2 things have been troubling me lately:

1. The notion that recognizing the nuances & uncertainties of SARS-CoV-2 transmission is somehow "denying" that respiratory transmission occurs.

2. This is all @WHO's fault for giving bad guidance.

Are these true? Let's look at the data.
1. SARS-CoV-2 is a respiratory virus. That means it infects cells of the respiratory tract in both the upper (nose) and lower (lungs) airway. Naturally, this means you become infected after exposure to virus via inhalation, direct contact (droplets), or indirect contact (fomites)
Infection occurs not from exposure to purified virus, but from virus that's emitted in particles of saliva and mucus that an infected person exhales (or speaks, sings, etc).

Go outside on a cold day and breathe out. That cloud of steamy breath? Those are respiratory particles.
These particles are all different sizes, from large droplets of snot/spit expelled with a sneeze all the way down to tiny aerosols that you can't see with the naked eye. Over the years, different disciplines have distinguished these by size, trajectory, and behavior over time.
The distinctions in terminology have led to a lot of truly exhausting arguments. For example, some think you can't inhale droplets because they are ballistic, but some think you can inhale the smaller ones if you define them only by size.
Some people define droplets as anything > 100 microns (um) in diameter, some define them as anything > 5 um. A 95 micron difference is actually pretty big regarding how long a particle can remain suspended in the air, because that's a big difference in volume and thus weight.
Since it's also a big difference in volume, that can also impact how much virus is contained within. That, in turn, is highly variable from person to person, depending on where they are at in the course of infection and how much virus they are shedding and where it's being shed.
All this is to say that there's a lot of uncertainty and nuance going on with this topic, which can make it seem as though scientists from one discipline are "denying" transmission by one route or another, when in reality the differences are largely semantic.
Furthermore, the routes of transmission themselves are not straightforward. "Droplet" transmission doesn't mean the sneeze version of Luke Skywalker hitting a bullseye of the Death Star's thermal exhaust port with his proton torpedoes.
Droplet transmission is also sometimes called "direct contact" transmission because that refers to direct contact of virus-containing material with the body. You can sneeze on someone's hand and then they touch their nose or mouth...
Adding to the confusion: snot and saliva are mostly water, which will evaporate. This reduces their size and can change their physical behavior. For particles on the smaller side, this means that a "droplet" can become an "aerosol."
So that brings us to "denial" of "airborne" transmission. This "denial" is usually actually a disagreement on terminology as well as a debate on which form is dominant. It's clear that fomite transmission (contaminated objects or surfaces) is less common for SARS-CoV-2.
Part of the reason for that is the nature of viruses. They are obligate parasites and require a host to reproduce. When they are in the environment for extended periods of time, they eventually become non-infectious. This depends on both the environmental conditions & the virus.
SARS-CoV-2 is an enveloped virus, which means that it is less stable than a non-enveloped virus. The amount of time it remains infectious in the environment is determined by temperature and humidity.
Other non-enveloped respiratory viruses, like rhinovirus or adenovirus, are more resistant to these changes, but it's very dependent on the environment. Fomite transmission has been demonstrated for most respiratory viruses.
So what about aerosols and droplets, then? Why can't we figure out which one is contributing more than the other?

