WHAT'S NEW - COVID-19 | Transmission Update - October

COVID-19 | Transmission Update - October

By Sean Derrig

Headlines

Navigating our way through the headlines about this virus is challenging. What do we really know? We do know a great deal more now than we ever did – it’s just a case of separating the science from the spin. To separate those, an evaluation of the source scientific papers is required. We do that so you don't have to.

1. A recent paper has suggested the virus is "extremely robust," surviving for 28 days on smooth surfaces such as mobile phone screens and both plastic and paper banknotes.

But the study was looking at an incredibly contrived set of circumstances and contributes little to our knowledge of the virus - but lends a lot to sensationalist reporting.

2. It’s now becoming clear that most people who catch the virus hardly pass it on at all but 10-20% of people who have it are responsible for 80-90% of onward transmission – what does this mean for productions?

3. Herd Immunity has been in the news too. The challenge is herd immunity comes from vaccines, not allowing the virus to run unchecked through a population.

4. Whether the virus spreads via ‘airborne’ means continues to be debated – some are suggesting it might be less trivial than we thought but what impact might this have on our behaviour?

It’s important to note that nothing in this bulletin changes our previous advice regarding distancing, masking, hygiene, and other common-sense interventions. But new research does help our understanding of the virus’s transmission and what we can do about it.

CAN IT SURVIVE ON SURFACES FOR 28 DAYS? 

A recent study (1) in a low-impact, open access journal has concluded that: 

“The data presented in this study demonstrates that infectious SARS-CoV-2 can be recovered from non-porous surfaces for at least 28 days at ambient temperature and humidity (20 °C and 50% RH).”

“These findings demonstrate SARS-CoV-2 can remain infectious for significantly longer time periods than generally considered possible.”

They make the point that: 

“Fomite transmission has previously been shown to be a highly efficient procedure, with transmission efficiencies of 33% for both fomite to hand and fingertip to mouth transfer for bacteria and phages.”

Yes, but not for SARS-CoV-2. There has not been a single, proven case of SARS-CoV-2 being transmitted via a surface (fomite) that could not be explained by its preferred, more social mode of transmission.

That’s not to say it can’t happen or hasn’t happened; it is entirely plausible, indeed other coronaviruses have been transmitted via surfaces. But it is certainly not its principal mode of spread.

But as above the paper quote transmissions efficiencies for bacteria – which is quite simply irrelevant - and (bacterio)phages which are viruses that infect bacteria, not humans. This isn’t just irrelevant, it shows a breathtaking ignorance of basic virology and makes one question the peer review process of this journal too.

The central claim of this article rather turns the accepted consensus on its head. Previous studies have come up with far shorter periods – but previous studies have been flawed.

Many used the presence of viral RNA on a surface as proof of the presence of infective virus (or airborne virus spread over great distances) which is simply not the case. Others put virus on to test surfaces and then tried to recover live virus after different times had elapsed. The problem is even this approach still doesn’t tell us the likelihood of someone getting an infection from a surface, plus such high starting concentrations of virus were used it doesn’t reflect ‘real life’ scenarios.

In science, extraordinary claims require extraordinary evidence. So, does this paper present that and is it the study to end all studies? Sadly, no

What They Did

They took live virus and applied it to various ‘coupons’ (as they’re known in the biz) made of different substrates to see how long you could recover viable virus from them at different temperatures and humidities.

Why This Is Different

Other studies have asked very similar questions but were looking for viral RNA which will hang about for far longer than viable virus – so this method is rather like finding a dinosaur footprint and citing it as proof T Rex has returned. At least this was looking at actual viable virus – but under VERY artificial and contrived conditions.

What Does This Tell Us?

Not a great deal that is useful, unfortunately. It does show that under quite unnatural conditions you can make a few virus particles remain viable for a while, but there are serious technical limitations to the study:

  • Experiments were conducted in the dark. The virus is rapidly inactivated by light. This isn’t helpful in making ‘real life’ comparisons.

  • It was conducted at 50% relative humidity. Heat, light and people in an enclosed space like a studio or gallery will likely lead to RHs higher than this. The virus is less viable the higher the humidity so again, not ‘real life’.

  • The concentration of virus (the ‘titre’) used in the samples was orders of magnitude greater than one might find in a patient, let alone on a fomite (surface).

