College football continues to corrupt our universities. At least we could pay the players

More than ten years ago, I wrote that it was time to get football out of our universities because the sport was corrupting the universities’ mission. Not surprisingly, I got a lot of pushback about that, but I’ve continued to make this point, both here at Forbes and in The New York Times.

This weekend, I watched a college football game for the first time in years. I was struck by how much worse things are–and by worse, I mean driven by money.

Don’t get me wrong. Football is entertaining for its millions of fans, and college football is extremely popular, especially for those who live in cities without a professional team. I’m not so naive as to think people will give this up.

The problem is that major college football is a professional sport where everyone makes money except the main participants: the players. Worse, the players are being told by their coaches, assistant coaches, athletic directors, and university presidents that they’re getting a great deal. We give you free education! And you get to play football for our great team, and everyone will cheer for you!

If this is really so great, then why don’t the coaches work for free? College football coaches are paid multimillion-dollar salaries, usually far higher than anyone else at the same university, even the university president. The average salary of NCAA Division I coaches this year is $1.75 million, and some coaches make over $10 million. In most states, a football coach at a public university is the highest-paid state employee.

But the players get zero. This situation, to put it bluntly, is unethical. Universities with large football programs are profiting handsomely off the unpaid labor of their own students.

Universities have been told this before. In 2011, civil rights historian Taylor Branch wrote a ground-breaking cover story in The Atlantic titled “The Shame of College Sports,” As Branch wrote then:

“Big-time college sports are fully commercialized. Billions of dollars flow through them each year. The NCAA makes money, and enables universities and corporations to make money, from the unpaid labor of young athletes.”

That was 11 years ago. The situation has only gotten worse.

What’s striking about watching a college football game on television, as I did this past weekend, is the degree of commercialization of the sport. The game is interrupted constantly with advertisements from sponsors, and the stadiums are decorated with ads as well. ESPN has a large, professional team of announcers covering every aspect of the game. The television work is highly coordinated and professional, with many cameras covering every angle of every play.

There is a LOT of money in college football.

I listened to interviews with some of the (winning) players after the game. They were excited, and they praised their coaches and fellow teammates as they were supposed to. They seemed to believe that the game they’d just won was supremely important, and that their performance (an upset victory) was meaningful and even “historic” (as one player said).

But it wasn’t. Football is just entertainment.

What’s especially sad, to me, is that nearly all of these players are getting short-changed on their education. They spend most of their time on football for a good portion of their year, despite the laughable pretense by the NCAA that these are “student athletes.” They’re athletes, certainly, but they don’t have time to be students, not during football season. The universities (and especially the football coaches) just don’t seem to care, despite their continual protestations to the contrary.

Only 1.6% of college football players make it into the NFL. Or to put it another way: at the end of their college years, 98.4% of college football players will be spit out into the real world, with poor job prospects because they didn’t focus on their education.

And it’s actually even worse than this. We’ve learned in recent years that football carries serious risk of permanent neurological damage, due to repeated blows to the head that happen to many players. It’s a violent contact sport, and the ever-greater size of today’s players has made it much more dangerous than in its early years in the mid-20th century. (I wrote about this too, back in 2019.)

Universities could start to fix this unethical situation by paying the players what they’re worth. Here’s one idea: if universities are seriously concerned about the education of these young men, they should separate their football programs from their education programs. Teams could pay to license the university’s name, hire and pay players, and pay fees to use the football stadiums. (Football fans claim that the sport makes a profit, and if this is true, the teams should do just fine in this scenario.) The athletes could be offered full 4-year scholarships that they could use after their playing years were over, or perhaps in the off seasons, so that they would be able to truly focus on their education.

But meanwhile, as The Atlantic‘s editors put it over 10 years ago,

the real scandal is the very structure of college sports, wherein student-athletes generate billions of dollars for universities and private companies while earning nothing for themselves.

Pay the players. That’s the only way to fix this.

New report says COVID was probably a lab leak: should we believe it?

 

A week ago, Vanity Fair and ProPublica published a long exposé on the origins of Covid-19, in which they revealed new evidence of a lab leak in the Wuhan Institute of Virology (WIV) in November 2019.

The big reveal: the report makes it appear much more likely than before that Covid-19 originated through an accident at WIV, where presumably one of the scientists was exposed to the virus. The new evidence in the ProPublica report largely centers on the work of a translator, Toy Reid, who claims to have a unique gift for interpreting the “secret language of Chinese officialdom.” Even native Chinese speakers can’t really follow it, he claims in the article.

Reid scrutinized a collection of internal and external communications from WIV, and says that he found messages in the fall of 2019 that indicated “inhumane working conditions and hidden safety dangers.” And most significantly, a message on November 12 refers to some kind of biosecurity breach, which might have referred to an accidental exposure of someone in the lab to a virus.

The date of this incident appears to coincide with an incident described in a 2021 article in the Wall St. Journal, which reported that 3 WIV employees sought hospital care in November of 2019. This incident has never been confirmed to involve Covid-19 infections.

To add some context: Reid’s findings were released by a Republican U.S. Senator, Richard Burr, in a report that was not endorsed by the full Senate committee investigating COVID-19’s origins. Burr’s report concluded that Covid-19 was “more likely than not, the result of a research-related incident.”

Not surprisingly, this new report has been getting a lot of attention.

The report initially might seem convincing, until you realize that it doesn’t include any actual biological evidence: no reports of actual infections, and no specifics about any viruses that might have escaped from WIV at the time. It seems to be based entirely on the translation super-powers of Toy Reid.

It didn’t take long for other experts to weigh in. There are plenty of Chinese-language speakers out there, including native speakers who are likely much more fluent than Toy Reid. One translator wrote on Twitter that Reid “screwed up.” Another said that a critical passage identified by Reid “doesn’t suggest a biosafety problem had occurred at all.”

Hmm. Here I have to admit that I have no idea who is right here, since I don’t speak or read Chinese. However, it does appear that ProPublica and Vanity Fair may have put too much faith in a single translator who might have had a political bias.

And there’s more. A number of virologists weighed in to point out that the Vanity Fair piece had ignored work that pointed to the Huanan Wholesale Seafood Market (in Wuhan) as the source of the virus. I wrote at length about that research in March, when 3 new scientific papers had just appeared (as preprints), all pointing fingers at the seafood market as the source of the pandemic.

Unfortunately, all of the evidence in those papers was circumstantial. None of them found an infected animal that was the true source of Covid-19. Instead, they found that many early cases in people were centered on the seafood market. Even supposing that is correct (and it might not be, because China never allowed outside scientists to go to Wuhan and test people all over the city), it is still just circumstantial. Perhaps a scientist from WIV got infected and stopped by the seafood market that day–we may never know.

But let’s return to this week’s controversy, shall we? A virologists who led one of the papers I discussed back in March, Michael Worobey, was also quoted in the Vanity Fair article. He had major objections to what they wrote, and he posted them in a lengthy Twitter thread here, which is well worth reading.

Vanity Fair described Worobey’s work as providing evidence that a natural zoonotic origin (in other words, an origin in an animal at the Wuhan seafood market) for Covid-19 was “plausible.” Worobey objected, pointing out that his comments were much more definitive, and that his position is that:

"OUR TWO RECENT PAPERS establish that a natural zoonotic origin is THE ONLY plausible scenario for the origin of the pandemic." (all-caps in original)

After Worobey’s Twitter thread appeared, Vanity Fair and ProPublica updated their stories to include exactly that quote, without the all-caps.

Worobey makes a compelling case that Vanity Fair and ProPublica misquoted him (or at least omitted important details), and it seems they have fixed that error. However, neither the Twitter thread nor Worobey’s scientific paper make a definitive case that, as he puts it, a natural origin is the “only plausible scenario” for Covid-19.

Not at all. The paper by Worobey and colleagues concluded that “the earliest known COVID-19 cases from December 2019 were geographically centered on this market.” Let’s grant that this statement is accurate: even so, their data does not prove that the market was the “origin” of the pandemic, especially because they failed to find any animals infected with Covid-19 from that market. They only found human cases. This leaves open the question of where the very first human case occurred: it’s entirely possible that the first human was infected elsewhere–perhaps at the Wuhan Institute of Virology–and that human visited the seafood market while actively spreading the virus.

And their data relies on samples collected in Wuhan, which is of course controlled by the Chinese government. Note the wording of that conclusion from the paper, which refers to “the earliest known cases.” China does not want the world to think that the Wuhan Institute of Virology might have caused the pandemic, so how can we ever know if there were early cases originating from WIV?

On the other hand, as I wrote back in March, China has known for decades that their live animal markets are a source for novel human viruses, including the 2003 SARS outbreak and multiple cases of avian influenza jumping from birds into people. And yet they have done nothing to shut down those markets.

So it’s complicated. In any case, as Matthew Iglesias pointed out in The Guardian, even if the entire Vanity Fair article is wrong, the lab leak hypothesis is still plausible–very much so. The fact remains that one of China’s major virology research institutes, which was known to be conducting research on SARS-like viruses, and which was known to be collecting viruses from bats, is located just a few miles from the live animal seafood market. That’s one heck of a coincidence.

Finally, let’s take a step back: why all this attention to whether the virus originated from a virology institute or from a live animal market? Either way, the implication is that humans caused this pandemic. As I wrote back in March, we should take away at least two lessons from this experience: first, that live-animal food markets should be shut down, especially those that sell wild animals rather than farm-raised ones; and second, that gain-of-function research on deadly viruses should be shut down as well.

So let’s stop arguing about the precise origin of the pandemic, and start taking steps to prevent the next one.

Gain-of-function experiments at Boston University have created a deadly new COVID virus. Who authorized this?


Schematic of the Covid-19
 virus, SARS-CoV-2

After all the controversy over the past few years about gain-of-function research on viruses, especially the Covid-19 virus, I thought this kind of work was on hold, at least in the U.S. Indeed, the controversy grew so hot that NIH issued a statement in May of 2021 declaring that it wouldn’t support such work.

Nonetheless, some scientists continue to pursue gain-of-function work. In a new study, just released on the preprint server bioRxiv, a group of virologists at Boston University did the following. They took the Spike protein from the Omicron BA.1 strain of SARS-CoV-2 (that’s the strain that spread throughout the world last winter, often slipping past the protection offered by vaccines) and combined it with an early 2020 strain of the Covid-19 virus.

This experiment gave them a brand-new, never-before-seen strain of Covid-19. Was it more deadly? You bet!

In their experiments, the BU scientists infected laboratory mice with the original Omicron virus, which caused “mild, non-fatal infection.” But when they infected mice with their new, recombinant virus, which they called Omi-S, 80% of the mice died. To quote from their article:


“the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”


Well, that’s just great. Making matters worse, the researchers found that the new recombinant virus also replicated much faster in mice: “Omi-S-infected mice produced 30-fold more infectious virus particles compared with Omicron-infected mice.” Yes, you read that right: Omi-S might grow 30 times faster than the garden-variety Omicron strain.

This, dear readers, is what we mean by “gain of function” research. The scientists took sequences from two different strains of the Covid-19 virus, one of which was relatively mild, and created a new strain that is far more infectious and far more deadly. As many scientists (and others) have pointed out, research like this carries great risks, foremost among them the chance that an accidental lab leak could create a new pandemic, killing millions of people.

And the benefits? There must be some pretty major benefits to offset this risk, right? Well, not exactly. The researchers say that these experiments show that the pathogenicity of the Covid virus is determined primarily by something other than the Spike protein. That’s a pretty narrow finding, and the authors don’t seem to consider that they might have learned this without creating an entirely new, more-lethal virus.

Does this work violate NIH policies? The NIH director has stated that

“neither NIH nor NIAID have ever approved any grant that would have supported ‘gain-of-function’ research on coronaviruses that would have increased their transmissibility or lethality for humans.”

First, let me point out that this is a very narrow statement: the NIH doesn’t deny that it funds gain-of-function work on viruses, because it does. They even put a “pause” on such work for 3 years, but they lifted it (regrettably) in 2017. I wrote about that at the time (“NIH Re-opens the Door to Creation of Super-Viruses,” December 2017).

Second, the NIH policy carefully says they don’t support work that would make viruses more deadly for humans. The BU study only looked at mice, so one might argue that it wasn’t making the viruses more deadly in humans–but there’s simply no way we can tell that, not unless we intentionally infect someone. Having read the paper, this work seems to me to be a clear violation of NIH rules.

Boston University and the researchers who led the study disagree. In a statement issued last week, BU officials wrote:

“First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-CoV-2 virus strain or make it more dangerous.”

Let’s take a look at this denial, shall we? First, let me reiterate that the new experiments combined 2 strains of the Covid-19 virus: the Omicron strain, which has been the main strain infecting humans since last winter, and an earlier strain that was collected from a patient in Washington state in 2020. The Omicron strain causes only mild infections in mice, but the new Omi-S strain–the one that Boston University scientists created in their lab–kills 80% of them. The Washington state strain, which is no longer circulating in people and thus isn’t a current threat, kills 100% of mice.

So that is the BU argument: because Omi-S is less deadly than one of its parental strains, the research doesn’t meet the definition of gain-of-function.

Sorry, but this argument is just nonsense. You don’t get to redefine gain-of-function in the same sentence where you’re denying you’ve done it. These experiments created a brand-new, recombinant strain of Covid-19, and that strain was much more infectious and much more deadly than Omicron, which is one of the strains it was created from. This is precisely what most scientists mean when they describe gain-of-function research and the risks that it carries.

Furthermore, we have no idea how this virus will behave in humans. It might be far more deadly than Omicron in people. Let’s hope we never find out.

And what about that 80% mortality rate? According to Prof. Ronald Corley, Director of BU’s National Emerging Infectious Diseases Laboratories (NEIDL), “This was a statement taken out of context for the purposes of sensationalism, and it totally misrepresents not only the findings, but [also] the purpose of the study.”

Out of context? Well, here’s what the scientists themselves wrote in the very first paragraph (the abstract) of their paper: “We generated chimeric recombinant SARS-CoV-2 encoding the S gene of Omicron in the backbone of an ancestral SARS-CoV-2 isolate and compared this virus with the naturally circulating Omicron variant.... In K18-hACE2 mice, while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”

That’s the scientists’ own statement, and it’s not out of context. The authors themselves were emphasizing this dramatic mortality rate.

The experiments also present another problem for BU. Despite being funded by multiple NIH grants, neither the scientists themselves nor Boston University appears to have informed NIH about this work, which is a requirement for gain-of-function research.

BU officials addressed this problem by stating, first, that the NIH funds only supported some of the underlying “tools and platforms,” and that NIH funds did not directly support the research. Really, BU? How stupid do you think we are? Money, as we all know, is fungible.

Second, according to BU, “there was no gain of function with this research. If at any point there was evidence that the research was gaining function, under both NIAID and our own protocols we would immediately stop and report.” (Read the full BU statement here.)

Well, I would say that when those mice started dying, you had some pretty good evidence that “the research was gaining function.”

I’ve been in touch with multiple virologists who take a similar view. Simon Wain-Hobson, an Emeritus Professor at the Pasteur Institute, wrote to tell me that the BU research “is a GOF outcome in that the recovered virus is more pathogenic than the parental (backbone) virus, albeit in a transgenic mouse setting.” Prof. Wain-Hobson also pointed out that this work “provides a road map to [creating] a virus that might be dangerous to man. By posting this, these authors are making life easier for the next person or copycat.”

Another virologist, Dr. Valentin Bruttel of the University of Würzburg, pointed out the same problems and more, writing that:

• [the experiments] could have produced a virus that is “way more lethal” than the original SARS-CoV-2 strain
• “the study is useless for the general population, because the chance that exactly this Omi-Spike [would] recombine with an extinct variant [the Washington state strain] are zero,”
• “the chimeric virus could cause more severe disease in humans than estimated from mouse data.”

Like Prof. Wain-Hobson, Dr. Bruttel also pointed out that “any terrorist group could copy the BU group’s protocols.”

What does NIH think? They don’t appear convinced by the BU denials. According to an article in The Hill, “NIH is examining the matter to determine whether the research” fits the definition of gain-of-function. And as reported by Helen Branswell in Stat last week, an NIAID official said that NIH should have been informed, at a minimum so that they could determine whether or not the research was permitted under NIH’s gain-of-function rules.

I contacted the lead author of the study to get his response, but he did not reply.

The bottom line here is that some virologists (by no means a majority) believe that conducting gain-of-function research on the Covid-19 virus is just fine. Many other scientists disagree, and strongly. Some have pointed out that this work is qualitatively no different from biowarfare research. I’ve been warning about the risks for years, and I’m certainly not the only one.

Merely requiring scientists to inform the government, which is the current NIH policy, is not enough. We need to shut this research down and take a long, hard look at it before any such experiments can go forward again.

Why the new COVID vaccine boosters are safe and likely very effective

In case you haven’t heard, there’s now a new set of vaccine booster shots that protect against the latest variant of Covid-19, BA.5. This new variant is highly infectious, and the original vaccine doesn’t protect people against it as well as it protected against earlier variants.

Now, before someone takes that last sentence out of context, let me emphasize that the original Covid-19 vaccines are still highly effective at preventing severe disease and hospitalization. Anyone who isn’t vaccinated would be well-advised to get one of those, if that’s their only option.

But the new vaccines protect against two different strains of Covid-19: the original strand and the latest Omicron variant, BA.5. BA.5 just emerged in August, and it’s spreading extremely fast–it now accounts for 88% of the cases in the U.S. The FDA authorized these “bivalent” boosters on August 31.

My main point today is to explain how this happened so quickly, and why it didn’t involve many months of clinical trials the way that the original vaccines did. Some people have expressed suspicion about the speed with which these boosters appeared, but those suspicions are entirely unfounded.

First of all, we do have data showing that the new vaccine boosters are safe: a study showing these data for the Moderna booster just appeared in the New England Journal of Medicine. That study also showed that people generated robust antibodies against the BA.1, BA.4, and BA.5 Omicron variants after getting the new booster.

Second, to explain why that’s all the data we need, let me explain something about the flu vaccine. Many people are well aware that we have a new influenza vaccine every year–but what they might not know is that each year’s vaccine contains a different strain of the flu virus from the previous year. (Actually, it has up to four different strains, and any or all of them could be new.)

And yet we don’t run large, months-long clinical trials of the flu vaccine each year to measure it’s efficacy. Why not? Well, the basic designs of the flu vaccines (there’s more than one) have been tested in large clinical trials, and we know they’re safe. Replacing the vaccine strain with a new one doesn’t affect the safety of the vaccine, as decades of experience with the flu vaccine have now demonstrated. And because flu mutates quickly, we need to change the vaccine strain every year if we want the vaccine to work.

So that’s what we do: we change the flu vaccine strain to match whatever seems to be circulating, but everything else about the vaccine design remains the same.

This is exactly what scientists have done with the new Covid-19 booster shots from Pfizer/BioNTech and Moderna: they simply added a new strain, in this case to match the latest Omicron variant.

Both of the new boosters are mRNA vaccines, which means the vaccine contains a tiny bit of genetic code (mRNA) with instructions on how to make the “spike” protein from SARS-CoV-2, the Covid-19 virus. When you get the vaccine, your own cells follow those instructions to make a limited number of copies of the spike protein–but nothing else. The virus itself can’t be created without many other genes, and the spike protein alone can’t form a virus.

But your immune system recognizes that an invader is present–that spike protein–and it generates antibodies against it. After that, your immune system is primed to recognize and defeat Covid-19, if it ever infects you.

So the new boosters contain mRNA from the BA.5 spike protein as well as the original spike protein, and now you get protection from both old and new strains. Other than that, it’s the same vaccine as before.

The vaccine makers have produced safety data showing that the booster is just as safe as the original vaccine (see that NEJM article I mentioned above). But the FDA didn’t require them to prove that the booster really works better against BA.5, because that would require months of trials, and by that time the virus could mutate again. So while it’s possible that the boosters won’t help against BA.5, it’s very, very likely that they will.

One of the big advantages of mRNA vaccines is precisely this: we can swap out the mRNA easily, allowing us to respond quickly to mutations in circulating viruses. That’s a good thing, and it might be our only path to controlling Covid-19.

The bottom line is that the new boosters should be very safe, and they will likely provide much better protection against the current strains of the Covid virus. I’ve already gotten my booster, and I hope everyone else will too.

Covid patent fight is about greed, not human health

I suppose I shouldn’t be surprised: one of the companies that developed mRNA vaccines for Covid-19, Moderna, has just sued the companies who make the competing mRNA vaccine, Pfizer and BioNTech, claiming that Pfizer/BioNTech is violating its patents.

Pfizer was surprised though, according to news reports. (Or at least they said they were.)

Moderna had announced, back in 2020, that they wouldn’t enforce patents on their vaccine during the pandemic, but they seem to have changed their mind. Apparently, billions of dollars in profits isn’t enough: they’ve decided the time is right to try to grab even more money.

Let’s make no mistake here: this is purely about greed. Apparently Moderna understands this, since they proudly advertised their earlier plans not to enforce patents on the Covid-19 vaccine. They realized that the public good will generated from such an announcement was valuable.

Not that valuable, apparently.

It’s not even clear that Moderna should have been given the patents it holds. According to a recent story in Science, the key technology behind one of Moderna’s patents was invented, and patented, years earlier by two scientists, Drew Weissman and Katalin Karikó, at the University of Pennsylvania. Their work discovered a way to modify the RNA in the vaccine that would make it much more effective. (Here’s a link to the patent.)

As I wrote last year, patenting the Covid-19 vaccine is unethical. At the time, the US had announced support for a “vaccine waiver” that would allow any country to develop vaccines against Covid-19 without licensing the technology from one of the companies that currently holds a patent. That policy sounded too good to be true–and apparently it was, because no such waiver is in effect now.

The patent system is a creation of modern governments, and they don’t have to let companies get away with this. The profits of a few companies are far, far less important than the lives of millions of people. Allowing companies to restrict Covid-19 vaccine development is, crudely put, defending money over human lives. Maybe it’s time for the international community to institute the vaccine waiver, at least until the pandemic is truly over. 

And make no mistake: even though we have vaccines now, they still need improving, and better vaccines will save lives. Patent disputes will slow down or even prevent work on better vaccines, since the patent holders will have a monopoly. Even the threat of a lawsuit can stymie progress; after all, why would someone invest time and effort on a vaccine that they might never be able to deploy?

Moderna is far from the first company or institution to let greed guide their actions: way back in 2010, I wrote about how MIT and Harvard had filed a patent that was, as I wrote at the time, both inappropriate and harmful. In that case, MIT and Harvard had an incredibly broad patent on a human gene, NF-kB, which plays a key role in our immune system’s response to infections. Granting a patent on NF-kB, as the US Patent Office did, was akin to granting a patent on all drugs that affect nearly any human gene. The universities licensed the patent to Ariad Pharmaceuticals, who filed a lawsuit the day the patent was granted. Neither Ariad nor MIT developed any treatments, but they initially won $65.2 million just because of the patent. (Need I point out that the Harvard and MIT work was mostly funded by the public?)

Fortunately, in the 2010 case, an appeals court threw out the patent, ruling that people and companies cannot patent human genes, because genes are products of nature, not inventions. The mRNA patents, though, don’t fall in this category.

Should I also mention that much of the basic research behind mRNA vaccines was also funded by the public? Or that NIH (and therefore the US government) has patent rights to some of the technology behind the Moderna vaccine?

Moderna, Pfizer, and BioNTech looked like heroes when they first announced their vaccine results–and in some ways, they were. The world was desperate for vaccines against Covid-19, and the mRNA vaccines have saved millions of lives.

But my message to Moderna is simpler: you’re already making billions in profits on the Covid-19 vaccine, so don’t be such greedy assholes. And don’t be evil: drop the lawsuit.

Scientists have re-created the deadly 1918 flu virus and used it to infect animals. WTF?

With all the controversy about gain-of-function research and all the concerns about how dangerous it is, you might think that scientists have stopped doing that kind of work.

Well, no.

In the latest news, a team of scientists in Canada and the U.S. report that they have re-created the 1918 influenza virus and used it to infect macaques. Let’s be clear here: the 1918 flu vanished from the Earth, long ago. It’s simply not a threat, or it least it wasn’t, until someone figured out a way to bring it back.

Why would anyone do this? I’ll get to that, but first a little background.

The 1918 flu pandemic was the worst plague since the Black Death, which occured in the mid-14th century. During World War I, a new flu virus swept the planet, killing upwards of 50 million people. It probably infected a third of the entire world population at the time.

Since Covid-19 appeared, the 1918 flu pandemic has been cited often (sometimes called the Spanish flu), usually to compare or constrast it with Covid-19. Sure, Covid is bad, but at least it’s not as bad as what the world experienced in 1918.

About 20 years ago, a small team of researchers led by Jeffery Taubenberger and Ann Reid figured out how to sequence the genome of the 1918 flu. In a series of papers spread over six years, they described how they recovered pieces of the flu virus from human samples that had been frozen for nearly 100 years, including corpses buried in the permafrost of Siberia and Alaska. In 2005, they reported the complete sequence in the journal Nature. Their main discovery was that the 1918 flu had originally been a bird flu, which jumped into humans sometime before 1918. Taubenberger and others, including Adolfo Garcia-Sastre at Mt. Sinai School of Medicine, also re-constructed the virus and tested it on mice, that same year. Not surprisingly, the mice died.

It didn’t take long before gain-of-function researchers said “hey, why don’t we reconstruct the flu virus and see what happens in primates?” The tools of modern genetics make it possible to reconstruct a virus from scratch, using just the sequence.

In 2007, only two years after the 1918 flu sequence was completely decoded, influenza researcher Yoshihiro Kawaoka at the University of Tokyo and the University of Wisconsin described, in a paper in Nature, how he and his colleagues used the sequence to create live, infectious 1918 flu viruses. To demonstrate that these really were flu viruses, they infected 7 macaques with them. Not surprisingly, the macaques got severely ill, and the scientists eventually euthanized all of them.

(Insiders may recognize Kawaoka’s name: he and Dutch scientist Ron Fouchier are widely known for their gain-of-function research that aimed to give deadly bird flu the ability to infect mammals. I’ve called them out on this in the past, and I’ve openly asked why NIH was funding this work.)

In the new paper, a team of researchers at the Public Health Agency of Canada, the University of Manitoba, and Oregon Health & Science University re-created the 1918 flu virus again, and infected 15 macaques. This time they used more realistic doses, and the macaques didn’t get so sick, suffering only “mild” or “moderate” disease. Maybe macaques “are not ideal for the development and testing of novel pandemic influenza-specific vaccines and therapies,” they concluded.

So let’s review: flu scientists have been using the sequence of a long-vanished, extremely deadly virus to reconstitute the virus and infect animals, and then observe how sick they get. (Kawaoka did it a second time, in a study published in 2019.)

Why do they do it? All of the papers give essentially the same reason: these experiments, they say, will help us develop animal models in which we can test vaccines. These same justifications have been used for decades, but flu vaccines haven’t improved one whit, as far as I can tell.

But hold on a minute! Even if you accept their argument that infecting macaques and other animals with influenza virus will help develop better vaccines, why use the 1918 influenza virus at all?

They don’t answer that question, because there really is no good answer. The fact is that the experiments will be more relevant if they use currently circulating flu strains–because those are the strains that we need vaccines against.

I imagine that the scientists doing this work truly believe the arguments they make, about how their work will help design better vaccines and therapies. But they’ve been making similar arguments for decades, and it just hasn’t played out that way.

The 1918 flu disappeared long ago, and there’s no way it could possibly re-appear naturally. There’s only one way that the 1918 flu becomes a threat to human health again: through a lab leak. Re-creating the virus in a lab makes that possible.

We’re still trying to figure out if Covid-19 had a natural origin or whether it started as a lab leak. Even if it turns out to have a natural source, the intense discussions about the lab leak hypothesis have been useful, because they made it clear that lab leaks happen, and that they should be considered a genuine risk.

In recognition of this risk, scientists and non-scientists alike have called for a worldwide ban on gain-of-function research. That hasn’t happened yet, although NIH has issued a carefully worded statement about the kinds of work that it supports.

Most of the recent controversy over gain-of-function research has focused on research that makes viruses more deadly. I hope it’s clear that re-creating a deadly virus from scratch is another form of gain-of-function research, one that carries equally great risks with little or no potential benefit. We should put a halt to both types of work.

There’s an easy way to eliminate the risk that a lab leak might release the 1918 influenza virus into the human population: stop re-creating the virus. The 1918 flu disappeared from the natural world long ago–or to be more precise, it evolved into a much, much milder form of influenza. The deadly form that was recently re-created in several labs does not exist in nature today. Let’s keep it that way.