Thinking Problems - Transmission

This is a follow-up to Thinking Problems – Lab Leak.  One could have thought that, by now, the issues of COVID would have faded into the background, but no.  Misinformation about the COVID vaccine is still circulating.

In discussions with JP, there was a common claim that “they” had said that the vaccine would prevent transmission.  For example, in August 2021, JP was housebound because he was worried about a local outbreak.  I asked about his vaccine status and his reply indicated that there would have been little consolation in having a second jab if he could still spread it.  A month later he was claiming that the “initial focus was on preventing spread”.

The problem is that the issue is very complicated.  I know that I am going to overly simplify things here, but I do so with the intent of getting past an apparent blockage on the part of some of the more conspiracy minded among us.

For a virus-based disease, there is sequence of events somewhat like this:

When thought of like this, it is clear that having a vaccine cannot help with certain stages.  You are either exposed or you are not.  With infection, that’s more a question of whether you ingested the virus or not.  Here things are a bit blurry because there is you and there are your cells.  There is also the virus and there are virions.  It’s possible that a virion (one particle of the virus) got into you, but did not enter a cell (thus infecting it) before being excreted or destroyed.  Did you (the human) get infected by the virus?  You certainly got closer than if you were merely exposed to the virus (ie sitting in a room in which virions were floating around in the air that you breathed, but you didn’t happen to breathe in one).

What about if one or a few of your cells did get infected, but your immune system immediately identified the threat and destroyed the infected cells before they could set up their virus replication process?  You didn’t contract the disease, your body as a whole didn’t get infected, but you were partially infected.

What about if you did get widespread infection of cells by the virus, your immune system swung into gear mounting an effective response, but you never got any symptoms – meaning that, strictly speaking, you never developed the associated disease?  This is non-symptomatic infection, which in hindsight appears to have happened with considerable frequency.  Usually, being non-symptomatic means you are not contagious.  But not always (as the Typhoid Mary case demonstrates).

I am going to just highlight a grey area between infection by the virus and development (or contraction) of the disease.  For the purposes of this argument, I am counting disease as including the non-symptomatic who produce enough virions to be contagious.

If viruses didn’t cause disease, we probably wouldn’t care about them.  It is worth noting though that not all the symptoms of an infection are due to the pathogen (virus or bacteria) per se – some of them are the immune system fighting against the infection (fevers for example).

The job of a vaccine is to prepare the immune system for fighting a specific pathogen (or suite of pathogens).  The better prepared the immune system is, the less likely it is that the disease will take hold.  This can range from preventing symptoms entirely, making the symptoms less severe and reducing the time that it takes for the immune system to eliminate the disease.

Viruses are particularly nasty because they take over the cells of hosts and redeploy them to replicate virions.  It’s rarely a friendly take-over, with the replication machinery set to keep working until the cell bursts, releasing thousands of virions which go on to infect new cells.  Quickly, the body is riddled with virions which then get into various liquids in the body, including those in the lungs, meaning that when an infected person breathes out, there are virions lurking in droplets that we inevitably spread about us.

This is transmission in the schema above.  The virus effectively uses us to spread itself around us in a fog of about 1.5-2 metres (as is most visibly noticeable on a cold day).  But note that transmission does not mean reception (exposure or infection).

If you have a viral disease, the only way to prevent transmission is to prevent droplets getting out and to another person.  The right sort of mask, when worn properly, can do that.  Or keeping away from others (social distancing).  Or not going out in public (isolating).  The vaccine will not help you, if you already have the disease.  Your having been vaccinated will also not help you if it is not you who has the disease, it won't stop stop someone else transmitting.

What the vaccine will do is increase the likelihood, if you get virions into your body, that your immune system will prevent an infection progressing to disease, reduce the seriousness of the disease if you can't prevent it (and possibly reduce the number of virions you produce that can then be transmitted to someone else) and shorten the period in which you have the disease (and are contagious).

In that sense, the vaccine can certainly minimise spread of the disease.

But it will never prevent contagious people from transmitting the virus, nor will it necessarily prevent you developing some form of the disease if you are infected (although it's much more likely to be mild, or even asymptomatic, rather than severe).

That’s not to say that there aren’t sterilising vaccines or other treatments –that are hugely effective and prevent you from producing virions if treated.  It’s simply that the covid vaccines were never advertised as those.  The effort was all about preventing severe disease, which is why they are described as COVID-19 vaccines not SARS-CoV-2 vaccines.