  • The concentration used equated to a PCR cycle threshold (Ct) value of 14 which they felt was ‘plausible’ but represents a far higher amount of viral RNA than usually found in clinical specimens. They do admit that using over 100-fold the titre used in other studies

“may account for the longer survivability.” 
  • They used a liquid to mimic the properties of saliva – but real saliva also contains many antiviral proteins, antibodies, white blood cells and other factors that make saliva very inhospitable to invading pathogens. The whole experiment is designed to enhance survival, our bodies do the opposite.
Again, this means the results tell us very little of relevance to real life.











They did calculate the ‘half-life’ of the virus under these very contrived and favourable conditions. The half-life is how long it takes the amount (titre) of virus to drop by half.

It varied a little depending on the surface and the conditions as one would expect but the longest was around two days. So viable virus would be down to 50% on Day 2, 25% on Day 4 and so on.







If we continue with that progression, on Day 28 there would be 0.006% of the starting amount left. 
We find this study unhelpful. While it may have (limited) technical interest to those working in the field, it does not tell us anything useful in terms of controlling the spread of COVID-19. They assert in the conclusion: 












"This persistence of SARS-CoV-2 demonstrated in this study is pertinent to the public health and transport sectors. 












This data should be considered in strategies designed to migitate the risk of fomite transmission during the current pandemic response."

This is quite simply hubris.  This study demonstrates no such thing.

In fact it's undeserved and wide dissemination in the media is likely to cause unnecessary confusion, anxiety and may encourage people to focus on a very minor potential route of transmission at the expense of concentrating on the far larger and provn risk factors.

THE IMPACT OF ‘SUPERSPREADERS’

Many questions still remain unanswered about how COVID-19 spreads. But we do know a lot more than we did and there is now a large body of evidence underlining the impact of ‘super emitters’ and superspreading events.

Key points are:

 The much-quoted R0 doesn’t tell us as much as we might think about how SARS-CoV-2 spreads;
Most people who catch the virus don’t pass it on to anybody
10-20% of people who have it are responsible for 80-90% of onward transmission;
Its transmission dynamics are very different to flu – which wasn’t realised early on and this knowledge can help inform future preventative measures.

Background

One of the biggest mysteries with COVID-19 is how some regions were very hard-hit at the start of the pandemic but other areas with similar populations, climate and other factors weren’t.

Milan and New York but not Tokyo? And why are there such huge variations between demographically-similar towns and regions in the UK? Many explanations have been proposed –schools, students, pubs, vitamin D, weather – and of course the responses of various governments.

All of these may well play a part but there were some assumptions made early on that have skewed our thinking but – as ever – science is catching up.


The data that most transmission is at ‘superspreading’ events is shouting ever louder yet – as was seen in the White House recently – that message might not have reached policymakers yet.

But then all the best disaster movies start with scientists being ignored. 

First we need to forget a couple of things. 

R0, Re, Z and k

We have all become used to politicians talking about the ‘R’ number. There are other metrics such as excess deaths - but the problem with R is it’s an average. It comes loaded with an assumption that spread is linear and predictable – in the jargon of epidemiology the pattern is ‘deterministic’ - like flu. The problem is, it isn’t.

To illustrate: 

Ꙭ | LIMITATIONS OF R

Bill Gates walks into Starbucks to buy his venti soy milk matcha green tea frappuccino with pumpkin spice.

There are 100 other customers there. The instant he walks in the average worth of each person in the place exceeds $1bn. But that average doesn’t tell us anything about the distribution of wealth in that Starbucks or how we might change it. And if someone with COVID were to walk in, and it’s loud and poorly ventilated chances are everyone might get it. 

We need some more jargon. Sorry. With deterministic spread (like flu), what happened last week helps us predict what might happen next week. R is helpful in these situations.

But the data now shows that trajectory of COVID-19 is stochastic. That means it has an intrinsic randomness and predictions are difficult because the same inputs can give markedly different outputs – which is what we’re seeing with large outbreaks going out of control in some places yet other places with many similarities remain largely untouched.

This confuses humans: we like phenomena with a clear arrow between cause and effect so we furiously seek the cause of an outbreak. Stochastic is the opposite of that – it’s inherently random - but we still we try to look for correlations where none exist and R doesn’t help us.

Why? This is an overdispersed virus which means it spreads in clusters. And its level of ‘overdispersion’ (k) can be measured. A recent paper (2) analysing an outbreak that was subject to extensive testing and tracing found about 19% of cases were responsible for 80% of transmission and 69% of cases didn’t infect anyone else.

