see that cases start to turn from about here (this is earlier than I'd supposed on the original post).  If it is going to turn it should have done so by about 23rd Sept.  If it doesn't turn by about then it means either that the most recent superspreader 'didn't find another superspreader to infect' or that it is all bollocks.

Edited by dgul
Never apologise, never explain.
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2 hours ago, dgul said:

I've gone through the data  from other countries and got a range of 'the most plausible' times for the superspreader theory (essentially a 90% probability) for a new superspreader to be formed.  Min 1.5 weeks or so, max about 3.5 weeks from the peak of the first superspreader's cases.  I still think this looks short, but that's what the stats show.

So we might see that cases start to turn from about here (this is earlier than I'd supposed on the original post).  If it is going to turn it should have done so by about 23rd Sept.  If it doesn't turn by about then it means either that the most recent superspreader 'didn't find another superspreader to infect' or that it is all bollocks.

Cases in Canberra (ACT) appear to be following a similar trajectory.  According to this model (and assuming that Canberra is 'rather isolated', following Aus lockdown rules, etc) we should see an imminent reduction in cases down to about 10 a day, and then bounce back significantly sometime between 20th Sept and 4th Oct (ish).

Again, we'll see how it turns out.

 

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  • 2 weeks later...

This paper is doing the rounds re. facemasks: https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciab797/6370149   Infectious SARS-CoV-2 in Exhaled Aerosols and Efficacy of Masks During Early Mild Infection

This is being pushed because they found facemasks halved the amount of virus being breathed out by people with active infection and symptomatic disease (well, 3 were asymptomatic).  They then use this fact to promote the wearing of facemasks in their conclusions.

They are right -- the facemasks did halve the amount of virus found.  

The problem with the work is that the amount of virus found was trivially small.

Over a 30 minute period for original variant and without facemasks they found a geometric mean (the right type for this analysis) of 7 and 18 viral particles (for coarse and fine droplets respectively).  That's nothing.  They even included coughing, shouting and singing within the 30 minutes to get the numbers up -- this clearly didn't help to bring numbers up.   This absolutely says that there was no point in the mask wearing mandate for original covid. 

That said, they did find a small number of people who were symptomatic and had virus levels in their exhaled breath of about 25,000 virus particles over the 30 minutes.  IMO this supports the 'superspreader' theory of covid -- that is, it is a relatively small number of people that are doing all the spreading.  I'm still a bit suspicious, however, because that's still rather low -- using the same method for influenza you'd expect to find a geometric mean of over 25,000 viral particles per 30 minutes, with the 'superspreaders' rising to the tens of millions of detected viral particles exhaled per 30 minutes.

For Alpha variant they found a geometric mean of about 500 viral particles (fine droplets -- less for coarse) per 30 minutes -- significantly greater than for original variant, but still very very low.  Surprisingly, the 'superspreaders' in this case were only at a similar level as for the original variant -- IMO this is reflected in case numbers, which weren't substantially different for alpha cw original variant, and certainly not the several-orders-of-magnitude-worse suggested by the geometric mean of exhaled virus particles.

Back to the original point -- facemasks.

For a start most symptomatic-infected people had no detectable viral particles in their exhaled breath (over 50% of them).  These people saw no reduction in viral particles exhaled with facemasks (duh).

For the rest, the masks seemed to reduce loads from about the 500 viral particles per 30 minutes level (fine droplets) to maybe 250 or so.  And that was with the individuals coughing, singing and shouting within the 30 minutes.  It's really really low.  To put this into perspective, it is generally thought that about 100 viral particles will cause an infection (clearly the answer to this really is 'one viral particle will cause an infection', but we're talking about averages).  Now, I'd accept that they're not going to have detected all of the virus particles in their experiment, but it is still low (note the numbers for influenza, given above).

To me this study's recommendations are backwards.  Instead of supporting facemasks it suggests that they're going to be pretty much useless (as seen in other facemask studies).  It also suggests that the SIR model isn't accurate if based on respiratory transmission, and that there likely are superspreaders within the infected community that are doing all the work.

I'd note again that these results are for symptomatic individuals.  I can only presume that viral loads will be even lower for asymptomatic individuals (though I worry that vaccinated-infected-asymptomatic might have much higher viral loads). 

I'd suggest that this is yet another paper suggesting that facemasks aren't doing anything to control covid outbreaks.

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