Thinking Problems - Lab Leak

This is Fu (it's his name in PowerPoint).  He's our nominal Patient O (also sometimes styled as 0, or Zero) for Covid-19, caused by the virus SARS-CoV2.  Behind him is a potential other person in the chain, we can call him Fu2, he's a hypothetical intermediate human carrier of the virus who didn't come down with Covid-19 - who may or may not exist.  As they collectively are the portal of the virus into humanity, we can just refer to the Fu/Fu2 nexus as Fu, just keeping in mind that there may have been that human-human mechanism right at the start.

We don't know how Fu got infected with SARS-CoV2, but there are some theories, indicated by the lines.

It could be entirely natural, noting that there are some variants of that, some of which have the virus being shared between different animal vectors as it evolved (some of which might have been human).  That's what the additional dotted box means.  Fu interacted with an animal in the wild, at a market or somewhere else that had the virus and got Covid-19.

SARS-CoV2 could have been genetically engineered in a lab and then Fu could have been deliberately infected with it.  This would imply that SARS-CoV2 had been developed as a biological weapon.

Alternatively, there could have been infection from a petri dish, test tube or surface in a lab where the virus was being genetically engineered, as a biological weapon, in a gain of function effort to develop better methods for treating coronaviruses more widely (vaccines, retrovirals, and the sort) or just out of scientific curiosity (i.e. pure research).

Finally, there could have been a crossover from an animal infected with SARS-CoV2 that was being treated, dissected, studied or whatever in a lab.  This may have been with the intent to develop a biological weapon, or do some gain of function for benign reasons, but in this case there had not (yet) been genetic engineering carried out.

Note that the purple arrows are pointing at the boxes, not any of the other arrows.  The amount of evidence for each event is nominal, the size of the bubble could also relate to the quality of evidence, rather than a mere quantity.  Note that it's evidence, not proof.  Some evidence might support multiple possibilities.

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I think I have captured all the possibilities being thought of seriously.  Even if there is some bizarre vector, like aliens or the New World Order doing the genetic engineering and deliberately injecting Fu, this still falls into the category "Genetic Engineering".  Same with a god doing it, it's just that the technology would be different (supernatural genetic engineering).  If there is something that I have missed, I am more than happy to go through it and try to weave it in.

Note that even with genetic engineering, there was still a natural origin of the base virus that was being fiddled with.  So, there is naturally going to be a lot of evidence for natural origins.  I'm not really thinking about evidence that supports all cases, just delta evidence.  Those cases are (arrow type):

• purely natural – Natural Origins→Fu (large red)
• simple leak from a lab – Natural Origins→Leak from a Lab→Natural Origins→Fu (small orange)
• deliberate infection – Natural Origins→Genetic Engineering→Fu (tiny grey)
• complex direct leak from a lab – Natural Origins→Genetic Engineering→Leak from a Lab→Fu (large green)
• complex indirect leak from a lab – Natural Origins→Genetic Engineering→Leak from a Lab→Natural Origins→Fu (small blue) – so we can think of zoonosis as “natural”, in a sense, even if the virus were to be tinkered with at some point.

There is one other that I identified after I put the image together, namely Natural Origins→Leak from a Lab→Natural Origins→Fu.  The notion here is that the virus was transferred from where it normally is (in a bat, in a cave, somewhere in southern China) to a lab and gets into another animal (pangolin, civet cat or one of those adorable raccoon dogs), and then that other animal becomes the vector for transmitting SARS-COV2 into humans.

There is also the possibility of a pre-SARS-COV2 virus being carried from a lab to the animal (via an intermediate human infection), with mutation(s) then happening in an animal or range of animals – resulting in a variant that became known as the Wuhan strain of SARS-COV2.

I’m not specifying a lab, although there are two candidates that seem more reasonable than any others given the location of the first outbreak – Wuhan Institute of Virology and the Wuhan Centre for Disease Control (about a quarter of a kilometre from the Huanan Seafood Market [also variously known as the Huanan Wholesale Market and Huanan Wholesale Seafood Market]).  It’s somewhat less likely that any leak occurred at another of the many labs in large cities in China and then got carried to Wuhan to break out there.  About as likely as Chinese authorities deliberately releasing a deadly virus on the doorstep of their major virology institute.

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The problem, as I see it, is that the light blue ellipse encompasses what some people refer to as a "lab leak", also indicated by the larger green arrow – implying genetic engineering in a lab with an accidental release, possibly of a biological weapon but, at the very least, some questionable gain of function research.  Then they take any evidence that there might have been a leak from a lab as evidence for genetic engineering, which it isn't.

