Science Friday - Coronavirus Immunity, Ask A Cephalopod Scientist. August 28, 2020, Part 1

Episode Date: August 28, 2020

How well you fare in fighting a new pathogen like SARS-CoV2 depends in large part on how your immune system responds to—and kills—the virus. The immune system’s job is to protect you from invasions, both right after you’re infected as well as when you encounter similar viruses in the future. As the pandemic marches on, we still don’t know exactly how our immune systems tackle this virus. The people who get the sickest seem to have an exaggerated, but ineffective immune response that turns on their own bodies. Others have lasting symptoms, sometimes for months. Immune responses even seem to vary based on your sex. Increasingly, research suggests that COVID-19 is a disease like many others, at least in some important ways. Your body remembers the virus, and may therefore fight it more effectively the next time you encounter it—which has big implications for eventually developing an effective vaccine. Immunobiologist Deepta Bhattacharya and New York Times science journalist Katherine J. Wu talk to Ira about the complicated and varied response of the immune system to SARS-CoV2—and why current research suggests we can be optimistic about gaining long-lasting immunity from future COVID-19 vaccines. Plus, cephalopods—mollusks like octopus, squid, and cuttlefish—seem to universally excite people. Many marine enthusiasts have a favorite, from the color-changing octopus to the multi chambered nautilus. But these smart, colorful undersea creatures also raise a lot of questions. How do they move? How do they change shape and color? How intelligent are they? How do researchers study these animals? Squid biologist Sarah McAnulty answers listeners’ questions, and catches us up on the latest cephalopod news.  And Hurricane Laura made landfall Wednesday night in Louisiana after strengthening from a Category 1 to a Category 4 storm in less than a day. As residents try to find shelter in pandemic-safe ways, meteorologists are warning of an “unsurvivable” storm surge reaching as far as 30 miles inland. National Geographic editor Nsikan Akpan describes the factors that have caused the storm to so quickly gain strength. Plus, why recent changes to the Centers for Disease Control and Prevention recommendations on who should get a coronavirus test and when people should quarantine are alarming epidemiologists and other experts—and other news from the week.  Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

This is Science Friday. I'm Ira Flato. It's been an historic and devastating weather week. Hurricane Loras, mass ashore in the Gulf with 150 mile per hour winds, storm surge, and predicted unsurvivable conditions. We haven't ever heard that, I don't think. And historic because of two storms in the Gulf at the same time. Here to talk more about the rare, nearly record-breaking double feature and how a storm like Laura can get so fierce, so fast, plus this week. week's other science news is Sikhan Akpan, science editor for National Geographic based in Washington. Welcome back. Hi, Ira. Thanks for having me. You have to talk about the storm. Residents of the Gulf and other inland areas are still dealing

with the flooding, the wind damage from Laura as we speak. And it turns out of the two storms there, Laura was the one to worry about, right? Yeah, absolutely. You know, every August, I feel like I switch from being a science journalist to being a meteorologist for about two to three months, especially in the past few years. And it isn't looking great. Hurricane Laura smashed ashore near Cameron, Louisiana, just after midnight on Thursday. Its wind speeds were just shy of making it a category five, but it's still going to go down as the most powerful hurricane to hit this section of the Gulf Coast since records started being kept in 1851. You know, as you described, officials said that the storm surge would be unsurvivable. And that surge stretched from near Port Arthur,

Texas to intercoastal city Louisiana. So that's more than a hundred miles of coastline. When I checked the tide trackers, water levels rose six to ten feet when Laura made landfall in that region. And the National Weather Service predicted that the surge could penetrate up to 40 miles inland. And the thing is that that flooding will likely last for days to come. You know, how does a storm go from a one to a category four in less than 24 hours? Yeah, it's remarkable. You know, Philip Klotzbach, a Colorado State University meteorologist, said it tied the fastest intensification on record, which was set by Hurricane Carl in 2010.

And Loris Gusto was fueled by a bunch of things, but, The biggest factor was probably warm waters, which were 1 to 2 degrees Celsius above normal as the storm was churning through the Gulf. That was like, what, 90 degrees in the Gulf, the water? Yeah, it's about that, exactly. That was the temperature. But relative to average temperatures in the Gulf, it was about 1 to 2 degrees more. And that's surprising because Hurricane Marco had just passed through the Gulf earlier this week. And the thing about hurricanes is that they tend to sop up heat as they go along and then cool off the sea.

But, you know, despite Hurricane Marco likely siphoning off some of that energy, Laura still was able to come through and hit with a fury. And, you know, I know what everyone's probably thinking right now as they listen to this, global warming. But it'll take time for researchers to really decipher the degree to which climate change influenced this storm. But this is what we're expecting. We're expecting this type of pattern as the years go on. You know, warm waters are going to keep fueling these megastorms. Yeah, they say, you know, it's not more storms.