There have been many other studies giving very similar numbers. 

What Does This Mean?

This does have impacts for policy and contact tracing strategies we’ll not delve into, but it’s interesting to observe there were early fears that Tokyo, with its population density and quite aged population, could have been very badly hit. It wasn’t’. Many possible reasons for that have been suggested such as local custom regarding masking and social interaction etc but none has been very satisfactory.

Japan focused on the impact of COVID-19’s over dispersion from early on, and their approach has been likened to looking at a forest and trying to find the clusters rather than the trees, unlike many countries which were trying to trace each individual tree and getting lost in the forest. Essentially you need to identify transmission events rather than concentrate on infected people.

Which is all well and good and interesting, but what does it mean for productions? Well, not a lot, really. 

  • It highlights the utility of rapid and frequent testing;

  • It reinforces our previous advice to avoid crowded places, close contact and close conversations – the main risk remains in poorly ventilated, indoor environments where people congregate for extended periods, especially when there is loud talking or singing without masks.























If prolonged contact, poor ventilation, crowding and poor mask adherence occurs, all it takes is one infectious person (especially if they are a ‘super-emitter’) and you have the perfect recipe for a super-spreader event.

It’s not a fail-safe recipe in that there is a degree of chance, but consider recent events in Washington DC – relying on an antigen based diagnostic test as a screening test, ambivalence to masks and respiratory hygiene generally, and lots of people in close contact for an extended period..

HERD IMMUNITY 

There has been much interest in a ‘declaration’ from a US libertarian think tank calling for ‘focused protection‘ for the elderly and vulnerable to allow the rest of society to return to normal life and build up herd immunity.

We already operate a form of ‘focused protection’ for seasonal flu in the UK – we vaccinate not just the elderly and vulnerable but also those that may spread flu to them – children. And if they do get flu we have zanamivir and oseltamivir. But that’s the point – we have neither vaccines nor therapeutics in the toolbox for COVID-19.

This declaration has garnered much press coverage and speculation and gathered the signatures of many ‘respected scientists and medics’ - but the only qualification required is an internet connection. Anyone can sign and many have, including the late Dr Harold Shipman. Several times.

Anyway, can this strategy work?

No. It sounds plausible but it defies the known laws of biology. Eminent scientists and public health experts who actually work in this field and so are qualified to pronounce on it have condemned it as “a very bad idea” and “dangerous to national and global public health”.

What Is Herd Immunity and How Is It Achieved?

Herd immunity occurs when a large proportion of a community (the herd) becomes immune to a disease. This means the virus has difficulty finding susceptible hosts and so the spread of disease from person to person is halted. As a result, the whole community becomes protected — not just those who are immune.

The proportion of the community needed to achieve this varies; it can be as low as 50% but this is rare. It’s usually more like 90%, especially for something really contagious.

There has been modelling suggesting COVID-19 may need a lower number than this but that’s speculation – and isn’t really relevant for two reasons.

  • The only way to achieve herd immunity is with a vaccine.


    No disease ever has achieved ‘natural’ herd immunity in the way proposed by this manifesto. In the past, infections such as measles would pass through communities and a certain degree of immunity would occur. So you’d get smaller outbreaks most years and epidemics other years. This is not herd immunity – it’s just the size of the wave year-on-year.
  • To achieve any sort of herd immunity you need that immunity to be long-lived.


    If protection is not long-lived the immunity in people who are infected early on will be waning by the time people who get it later become infected. And more and more data are stacking up suggesting we only get protective antibodies against SARS-CoV-2 for some months, not years.

So, biologically the idea doesn’t hold up. If a disease doesn’t provoke long-term immunity, you can’t have herd immunity and herd immunity is a product of vaccination, not ‘natural’ infection.

It could be like flu in that you get protection from a vaccine that lasts – say – a year and next year you get the new shot. In flu this is because the virus mutates like hell. COVID-19 mutates at a much lower rate than flu.

It could be that a future vaccine will offer longer-term immunity – we just don’t know yet. 