I suspect that there's a similar problem on the other side in that initial discussions of a "lab leak" included the assumption that it encompassed both a leak from a lab and genetic engineering, so they weren't counting direct transmission from an animal to a human inside a lab (or even just a SARS-CoV2 sample from an animal, onto a surface or into a test tube and thence to a human) as a "lab leak".  So they were saying that a "lab leak" was considered extremely unlikely where, in reality, a leak from a lab is entirely possible and they should have said more clearly that genetic engineering is extremely unlikely (for various reasons) but not entirely impossible.

It isn't helped by the fact that dog-whistles are used on both sides, and the one term sometimes means quite different things.

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If something seems unclear, please let me know.

The Death of Nuance

 On 20 Jul 2023, Alex Gutentag, Leighton Woodhouse and Michael Shellengberger published a piece titled Covid Origins Scientist Denounces Reporting On His Messages As A “Conspiracy Theory” (archived) which contains links to two documents, one containing Slack comments and the other containing emails between Kristian Andersen, Andrew Rambaut, Edward C. Holmes, and Robert F. Garry – the authors of “The proximal origin of SARS-CoV-2” (archived pre-print | published).

 

The existence of this was hinted at by JP (of climate denial fame, see earlier posts that started in earnest at Ice Extent Challenge).  He didn’t, of course, just say “interesting piece at this website”.  Oh no, it was a single SMS, “And now we have covid-gate.  Grist for the mill.”  I actually thought it was a joke.  Unfortunately no.  About two hours later I dug a little and found the article mentioned above.

 

And, naturally, he wasn’t going to actually read the slack messages and emails.  He’s too busy, but he was nevertheless convinced that the paper (The proximal origin of SARS-CoV-2 – let’s call it “Proximal Origins” as Shellenberger etc do) should never have been published.  He wasn’t even going to read the paper (although he later said he had skimmed it and knew the main conclusions, which on cajoling he summarised as “Lab leak is bunkum. Only explanation is zoonotic source”).

 

Ok.  So, I am not going to go into detail of why it’s probably better to look at original documents than rely on videos that come up in your YouTube feed.  This post is about the death of nuance.

 

JP is all about nuance.  There’s no grand conspiracy, it’s all social contagion, social pressure.  You just need to listen to the heterodoxes for your serving of truth, but you need to be discerning because sometimes even the most brilliant people might say something that isn’t 100% true.  So, you know, nuance.

 

My view on nuance is a little different.  Things are complicated.  Some things we simply can’t know.  Sometimes we know that we can’t actually know something for sure, but we can take a balance of probability approach.  The story which by necessity involves large groups of people acting together to deliberately and effectively hide the truth from us is probably not the real story – even if you can convince yourself that they are doing this organically rather than deliberately.

 

JP is also into narratives, whereas I prefer to deal in facts, despite knowing that sometimes those facts are not available.

 

And that is a problem.  I worry that this sort of big reveal by Shellenberger and friends, like the University of East Anglia email saga (also known as Climate-gate) will have a chilling effect on research, and the discovery/confirmation of facts.

 

Science works best if there is an open exchange of ideas, including bad ideas and partially developed ideas and preliminary ideas.  Get the ideas out there, discuss them, test them and ditch those that don’t stand up to scrutiny.  Sometimes, possibly rarely though, what initially seem to be bad ideas turn out to be really good ideas, the sorts of ideas that revolutionise science.

 

In this instance, there were a few credible ideas about where Covid came from – directly from bats, from bats via another animal, from culturing of a natural virus in a lab (and then accidental release) and from genetic engineering of a virus in a lab (and then accidental release).  Plus some much less credible ideas – deliberate insertion of HIV into the virus (release mechanism unclear), deliberate engineering and release of the virus to target white (and black) people, and so on.

 

In the early weeks of Covid, the authors of Proximal Origins discussed the possibility of a lab leak.  They actually favoured a lab leak as the origin.  But as evidence mounted, they changed their minds and began to favour natural origin, without declaring the lab leak impossible.  Proximal Origins was pre-published almost a month before the declaration of a pandemic.  Even the formal publishing was less than a week after that declaration (and had been in the works for a while before that).

 

The authors did not know for sure, at that time, that Covid would become a pandemic, nor that it would be as serious a pandemic as it came to be.  The signs were there and I recall, perhaps erroneously now, that I thought it was going to be a pandemic well before the official announcement – at the very least I had set up a spreadsheet and was already tracking the numbers as early as 10 February 2020 and I had never done that before.  But nevertheless, it was very early days when the Proximal Origins authors started putting together the paper.  This was a very good time to be considering all options, discussing furiously what seemed to be a good idea to you and what ideas from others seemed to have massive holes in them.