Well, the whole fomite tangent was to impress upon you that there's more going on here than just physical variables like droplet size or movement in the air.
Distinguishing aerosol vs droplet transmission in the real world is exceptionally difficult in epidemiological studies. People are often unreliable narrators at describing their prior actions ("I stood exactly 3.5 ft from this person for exactly 14.5 minutes in a 9x9' room")
And close contact alone doesn't distinguish between aerosols and droplets. How do you know if you breathed in an infectious dose, or if you just scratched your nose after someone's stray cough/sneeze/shout-propelled droplet landed on it?
Also aerosols that are exhaled by people are more concentrated in close proximity which brings us to the complicating factor of infectious dose. You likely aren't going to be infected by being exposed to a single infectious SARS-CoV-2 virion.
There are multiple barriers to infection: nose hairs that trap larger particles, mucus that covers susceptible cells in the respiratory tract, virus coming into direct contact with a cell expressing the virus receptor ACE2, and the innate immune system/interferon response.
To establish a productive infection in a new host, there needs to be enough infectious virus in the exposure dose to allow a lucky few to overcome all these barriers to infection. That's going to be more likely in situations where you're exposed to a higher dose.
Those conditions can be met through close contact exposure of any kind, whether by direct contact with droplets or inhalation of aerosols. In certain situations (enclosed spaces), enough aerosols can build up to also cause infection.
And those of us working on respiratory viruses for years, including virologists like me (I did my PhD on rhinovirus and have worked on flu and MERS-CoV for the last 10 years), epidemiologists, infection preventionists, etc. all KNOW this. Nobody has been "denying" it.
It all comes back to semantics. Different fields have different terms for different things. "Airborne" usually refers to long-range aerosol transmission, which only occurs for SARS-CoV-2 when the conditions allow for it. Using a term in a field-specific way is not "denial."
This debate is exhausting & unnecessarily contentious. I've been accused of killing people b/c I don't think the term "airborne" is specific enough. We desperately need unifying terminology, but we won't get that w/ one field telling another that academic disagreement = murder.
SARS-CoV-2 is a respiratory virus. It is transmitted by the respiratory route. That includes both inhalation of aerosols and direct contact with droplets. To a lesser but non-zero degree, it also includes indirect contact/fomite transmission.

Nobody is denying that.
Now let's move on to #2: this is all @WHO's fault for "bad guidance."

To start off, it's safe to say that the US didn't follow WHO (or CDC) guidelines. But which countries did? How are they doing?

What guidance did WHO issue that is, in fact, so bad?
Today is the one-year anniversary of a now infamous tweet from WHO that SARS-CoV-2 is not airborne. I just discussed how "airborne" can mean different things to different fields. WHO has gotten no end of pushback, ranging from constructive to accusations of genocide.
To refresh your memory, last summer WHO received a letter from a large group of scientists asking them to revise their guidance. They wrote a very thorough scientific brief in response.

They were still shredded for it.
In this document, they took a nuanced approach that was based on both contemporary data as well as other respiratory viruses. They carefully defined aerosols and droplets based on size, and defined "airborne" transmission as specifically long-range.
But no! Said people from other fields (and quite a few non-scientists). We don't like these definitions because we use a different definition for droplets, aerosols, and airborne. They aren't "admitting" that it's AIRBORNE! People are dying as a result!!!!
But is that true? Here are some examples of countries that have been applying WHO guidance:
New Zealand
South Korea
The list goes on and on. Not all these countries implemented WHO guidance the same way, but that just goes to show that there's more than one way to respond to an emerging health crisis.

But key to this? These success stories didn't depend on the virus being "AIRBORNE."
Not only is this particular criticism of the WHO demonstrably untrue, but it indicates a very poor understanding of what the WHO actually does.

The WHO exists to provide an international body, composed of member states, to address global health threats.
As part of that mandate, yes, they provide guidance. But they have no authority to demand that member states implement that guidance, nor do they expect that member states won't apply the guidance that works for them.
As such, it's unreasonable to expect them to issue guidance that calls for every country in the world immediately start overhauling their ventilation systems or distributing N95 masks to everyone.
Furthermore, many don't seem to realize that the WHO has many other functions, including responding to other public health emergencies of international concern (PHEIC)—of which there are many occurring at the same time.
They also are responsible for coordinating vaccination campaigns for COVID and other viruses, such as measles and Ebola, and other forms of relief for these PHEICs (food, medical supplies, etc).

All on a shoestring budget made up of voluntary contributions from member states.
So before you blame WHO for giving "bad" guidance that's actually quite good when you look at countries that have implemented it, or for "denying" aerosol transmission, maybe consider that global health is a lot more complicated than just screaming AIRBORNE into the void.
@WHO is not above criticism, but if you think that ANY one entity is singehandedly responsible for the pandemic, then your thinking is hopelessly facile and you really ought to rethink your qualifications for opining on this topic.
We live in a global world, and I'm thankful we have @WHO to respond to infectious threats in a global, multi-dimensional way. We can all do better. But that doesn't mean WHO is bad.

Let's try to remember that we're all in this together.

