I’ve been seeing some wild speculation that this pandemic is the product of genetic engineering — that it’s a biowarfare weapon that escaped from a lab somewhere. This is nonsense. I’ll refer you to an article in Nature Medicine, The proximal origin of SARS-CoV-2, which discusses a systematic analysis of the structure of SARS-CoV-2 in comparison to other coronaviruses.

It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted. Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone. Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) natural selection in humans following zoonotic transfer. We also discuss whether selection during passage could have given rise to SARS-CoV-2.

A little translation: the virus has a spike protein that binds to an enzyme on the surfaces of cells, called angiotensin converting enzyme, or ACE. This enzyme is important in regulating blood pressure, and is expressed by cells in lung capillaries (fun fact: your lungs play an endocrine role in sending out signals that maintain blood pressure). This is one reason the virus has such a dangerous respiratory effect — the lungs are the primary targets, where it can use the spike protein to bind to cells that express ACE and drill into them.

The RBD is the Receptor Binding Domain of the viral spike, and is the most variable part of the virus. This makes sense: the RBD is the key the virus uses to get access to your cells, and it varies because it confers target specificity. So there are all these different varieties of coronavirus, most of which don’t bother humans because they lack the human key — they are adapted to invade other animals’ cells. SARS-CoV-2 has acquired a spike with a human unlock code. Could some cunning super-villain have modified the spike?

Not likely, for several reasons. The virus has other similarities to coronaviruses in other animals; it’s not a de novo construct, but is a member of a large family of viruses. The modification to the spike protein is unusual. It works, but it’s not one that scientific experts would have used — they would have used something that would have been previously modeled. Then also bioengineers have lots of clever tools that could be used to stuff a desired sequence into a virus, but they all leave tool marks, little scraps of the molecule used to do the replacement. Those marks aren’t there. The best explanation is that we’re just seeing natural selection amplifying random variations in the spike.

While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

Yeah, see, if I were a nefarious super-villain, we already have an even better RBD we could yank out of other viruses, and I would have used that to build a deadly virus. But instead, the SARS-CoV-2 RBD is some clunky variation that came out of nowhere, by accident, without any other signs of intentional manipulation.

They also consider the possibility that this was an accidental variation acquired in a lab — if you pass a virus through a lot of host cells in a cell culture system, it will continue to evolve, and you might imagine the RBD might acquire a random variation that allows it to thrive in those cells, and then it accidentally escapes the lab. This is also unlikely, because it shares a lot of similarities with the pangolin coronaviruses. It’s more likely to have arisen from an existing pool of related viruses in the wild, then either acquired its novel binding site there, or after infecting humans and experiencing selection for better binding to human cells.

The best strategy is to look for intermediates in animals, or in the sequences of humans who were infected early in the pandemic.

The identification of a potential intermediate host of SARS-CoV-2, as well as sequencing of the virus from very early cases, would similarly be highly informative. Irrespective of the exact mechanisms by which SARS-CoV-2 originated via natural selection, the ongoing surveillance of pneumonia in humans and other animals is clearly of utmost importance.

Sorry, conspiracy theorists. The best explanation is evolution and natural selection, not Evil Intelligent Design.

Last week there was an article published by a guy named Aaron Ginn in Medium, which purported that the current pandemic was going to fade out relatively quickly and do far less harm than others expected. The article was spread widely — you might even say it went viral — and some big names in media promoted it. It was recently taken down, though, and I can’t link to it, nor would I, even if I could. It was a terrible article.

It was interesting as an exercise in critical thinking, though. The first week of my introductory biology course I share a bad science article with the students, and ask them to figure out how they would know whether to trust it or not. They quickly do the usual stuff — look at the source, look at the author, look at the quality of the data — which should have been the response to this article by Ginn…but no. It says things people wanted to hear, so it was disseminated uncritically.

What should have been noticed right away is that Ginn has zero qualifications in epidemiology, yet here he is claiming that the scientists were all wrong. You might be wondering what his qualifications are. He’s a silicon valley tech bro who claims to be an expert in “growth”, meaning how to increase the popularity of products online. Because he uses the word “virality” in his advertising and promotion work, surely he must be a master of the biology of real viruses. He even claims you don’t need a special degree to do epidemiology.

Jesus. Red flags and signal flares popping off all over that mess. The arrogance of these silicon valley dudes knows no limits, and we ought to be able to stop there. Except that Mr Ginn was quite annoyed when his silly, ignorant article was yanked, and he ran yipping and whining to other unqualified media personalities, like Brit Hume, Greg Guttfeld, and Steven Crowder (seriously, dude?), none of them with any qualifications in the subject, either. He’s being censored, don’t you know. He’s now frantically and rather indignantly defending his claims on Twitter. Someone ought to tell him that Brit Hume, let alone Crowder, isn’t exactly a smart guy to cite, and rather obviously his choice of who to beg for props is telling. Ginn writes for Breitbart in his spare time, and works with the California Republican party.

Anyway, ignore Ginn and his bad paper. Go read this Twitter thread by Carl Bergstrom, who actually knows what he’s talking about.

1. I hate to invest precious time on taking apart the atrocious @aginnt article pictured below, but it is getting too much traction here and even in traditional media.

This thread could be far longer than it is, but I'm doing my best to only discuss the most glaring flaws. pic.twitter.com/EFA7ATQRbX

— Carl T. Bergstrom (@CT_Bergstrom) March 22, 2020

Ginn is puking up exactly the kind of misinformation that ought to be filtered out — he’s cocky and full of himself, but he knows pretty much nothing about the subject he’s lying about.

I decided to get out of the house and take a walk. Everything is still dead and brown and frigid outdoors, but I had a cunning plan: I’d visit the university greenhouse! I was disappointed.

Oh, sure, there were colorful flowers.

But I was looking for spiders. The only arthropods I could find were some tiny ants scurrying all over twigs and leaves. You can’t escape ants.

There were some tantalizing dense cobwebs in a couple of close spaces, but the inhabitants weren’t hanging out. Probably lurking. I’ll have to come back and check again.

I miss working in a lab with a wall of fish tanks, the water gurgling, the little fishies darting about. It was rather soothing. Spiders have their charms, but they don’t dart, or flash, or move in swirling schools, they mainly just lurk. My lab is much quieter and dryer now.

I switched to spiders because I wanted an animal to study in their natural habitat, looking for interactions with other species. As it turns out, there was an alternative: I could have moved to the Bengal region of India, which is a magical place where the experimental animals frolic in great numbers in shallow ponds, and where I could be wading knee deep in warm waters while Danio rerio nibbles at my toes, like the Jutfelt lab is doing.

I was mesmerized by this video this morning, just lying in bed watching the lovely schools of zebrafish zipping around.

Spiders don’t frolic, either. They do murder small arthropods, though, in a vicious and personal way, which might better fit my mood nowadays.