 

However, if scientists know or fear that anything they say, in semi-private Slack chats, or emails, might be picked apart by hostile bloggers and commentators … they may well stay silent.

 

This won’t necessarily sound a death knell to all scientific collaboration, since it’s still possible to talk in person or over the phone, but as I said, it could have a chilling effect.  It’s often the case, for me at least, that it helps to get my thoughts down on paper, or in pixels, rather than trying to engage in a discussion which can often be hijacked by some other interest of the day (much as the intro to this post was, who the hell is JP after all? what do you care?)  I think many of us would lose a lot if we were badgered into not writing anything down for fear of some moron using it against us in the future.

 

A move away from being able to share ideas openly over email or other recorded mechanisms will only hurt us – all of us.

 

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And is there anything worrisome in the Slack messages and emails?  No, it’s just some guys talking about their work and one joke about the French.

Why the UK Variant (or Kent Variant) being More Lethal might be a Good Thing

Firstly, I must make it clear that I don’t want more people to die.  And I do realise that some people already have caught the UK variant (or Kent variant) of Covid-19, and it being more lethal is difficult to see as a good thing – for them.  However, there is a sense in which the new variant being more lethal, as well as being more transmissible, is a good thing.

 

Part of the argument is that the UK variant being more transmissible is a really bad thing.  There are reports that the UK variant is in the order of 50% more transmissible, which means that after 10 rounds (where a round is where those now infected have infected those that they are going to infect) about 40 times as many people will die (as would have with the original variant).  If it is only 30% more lethal, and not more transmissible, then it will kill 30% more people, so 1.3 as many people will die.  Combine the effects together and it’s about 50 times as many.  Which, at first blush, is not good.

 

However, the increased lethality of the disease only comes into effect once you have managed to catch the disease.  It’s entirely possible that people are going to be far more scared by the notion that they are 30% more likely to die with the new variant, and 50% more likely to get it, than they are by the notion that they will transmit it to 50% more people.

 

This might open up a channel into the mind of an otherwise unreachable and selfish individualist – especially if they can wrap their mind around the fact that it is not 50% more likely that they will get Covid-19 with the new variant.  That’s just 50% more likely to get it from each person with Covid-19 that they interact with, if they are interacting with more people (which will be the effect if infection rates are not otherwise stemmed) then there will be a compounding effect.

 

In other words, the increased lethality of the UK variant might just be the motivation that is needed for selfish people to act selfishly and, through acting selfishly, protect us all.

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On the mathematics side, if the 30% lethality was enough to scare the non-cooperative types into better behaviour such that it reduces the replication number by 10%, then this could halve the number of deaths – or more – over the long term (assuming just the increase in transmissibility).

Infectious Statistics

In A Worry of Climate Change Scientists (coming soon), I address a claim associated with the 97% consensus figure which the media, such as the Guardian, picked up and ran with.  It’s possible that they are using it ironically in the rubric “Climate Consensus - the 97%”, echoing the 99% quoted by the Occupy movement.

Any statistic, like the 97% figure, should be taken with a pinch of salt and an assortment of questions.  What does it actually mean?  What is it really measuring?  Were there any caveats associated with the figure?  And so on and so on and so on.

A recent example of a similar problem came to mind as I was developing that post, a time at which the novel coronavirus recently dubbed COVID-19 had been confirmed to have infected more than 60,000 people and killed more than 1300.  It’s a bit messy because China released additional figures based on a new detection technique, leading to a one day jump of more than 15,000 cases and the day after 100 people miraculously came back to life (that is during the early reporting hours, the numbers were adjusted down by 122 and later down by about 100).  For the purposes of this discussion, I am going to work from the basis of it being 12 February 2020 when the figures, although probably not accurate, were at least consistent.

There was a question occupying the minds of many people trying to work out whether they should be bothered by a virus that has, so far, killed in the order of 0.2-0.4% as many people as die each year from influenza.  Sure, the flu is everywhere, while COVID-19 had so far been largely contained to China, but it seemed unlikely that, by the end of the year, more than half a million people would die from it.

The question was: what is the mortality rate due to COVID-19?  An easy question, but not so easy to answer.  The official answer, to avoid any unnecessary concerns, is about 2%.  The figures are rubbery because we are unlikely to have a good idea of precisely how many have been infected until much later, we only knew the confirmed case numbers and these might have just been those who were sickest – sick enough to present to a medical clinic of some kind.