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More from @angie_rasmussen

19 Mar
No, you can’t. Kids being lower risk does not mean “same as an already vaccinated grandparent.”

I value other perspectives, like economics, in vaccine discussions. All are stakeholders in public health. But have the humility to know when you’ve hit the limits of your expertise.
This is insufficient. The problem wasn't just the headline. The problem is that two of the fundamental arguments are wrong.

1. Risk of infection is just as relevant as risk of disease.

2. Vaccinating only adults won't get us to herd immunity by summer.
And I should add there's another risk that wasn't addressed at all: the vaccines are not 100% effective (though they are very good). Failing to mitigate transmission risk by relying on flawed risk assessments still presents a danger, especially to more vulnerable adults.
Read 4 tweets
18 Mar
So, here's another great paper out today from my friend and colleague @DrSimonAnthony.

It will be of particular interest to those pondering possible SARS-CoV-2 origins, and viral evolution enthusiasts in general.

Brace yourself: it's about how different sarbecoviruses use ACE2.
In short: Dr. Anthony and his PREDICT colleagues found 3 isolates of a novel sarbecovirus (SARS-like betacoronavirus) in bats...from Uganda and Rwanda. Hey, that's nowhere near China, so what does that have to do with SARS-CoV-2?
A lot, actually. Sarbecoviruses are not exclusive to China or East Asia. That's where they've been studied most extensively, but they aren't restricted to that part of the world. Here's how these viruses and host bat species relate to each other and where they were discovered.
Read 19 tweets
12 Mar
The sequences from the Ebola virus outbreak in Guinea were posted on virological, and they are, to put it mildly, absolutely stunning.

The sequences are only 12-13 nucleotides different from those circulating in the 2014-2016 epidemic.

This suggests that this new outbreak resulted from transmission from a persistently infected survivor of the prior epidemic, which is bad for a whole host of reasons, including the further stigmatization of Ebola virus disease survivors.
This is also genuinely shocking to me scientifically.

Based on the known mutation rate of EBOV/Makona, we'd expect viruses that have been replicating for 5-7 years, even at low levels, to have many more mutations. Like hundreds. These have 12.
Read 8 tweets
11 Mar
Good grief. This isn’t even a study—it’s a preprint of a perspective piece advancing an untested hypothesis (pork shortages led people to seek other meat sources). You can poke holes in this without much effort.
For example, do the authors really think that ASF-induced shortages of farmed pork led people to start sourcing wildlife to replace it? It would take many metric shit-tons of bats and civets to replace the lost pork.
Why wouldn’t most shoppers just use a more readily available meat like duck?

I know when pork chops are sold out, I immediately start thinking about sourcing some rhinolophid bat meat to replace it. Then I realize that’s dumb and just grab a chicken or whatever instead.
Read 9 tweets
10 Mar
I'm writing about this (among other knowledge gaps still to be filled with regard to SARS-CoV-2) and Dr. Goldstein is right: I've been working on host responses to the big bad beta-CoVs since 2012, but haven't given much thought about tissue tropism of the other hCoVs...
This has led me to think about the relevance of fecal shedding for SARS-CoV-2 to transmission. The key to understanding SARS-CoV-2 transmission is that it's situational, even with more dominant modes (inhalation, direct contact) of transmission.
Dating back to SARS classic in 2003 & now with SARS-CoV-2, transmission via fecal bioaerosols is thought to occur when specific conditions occur with a building's plumbing. Despite lots of 🚨🚽🦠⛲️💩☣️-type tweets about it, people aren't getting COVID every time a toilet flushes.
Read 22 tweets
3 Mar
It has come to my attention that noted anti-vaccine zealot Robert F. Kennedy Jr. is releasing a film tomorrow targeting the Black community with some appalling misinformation.

It is not just filled with falsehoods. Despite claiming to be anti-racist, it is racist as hell
Medical racism absolutely exists, and underlies the disproportionate impact on the COVID-19 pandemic on the Black community. But correcting those disparities by claiming vaccines contribute to medical racism?

That's much, much worse.
You know what the result of discouraging Black people from getting the COVID-19 vaccine will be?

More preventable deaths in the Black community.

Race-based targeting with the goal of more Black people dying as a result?

It's morally bankrupt and outright racist.
Read 5 tweets

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