Herd Immunity by Numbers

Just by way of illustration let’s assume that you could achieve heard immunity in the way described without a vaccine. In this parallel universe where the known laws of biology don’t apply this would happen:

  • At the time of writing, in the UK we’ve seen over 600,000 confirmed cases, nearly 43,000 confirmed deaths and just shy of 150,000 hospital admissions.
  • If we look at infection rates (as measured by people who have antibodies against COVID-19), it varies regionally – 18% around London, the mid-teens in parts of the North and the Midlands and 5% or less in other places. Let’s say nationally 10% have antibodies against SARS-CoV-2 AND those antibodies give a degree of long-term immunity.
  • In order to reach the mythical 50% level without a vaccine that’s more than three million additional cases, another 215,000 deaths, and over 700,000 hospital admissions. There are 101,255 general and acute beds in the NHS






So even if the idea of herd immunity without a vaccine could work the human cost would be enormous. If – as is likely – we need immunity in more than 50% of the herd those numbers go up dramatically, obviously. It’s important to note these are crude calculations, populations are not homogenous biologically or socially and any further comment gets into the politics of this which is not for us. Roll on the vaccine...

Aerosol Transmission 

This keeps coming back!

There is a strong consensus - and no real doubt - that the primary way in which COVID-19 is spread is through large droplets. These come from breathing, talking, coughing, sneezing, shouting, or singing. Viral particles are encapsulated in globs of mucus, saliva, and water. These globs can spread several feet. Exactly how far is still a little controversial, but 6’ is generally considered to be a minimal safe distance. Or 2m in new money.

Indirect transmission through physical objects (fomites) is also possible but this is considered a minor (but not irrelevant) route of transmission.

Aerosolised spread refers to viral particles surviving in droplets so tiny they can remain airborne for a long time, unlike the larger droplets we already know about that tend to fall quickly to the ground.

This is important because cloth masks aren’t as protective against aerosols, you need proper PPE for that.

Also the distinction between ‘large’ droplets and aerosols is somewhat arbitrary -it’s actually a continuum, as is settling time because settling time is based on droplet size.

Two recent reviews have suggested: 

“Researchers have speculated that both droplets and aerosols generated from non-violent and violent expirations of SARS-CoV-2-infected people may be responsible for the airborne transmission of COVID- 19 disease. However, more research work should be conducted to understand the behaviour of virus- laden droplets and aerosols in different environmental settings, especially confined spaces so that the transmission of COVID-19 pandemic in the built environment could be fully ascertained (3).”

So, ‘more work needed, but it might be a thing’. 

Heating, Ventilation and Air Conditioning Systems (HVAC) are used as a primary infection disease control measure. However, if not correctly used, they may contribute to the transmission/spreading of airborne diseases as proposed in the past for SARS.

The authors believe that airborne transmission is possible and that HVAC systems when not adequately used may contribute to the transmission of the virus, as suggested by descriptions from Japan, Germany, and the Diamond Princess Cruise Ship (4).

Again this is not exactly a smoking gun.

Both these papers are quite equivocal and not in high-impact journals. Were the BMJ, JAMA, NEJM or one of the high-impact infectious disease journals to weigh in on the matter that might be different.

Nothing in these papers is startling enough for us to change our current advice but we shall continue to watch as science continues to pick at the scab until it delivers a definitive answer.

References

1. The effect of temperature on persistence of SARS-CoV-2 on common surfaces. Riddell, Shane, et al. 145, 7 October 2020, Virol J, Vol. 17.

2. Clustering and superspreading potential of SARS-CoV-2 infections in Hong Kong. Adam, Dillon C, et al. 17 September 2020, Nature Medicine.

3. Transmission of COVID-19 virus by droplets and aerosols: A critical review on the unresolved dichotomy. Jayaweera, Mahesh, et al. September 2020, Environ Res, Vol. 188.

4. Airborne route and bad use of ventilation systems as non-negligible factors in SARS-CoV-2 transmission. Correia, G, et al. 2020, Med Hypotheses.

5. Test sensitivity is secondary to frequency and turnaround time for COVID-19 surveillance. Larramore, Daniel B, et al. 27 June 2020, medRxiv.

6. Evaluation of Two Rapid Antigen Tests for Detection of SARS-CoV-2 Virus. Khairat, Sahar Mohammed, et al. 3, 13 Augst 2020, International Journal of Microbiology and Biotechnology, Vol. 5, pp. 131-144.

7. Panbio antigen rapid test is reliable to diagnose SARS-CoV-2 infection in the first 7 days after the onset of symptoms. Linares, Manuel, et al. s.l. : medRxiv, 23 September 2020.

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