A simple way to calculate the mortality rate is to take the number of deaths and divide that by the number of (confirmed) cases (all figures taken from here with downloadable datasets here):

Deaths	Cases	Mortality Rate
12 Feb 2020	12 Feb 2020	D/C
1117	45206	2.5%

So that seems accurate, about 2% just like the authorities were telling us.

However, there is going to be a lag between a person presenting with symptoms, being confirmed as having COVID-19, getting progressively sicker and finally succumbing.  Surely the mortality rate should be compared not against the number of people confirmed to have the virus at the time of death, but at time of confirmation.  The question then is what is the lag between confirmation and death?

For the man who died in the Philippines, that lag was seven days.  There appears to be a six-day lag between the downturn in the rate of new cases (6 Feb) and the downturn in the rate of new deaths (12 Feb).   Let’s use six days:

Deaths	Cases	Mortality Rate
12 Feb 2020	6 Feb 2020	D/C
1117	30808	3.6%

But it could be worse than that, should we not consider it from the time that the virus was contracted, which is two to fourteen days prior to symptoms developing.  Let’s split the difference there and say eight days before being confirmed as having the virus and fifteen days before succumbing:

Deaths	Cases	Mortality Rate
12 Feb 2020	28 Jan 2020	D/C
1117	6082	18%

Whoa Nelly!

That would be something to be worried about.

Another way to calculate the figure is to consider those who had run the course of the disease.  Some recovered, some died which permits another calculation to be made, the percentage who run the course of the disease but succumb to it:

Deaths	Recovered	Mortality Rate
12 Feb 2020	12 Feb 2020	D/(D+R)
1117	5123	18%

My rounding here hides the fact that one 18% is actually 17.7% and the other is 18.3%, making them look precisely the same when they are different by more than half a percent.  Also, an interesting thing happens when you push back a couple of days and run the previous calculation (deaths/cases, fifteen-day lag):

Deaths	Cases	Mortality Rate
10 Feb 2020	26 Jan 2020	D/C
910	2829	32%

What?!

Another two days:

Deaths	Cases	Mortality Rate
8 Feb 2020	24 Jan 2020	D/C
725	941	77%

Of course, that can’t be right.  I’m conflating the notion of people who contract the virus on a particular day with figures reported as confirmed on that day.  Phew!

Note that the 18% for deaths divided by the number of people for whom the virus has run its course still stands, but if I go back in time and check the figures, the mortality appears to be worse the further back I go, so that doesn’t seem right either.

What about the seven-day lag figure?  If I do the same thing, pushing back a couple of days:

Deaths	Cases	Mortality Rate
10 Feb 2020	4 Feb 2020	D/C
910	24506	3.7%

It’s not as much of an increase, but as I push back further, the apparent mortality rate goes up – slowly, but inevitably, eventually getting into the 20% range in the early days of the outbreak.

So what I did was project into the future, assuming that the number of case and deaths increases linearly (which as of 12 Feb was worst case, given that there seemed to be a slowdown in both new cases and deaths), and found that the mortality rate based on cases, irrespective of the lag time, tended towards about 3%.  Mortality based on number of people who run the course of the viral infection, assuming a fifteen-day illness and borrowing case numbers from the previous projection, also tends towards about 3%.

So, as of 12 Feb and depending on whether my objective was to be accurate, informative, calming, inflammatory or some combination thereof, I could possibly justify saying that the mortality rate was:

2% (official)

2.5% (current deaths divided by current cases)

3% (long term trend)

3.6% (current deaths divided by cases six days ago), or

18% (current death rate divided by current number of people who have run the course of the viral infection, one way or the other)

That’s quite a spread.

The point that I am trying to make here, long-windedly, is that unless I went to some serious effort to explain to the reader how I arrived at whatever percentage I provided, my use of an apparently more accurate figure (3.6% versus 2% or 3%) should not be thought of as providing you with any more confidence that my figure was accurate, or that it gave you the information that you thought it was giving.

The same applies to the climate consensus 97% figure – for the most part, when quoted by a denialist, it’s being used as a distraction with the intent to keeping rational people engaged on minutiae and, therefore, not on the scientific evidence that is so damaging to the denialist cause.

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Note, since writing this, the topic came up on More or Less.  I am not “Ian” so someone else out there is maintaining a spreadsheet and arrived at a figure of 18%.