It's just more intense storms. Exactly. And even though, you know, people are looking to the future to see this pattern, it really feels horribly familiar right now. Last year, Hurricane Dorian rapidly intensified just before devastating the Bahamas. And the same happened with Hurricane Michael and Hurricane Florence in 2018. And I think what people need to know, unless you witness it firsthand, it's very hard to fully grasp how long a hurricane's devastation lingers after the storm is gone, you know, after the TV crews

sort of go away. In 2018, I reported from a hard hit town along the Carolina coast about a month after Hurricane Florence. And outside every home was just a pile of mattresses, you know, couches, framed pictures, pianos. I saw piano. Yeah, we, yeah, we had Hurricane Sandy coming up years ago, and we understand that it took years to recover. Still, people still have not recovered from that. Exactly. And it takes everything from a home, you know, when we talk to people down there, they're just like, this is my home.

I want to rebuild, but I don't know if I want to do it if another storm is just going to come through and knock everything out again. And I think you see that echoed in the early footage from Lake Charles, Louisiana, and a lot of the places around where the storm made landfall. And we're not done, right? You know, the forecasters are expecting this to be an extremely active hurricane season, in part because Lenina, you know, the climate pattern cousin of El Nino is about to form, and that helps promote cyclones.

And we've already broken the records this year with nine named storms before August. And, you know, the conditions are so primed that forecasters say that we might even have to turn to the Greek alphabet to name all the storms that we have this year. Amazing. And of course, this all comes in the midst of a pandemic.

That's exactly right. If people visit National Geographic.com right now, they can see a story by my colleague, Sarah Gibbons, that dives into how COVID-19 is cutting off access to storm shelters and, you know, basic necessities that people need after a hurricane like this. And speaking of the pandemic this week, a lot of us were, I don't know if the, if puzzled is the right word here, when the CDC announced earlier that it was no longer recommending people without COVID symptoms to be tested. And they followed that up by removing the recommendations for

travelers to quarantine for 14 days. Why would either of these things be good ideas? Yeah, you know, if I had long hair, I would be sort of pulling it out. And I think members of public health Twitter sort of feel the same. There's been a real, real frenzy after these decisions came through. I mean, the first one sort of saying that people who think they've been exposed to COVID-19 don't necessarily need to be tested if they're not showing symptoms. You know, it really doesn't make sense. And also the way that the policy was put out, it was very quiet. It was a very quiet change. I think that's led to a lot of the uproar. And the Washington Post reported that the pressure to make the change came from the White House.

And after effect, there was an official from the Health and Human Services that said, you know, doctors on the coronavirus task force, you know, all the positions. on our coronavirus test force had endorsed the plan. But then later, Anthony Fauci told CNN, well, what are you talking about? You know, I was in a hospital last week receiving vocal cord surgery. And to quote him, he said, and was not part of any discussion or deliberation regarding these new testing recommendations. But I think the bigger issue is that, again, it really doesn't make sense to do this, right? If you went to a doctor and said, hey, I think my friend just poisoned me, and the doctor replied, sorry, I can't test you until you

show symptoms. You'd be like, wait, what? That doesn't make any sense. Like, I'm in trouble now. And early detection is even more urgent with COVID-19 because we know that up to 40% of cases have no symptoms. You know, the American Medical Association replied to this news saying, this is a recipe for community spread and more spikes of coronavirus. And the same goes for the other new guideline about how travelers don't need to quarantine if they're coming from a place that is a hotspot for disease. Why would you do that? We know that these arrivals are more likely to have the disease. And again, a lot of those people could be asymptomatic. It's just extremely, it's extremely dangerous. And we have a story out this week from one of our writers,

Craig Welch, where he talked to experts across the country, and their recommendations were incredibly uniform, right? Like, we still just need to do the basics. And I think part of doing that is embracing reality, right? Like, we're half a year into the worst public health crisis in a century. Aren't people tired? Like, don't people want to sort of go back to the way things were if they can as fast as they can? So, it's a lot. think to do those things, we just really need to focus on the basics, wearing masks, social distancing. And also, we need our leaders to have a uniform plan that they can give to us because creating all this confusion is just going to lead to more spread of the disease.

Well, let's see if we can end on a happier or a more hopeful note, a news story this week. And that is a ray of good news from the fight against a different. infectious disease. The African continent was declared free of wild polio this week. Can you explain that? Yeah, I mean, this is the end of a 24-year effort to eradicate wild polio, which, you know, is a devastating disease. It's a crippling disease. You know, there was a major campaign that was launched in 1996 called the kick polio out of Africa campaign. And back then, polio used to paralyze about 75,000 children on the continent per year. And through a public health outreach and through a mass vaccination campaign, they're able to reach this point where now wild polio has been eliminated

from the continent. So there's still a non-wild strain of polio left, right? How big a, big a worry would that still be for this effort to eradicate it? Yes. I mean, even with this progress against wild polio, there's still a strain of polio that's circulating due to an old vaccine that involved a weakened version of the polio virus. And unfortunately, what happened is some people took that vaccine and the virus sort of came alive again. And, and the virus sort of came alive again. and now we have this other strain that doesn't cause that many cases. You know, we're talking about 320 last year, 68 in 2018, but it's still out there, and we're still working to immunize with the polio vaccine that we know works now to fully eliminate

that other strain. And the pandemic, the COVID-19 pandemic, has sort of interrupted. did some of those efforts this year, and, you know, people are hoping that we can pick them back up once COVID-19 abates. Thank you, Sikhan. Thank you for having me. Sikhan Akban, Science Editor at National Geographic in Washington, D.C. We're going to take a break, and when we come back, the keys to COVID-19 are not just in

understanding the virus, but also our own immune system. How to wrap your head around all the knowns and unknowns of the body's complicated defense system. Coming up after the break, so stay with us. This is Science Friday. I'm Ira Flato. Let's talk about our immune system. As we keep hearing, it is complicated, an elaborate cellular machine whose job it is to protect you from anything that, well, isn't you, whether that's invading bacteria, parasites, and of course the virus that causes COVID-19. Your immune system has two departments. the innate response, which happens immediately,

and the adaptive response, the immune memory that our hunt for an effective vaccine hinges on. But if you tangle with the virus once, research is increasingly finding signs that your immune system will remember and protect you for at least several months to come. Could it be longer? How does it happen? Let's talk about it with my guests. Dr. Catherine J. Wu covers science and health for the New York Times, holds a Ph.D. in Microbiology. Welcome to Science Friday. Hi, it's great to be here. Dr. Deepta Batacharia, Associate Professor of Immunobiology at the University of Arizona in Tucson.

Welcome, Dr. Baticharya. Thanks for having me, Ira. Let's begin with Catherine. Walk us through the standard immune system response to a new virus. What should happen when we encounter this coronavirus for the first time? Yeah, thanks for that question, Ira. I'll speak here very broadly. because every virus is going to spark something slightly different in the body. But for a typical respiratory virus, you should expect an immune response in two kind of orchestrated waves. The first is full of immune cells that basically see the world in two shades, self or not self. If it falls into that latter category and we're talking about something that has nothing to do with the body that these cells grew up with, they're going to attack it pretty indiscriminately. That happens really fast. That sort of buys the

rest of the immune system time to mount a more specialized response in the form of T-cells and B-cells. B-cells are the cells that produce antibodies, those really important disease-fighting molecules that everyone has been talking about lately. And those are super specific. I sometimes call those types of cells assassins because they can really set their sights on something incredibly specific and go after it specifically. Catherine, do you want to tell us what, what is so unusual so far with how COVID-19 provokes the immune system initial response? The first thing I'll say is a lot of people do seem to be mounting what seems to be a pretty

typical and protective immune response. The virus gets in. The body says, hey, you don't belong here. We're going to attack you and get rid of you. You see those two waves come in, the innate system first, then the adaptive system. And the virus does end up cleared. If people feel sick for a little while, they are capable of passing that virus onto others, and that's when they should really be taking care of themselves, staying inside and seeking

medical attention if necessary. But then the virus leaves their body, and they seem to have the tools to be able to fight it off again. Now, whether that production is actually occurring still remains to be seen. We're only eight months or so into this pandemic. But it is looking promising. That said, that's absolutely not the case for everyone. For people who do really poorly with this virus, it seems that their immune system is totally confused.

The virus gets in, the innate system starts to react, but then it kind of never stops reacting. And eventually it just starts creating all this collateral damage that starts attacking healthy tissues and sort of takes the body down with the virus. And then when the adaptive immune system comes in, it seems like there's this total lack of coordination. It seems like it's firing on all cylinders. and it almost seems like the body can't tell whether it's fighting a virus or a bacterium or a fungus or a parasite like a worm. And it's just throwing its entire arsenal of weapons at the virus. And that just wreaks havoc all over the body. Why does it keep fighting this? What kind of memory do these antibodies and T cells offer? So as you said at the very beginning, what the immune system is really

trying to do is distinguish self, things that are normal from non-self. We encounter all sorts of things that are different than ourselves, things we eat, things we inhale, and we really don't want the immune system overreacting to those kinds of things. So the innate immune system has a series of molecules called pattern recognition receptors, and they're looking for really common traits and viruses or bacteria or fungi or parasites that then instructs the adaptive immune system, the B cells and the T cells, to make the right kind of response. So in a typical kind of response, then what happens is that there's this intense competition for the best B cells and the best T cells that recognize the pathogen at hand, in this case, SARS-CoV-2. And then at the end of it,

all you really left with are the winners of that intense competition, and those can persist for quite long periods of time so that they can respond very quickly if you see the virus again. How long does this memory last for in our bodies? So at the very beginning, during this competition process, there's this massive wave of both B cells and T cells that are attacking the virus, and they're not all that great. And so again, through this culling and competition process, there's a massive wave of death of the cells that are not very effective in dealing with the virus, so that only the best ones are left. So during that process, there's a decline in antibodies, there's a decline in the number of T cells. And what really follows is the stable wave of

memory cells that persist after that initial decline. And really, that's where the stage we're at right now. And it's a little bit difficult to predict exactly how long to last. But, you know, if we take some lessons, say, from the first SARS coronavirus, I think we can expect that those will persist for at least a few years. You know, it sounds like the immune system is really, really complicated. