World-renowned expert Ben Neuman shares which COVID vaccine he’d take, given the choice

This week virologist Ben Neuman answers questions from readers.

Before most of us knew what a coronavirus even was, Neuman was one of the world’s top experts on them. He’s science-world famous for growing SARS-type coronavirus in the lab and is a professor of biology, and Global Health Research Complex Chief Virologist at Texas A&M University. Soon after the discovery of the virus now shaking our world, he served on the panel that named it. (Officially, it’s not “the ‘rona.” It’s SARS-CoV-2.)

This interview has been lightly edited for length and clarity.

Lots of people had questions about new variants of this coronavirus. Could you talk about what a variant is? Why are some more infectious than others?

This is a whole thing where the public perception of what a virus is and does is different from what a virus actually is and does.

The public tends to think of a new strain, a new variant, as one that’s a little bit different and somehow just so much better at doing everything than the old version. But viruses are not that clean and tidy.

About one out of every two or three copies that the virus makes of itself will have some kind of mistake — an extra base, or one base missing. Something will change just randomly. So no matter which virus strain you catch, within just a few hours — a couple rounds of replication — that strain has actually made every possible variant that can exist under the sun.

So what are these new variants? Well, they’re kind of like the center of that cloud of virus that’s spreading. The virus operates as an entire squad of these little mutants that kind of cooperate without communicating. It’s a very strange thing called a quasi-species.

So here’s the thing: To replicate itself, the virus is running all these little assembly lines under whatever conditions it finds in a cell. Getting as much product at the end as possible — as many virus copies as possible — is all about lining up the assembly lines.

But a virus doesn’t have dials that let it turn up and down some of the machinery that it’s running. Those genetic changes, the mutations, let it adjust. Certain mutations will make each machine run a little bit slower or a little bit faster. That’s what’s really going on.

Now, to answer your question in a way that people understand: The new variant seems to be one that has completely replaced the old variants. The UK had these strains called 20A and the 20B. Each of these is a loose confederation of viruses that are more or less the same.

When you get a COVID-19 test, the lab is only looking for a little part of the virus that doesn’t change, so that test doesn’t tell you which strain you have. When a scientist gets around to sequencing the genome of the virus strains, then they will pick up a batch of just random positives, read them out and see what’s been going on. The last time I looked, you have to plunk down about $1,000 per sequence. So maybe every month or so this happens.

That’s what happened in the UK: They looked once, and it was 20A and 20B; they looked again in a month or two, and all of a sudden, those strains were almost gone. They’d been replaced by this new thing.

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That suggests that this strain is spreading a little faster or a little more widely — or at least, that it’s out competing with the other coronavirus strains that are out there. The thing is, we don’t know what that means.

A virus’s life is very hard. This thing has to get made in a cell that tries to kill it. It has to get past an immune system. All this sticky mucus is trying to trap it and destroy it. Then the virus has to get out into the world — probably by hanging in a little droplet for just long enough that somebody else can breathe it in. And then it has to go through that process in reverse to get into the new person’s cells and multiply.

It’s not always one particular kind of mutation that gives a virus greater fitness. A mutation might mean that virus does things more slowly. Or that it does them more quickly. Or it’s more stable. Or it’s more primed and ready to go. All the mutations will give the virus different properties, slightly different options.

Honestly, the only way to really figure out what this variant does is the real-world experiment that we’re all doing right now.

So we don’t know how these variants are physically different from the older versions?

No, we know exactly where the differences are. There are 28 differences in the genome. There are a couple mutations up in a protein called nsp1. Those might lower the amount of disease the virus causes. We think nsp1 is one of the things that is stomping on a part of our immune system that tries to set off alarm bells — the interferon system, the way that your cells let other cells know something bad is happening and they need help.

The variant has also got problems down the thing called “open reading frame 8” that nobody really knows all that much about. It seems to have the same sort of effect in us that it does in bats: It’s maybe about shutting down the interferon system. So probably, that change makes the virus a little less able to evade our immune system, and a little less dangerous.

Then there’s a whole host of mutations in the spike gene. There’s one right at the tip of the spike. The part of the coronavirus spike that binds to the human cell’s receptor looks sort of like a wishbone, the kind that you would grab after Thanksgiving dinner. One of these mutations is there, so it’s going to affect the part that actually clamps down onto the spike. And that may indeed, make the virus either more stable or less stable, faster or slower at binding particular receptors.

That’s the possibility. But we have to wait till the experiments are done. There’s just a lot about this virus that we don’t really understand.

That particular change — it’s called the N501Y mutation — has been circulating in the U.S. since spring, and it has not taken off in the U.S. So most likely it’s not that mutation alone that’s driving this spread.

The difference could be due to people infected with that strain at one or two super spreader events. You can only spread the virus you happen to have, and if you just happen to be the most popular person that the COVID party, then yeah, everybody’s gonna get your personal strain. Fantastic, right?

Or that variant’s presence could be due to a lot of this stuff. We don’t know. But I do know everybody’s worried about it.

The South African version is almost identical: one has 28 mutations compared to the original, one has 29.

About every two weeks a new mutation comes in. That’s just what these viruses do. We expect 30 mutations a year, it’s been a year, and we’ve got a 29 mutation variants circulating. That is exactly business as usual for a coronavirus.

So the viruses may be becoming more infectious but less deadly?

Possibly. Viruses don’t necessarily want to kill you. Viruses are generally optimized for whatever produces the most new viruses. And a dead person doesn’t do that.

We think these viruses are probably optimized for living in a bat. And whereas we have an immune system with lots of different components, bats rely very, very heavily on this thing called type one interferon. And so to survive on the bat, you have to be really good at shutting down type one interferon. I think at last count, there are seven different parts of this virus that are all dedicated to smashing type one interferon. That’s perfect for the virus’s long term survival in the bat: The bat doesn’t get sick, and the bat continues to spread the virus.

But people are not bats. We have a different immune system. We’ve only got a little bit of interferon, but it’s still really important. So when the virus turns that off in us, you get this long, lingering illness, which is what leads to the cytokine storms and other immune problems.

Several people are asking whether you should get the vaccine if you’ve already had COVID-19.

Yes. Definitely.

Why? What happens in your body if you’ve already had COVID-19 but then get the vaccine?

We put the vaccine into an arm muscle because we know that buried in each of your tissues, there are little sentinels. Something like one out of every 15 cells in the body is a white blood cell of some kind — part of that immune system family. They’re in your muscles; they’re circulating in your blood; they’re in your organs all over the place.

What we want to hit is called a “dendritic cell.” If we manage to inject one of those with either a bit of protein or a bit of messenger RNA that’ll make a protein, the cell will make a little bit of the protein, harvest it, cut it into little pieces, learn how to recognize it, and go show it to the rest of your immune system. Eventually it’s going to find some sort of cell able to recognize this. Then it gives it a little reward, kind of like a piece of candy — but, you know, in immunological terms (laughs).

The dendritic cell just keeps showing this little piece of the virus until it’s got a whole horde of cells that are ready to go out and hunt down just this one thing. It can’t react to anything else. They’re totally focused on COVID. You’re building up that little army.

From about two weeks after the first dose of vaccine with either of the mRNA vaccines — the Pfizer or the Moderna — it looks as though you have enough immunity to get at least short-term protection.

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So why have two doses? Well, they looked, and you get a boost of about 10 times as much protection. It boosts up your immunity.

Whatever the level your immunity starts at, it’s going to go downhill — either slowly or relatively quickly, but we think it’s at a pretty predictable rate. If you start higher, it takes you longer to get down to the bottom.

Now, if you’ve already had COVID, that’s fine. Effectively, COVID acted like your first vaccination, so your first shot of vaccine is going to be a boost. If you’ve had COVID, you might be able to get away with a single-dose boost — we don’t know — but why not take both of them? There’s no way that this can harm you. It is only training a population of cells. They are very loyal, good little soldiers, and they are out there to protect you.

Jef Rouner asks, “How do you respond to someone who says COVID has a 99.9% survivability rate?”

You say, “Well, you’re off by tenfold.” And then, you go into COVID’s other effects.

At the beginning, there was one paper that said that the fatality rate was something like 0.1 to 0.3%. That was based on a relatively small amount of data from California back when we weren’t doing a good job of testing. But later, much, much, much larger data sets put the fatality rate at somewhere around 1 or 2%.

A 1% fatality rate is a big deal, right?

Oh, my goodness, yes. We would not tolerate anything else in our lives that had a 1% fatality rate.

And it’s not just the fatality rate, though we tend to obsess about that. But many people — the studies ranged from 20% up to around 50% — have what looks like long-lasting or permanent heart damage. I mean, it’s too early to say “permanent,” but it looks like the permanent heart damage that you’d see from other causes.

There is also damage to the brain. They call it “COVID brain” informally. We don’t know whether that cognitive function ever comes back.

And there’s a lot of other bad stuff. There’s damage to blood vessels, those things that are going to be under pressure for the rest of your life. COVID has caused quite a number of aneurysms, which is a ballooning in one of those vessels, a weak spot that is eventually going to break.

So when it comes to COVID, Nietsche is completely wrong. Even if it does not kill you, it makes you very, very much weaker. So you should definitely avoid it.

A question from Rebecca Estrada: “I’ve heard that up to 40% of people are asymptomatic. Is that correct? How much should I worry about this?”

Great question. There is still some unsettled science.

So here’s what we know. There are some studies, like the early ones on the cruise ship, where they could literally test every single person that came off that ship and see exactly how many have the virus and exactly how many have symptoms.

We’ve found in a lot of animal models that you won’t see any symptoms in the animals, just like you don’t see symptoms in the people, but there is a little bit of damage that goes on in the animals’ lungs.

You wouldn’t notice that necessarily. Some people are going through a lot every day with allergies and whatever else, so they may not notice a particularly mild case.

Younger people are more likely to be asymptomatic. Or really, it’s not “asymptomatic.” It’s “low symptomatic,” or “don’t-bother-to-tell-people symptomatic.”

The number 40% seems to be in the right ballpark, I’ve heard as high as 50%; 40% seems reasonable.

There are other kinds of studies, like one I’m involved with. They take saliva samples from random people and check them, so you get a real nice little cross-section of the population — or of the population that’s willing to spit in a tube, anyway.

We have some little studies like that. We don’t have a giant study like that. But from the little studies, it does look as though one in three — or maybe one in two — virus-positive people don’t have enough symptoms that they notice.

We also have evidence from situations where some of those asymptomatic people have been the only person who has COVID, and the virus has spread. So we can logically conclude that they probably spread the virus.

So your not having symptoms doesn’t mean that you won’t infect anyone else. And it doesn’t mean that you won’t have symptoms down the line. We get people that relapse-remit. You get all kinds of crazy things with this disease because the disease is coming more from your immune system — it’s not so much the virus itself as the way the immune system is set off by the virus.

That’s also why we have such a hard time with the treatments for people on a ventilator or who have severe COVID. You can stop the virus, but once the virus has set off the chain reaction in the immune system, it’s the chain reaction that you have to stop. And we do not have a good way to do that. At all.

Amy Hoster Richards asks, “If I get the vaccine, could I still get COVID and be asymptomatic and spread it?”

This is possible. The true answer to this is, “We don’t know.” The reason why we don’t know is because they didn’t set up the clinical trials that way.

To check for that in a clinical trial, you could give everybody the vaccine — or give half of them the vaccine, half a placebo; or maybe give half other vaccine — and then you could test everyone every week and see who gives back a positive test. Then you’d know whether vaccinated people can be asymptomatic carriers.

That is not what Pfizer or Moderna did. What they did was to say that anybody who feels sick should go get a test, and then anybody who gets a positive test will be recorded. Later on, they will unblind the study and figure out whether you had the placebo or the vaccine.

So all we know is that fewer people get sick when they have the vaccine.

Olga Luiza Dentzien-Keller has a related question: “Is it true that the vaccines have been shown to prevent disease but not infection? And if so, how do we achieve herd immunity?”

Let’s start with the first part: Do the vaccines prevent disease but not infection? In animal models, we have examples of both. With something like a ferret, you can reinfect it again after about a month, and even though it’s infected, it doesn’t get sick, doesn’t get disease, the second time. It’s like the first infection vaccinated the animal against the second one.

But all the animal models get really, really mild disease, so they are not great points of comparison for the human disease, which is severe. We have yet to find a really good animal model. People are working hard on this, but it is it is tricky stuff.

So what about herd immunity? Can we achieve it if vaccines prevent sickness but not infection, so people are still spreading COVID?

“Herd immunity” is one of these squishy epidemiological concepts that exists as a formula in a mathematicians’ brains and occasionally in papers with those formulas.

Out in the world, the way we’ll know that we’ve reached herd immunity is that the virus will just go down. Even though people aren’t necessarily doing anything different, new cases will continue to plummet because the virus has nowhere to go, can’t find places to spread.

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Herd immunity theoretically could be achieved through vaccination — if either the virus can’t infect immunized people, or if it can infect them but then can’t spread to anyone new.

But as we just discussed, we don’t know for sure whether the virus actually prevents humans from getting infected or from spreading the virus. I think the experiments were done the way they were to get them done as fast as possible. Eventually, a year or two from now, we will probably have great studies that will answer all these questions.

Herd immunity with these vaccines is a calculated gamble, I would say — but I feel like rolling these particular dice.

Is anyone testing vaccines now to see if they prevent infection?

No, no, nobody is doing that. You have to do these enormous studies — say, with 45,000 people in them. So to do that study, you’d have to get 45,000 people to show up to be tested at a set time every single week, or maybe twice a week. That’s hard.

In these experiments, in the the vaccinated group, somewhere between 10 and 15 people actually end up with the virus; and in the unvaccinated group, it’s only something like 100 people. So you are doing tons and tons of work for very little actual usable data. And I think it just seems like a lot of work and a much slower path to approval.

To get full-on approval, and not just the stopgap emergency approval that all the vaccines have, they’ll probably have to do studies like that later on.

Olga Dentzien-Keller also asks: “If you had the opportunity to choose which vaccine to take, would you take one of the mRNA vaccines (Moderna or Pfizer), or would you take the AstraZeneca? And why? I know that Dr. Peter Hotez previously stated that he’d take any vaccine, but I’m looking for specifics.”

I like the mRNA vaccines. But if I’m king of the world in charge of vaccines, I would want to mix and match.

Each company does its own trials, so we don’t yet have any studies about whether you can do the first immunization with mRNA and the second immunization with an adenovirus-vectored vaccine like the Johnson & Johnson or the AstraZeneca or even the Russian one. There’s a trial like that going on in the UK, but it’s not done yet.

The reason I would want to go with different types of vaccine is that each of the vaccines is going to reach a different population of cells in a different way. With the mRNA, you are just blasting it out, delivering it to any random cell in the vicinity, hoping that one of those happens to be a dendritic cell. It’s basically like you’re leafleting every single door hoping that one guy buys a pizza.

That’s really effective, I should point out. It seems like it shouldn’t get the job done. But it does. People buy pizzas! These vaccines are pretty awesome.

The AstraZeneca model hides a little piece of DNA — DNA instead of RNA, but basically the same thing. It hides the DNA inside a little Trojan horse, which is the hollowed-out shell of a thing like a cold virus. That will then look for a particular set of cells that have a thing called the CAR, the chimeric antigen receptor.

Dendritic cells are one of the cells that have that receptor. So the vaccine will hit those but also some other populations of cells, some of which may also be able to do maybe half as good a job as a dendritic cell. You probably wouldn’t have hit some of those with the mRNA vaccination.

Basically, I want to buy as many lottery tickets as possible. I want as many possible ways to be protected as I can get. I would build the immunity with an mRNA vaccine, then sustain it with an adenovirus one.

The adenovirus ones have lower success rates in the trials we’ve seen, but I think that just means they’re not great at doing that one thing — at just saturating all the dendritic cells in an arm muscle, but they still probably have some use.

Vivian Ho asks, “I understand that SARS-COV-1 does better in cold temperatures. Does it both last longer and multiply faster in the cold? Is it more likely to multiply in your nasal passages when it’s cold outside?”

There are two layers of this answer. One part is the same reason why you put your meat in the refrigerator and not on the counter. Once the virus comes out, it is just like a little piece of meat. It comes from an animal cell. It’s made of all the same stuff as you are, and it will break down in 100 different terrible ways, all of which mean no more virus. Cold prevents that from happening to a large extent, and by inhibiting a whole bunch of bad things that could happen.

But there is another point there, and that is from a Volker Thiel paper from spring. He found that SARS-COV-2, the thing that causes COVID, grows pretty well in the upper respiratory tract where it’s a little cooler because we’re exchanging with room temperature air, although room temperature is a little different depending where you are.

The original SARS virus, SARS-COV-1, needed that bottom-of-the lung atmosphere, 37 degrees Celsius, high humidity. It did not do well in the upper respiratory tract.

So SARS-COV-2 is growing in a place that makes it easier to catch, easier to spread and more likely to take hold. That’s why it’s spreading so fast.

So should we do anything to change the temperature of the air we breathe?

You would have to change your body temperature. While it is possible to do that — if you’re David Blaine (laughs) — it is generally not medically advisable. Changing the room temperature in your house makes a very small difference. “Homeostasis” is the word: Your body tries really hard and spends a lot of energy to keep everything the same, no matter where you are or what you’re doing.

While we’re talking about temperatures: Lary Sides wants to know, If the Pfizer vaccine is stored at negative 80 degrees Celsius, will I get a brain freeze when injected?

(Laughs.) The question is, “How cold do you need to store this mRNA vaccine?” Pfizer is going old-school. Back when I was taught, it was, “If you’re going to work with RNA, you need to douse everything with sodium dodecyl sulfate. You need to wear gloves on top of your gloves. You need to wear some kind of masks so you don’t breathe out RNA-destroying enzymes. And whatever you do, you want to keep that thing at about minus 80 degrees or else bad stuff happens.”

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Moderna is working with an essentially identical product, but they’ve got maybe more a laid back California approach. Theirs doesn’t have to stay as cold as Pfizer’s because they’re putting a lot more mRNA in their vaccine. So even if you lose half of the material before it gets to you, you’re still getting a little more than with the Pfizer.

But basically those vaccines are the same. They do the same thing.

So back to the brain freeze: That shot isn’t going into your body at negative 80 degrees Celsius, right?

(Laughs.) Definitely not. It’s going into you at nice room temperature.

Another question from Vivian Ho: “If a person gets a COVID vaccine during the day, is it okay to have an alcoholic drink that evening?”

(Laughs) I was going to say, “Booze it up!” but that’d be classic bad advice.

I don’t know of any reason why you shouldn’t have a drink. I don’t know of any interaction between a messenger RNA and a dendritic cell and ethanol or ethylene glycol. So as far as I’m aware, I think having a drink is just fine.

You’re not supposed to drink when taking certain medications because they use the same enzymes that you use to break down alcohol. In those situations, it’s like you get a crowd coming through the door. That’s why bad things happen.

But the vaccine is not related to that process. So yeah, I think you’re okay to celebrate. Have one for me!

Here’s my own question: What research are you working on now?

I am about to start some research. We have ordered some SARS-COV-2.

You can order coronavirus?

You can. There are places. You need certificates upon certificates, and everybody up to the CEO and down to the lowest minion has to sign off on it.

I’m going to be at an animal facility, along with a couple of chemists with something like 100 or 150 drugs apiece, each of which looks as though it’s going to do some good. They want to test the drugs against the virus in cells, and they want to test them against the virus in something like a mouse.

It’s going to be really interesting work, and I hope we come up with something that does some good. It looks as though COVID is going to be around for a while.

Have you read any interesting research lately?

So much! The neatest thing was on the CDC’s influenza page. We should be about a third of the way through flu season right now, and the curve is just not there. Flu is almost completely suppressed. It’s at the lowest level that I’ve ever seen. It’s at the lowest level on any of these charts showing the last seven or eight years, since they’ve been keeping really good stats.

That is really cool. It looks as though flu was a relatively easy out. We could have stopped flu at any point during the last I-don’t-know-how-many years.

By staying home and washing our hands?

By staying home, washing our hands and occasionally wearing a mask. Flu is an easy out.

Unfortunately, COVID is a hard out.

Anything else we should be thinking about?

The vaccine papers are, and they are written in a way that I think is meant to be read by non-scientists. They’re designed to be really, really accessible. They have these big infographics.

The beautiful thing is, for the first time, they made both Pfizer and Moderna show essentially the same data on the same graph with all the same bars on the sides, so that you can directly compare the two. It turns out that they’re about the same, because the two products are just about identical.

But that is nice to see. Everybody’s been doing their own version of a test, either accidentally or on purpose, doing the tests in ways that are just different enough that you can’t quite compare them. Maybe now we can all just get along.

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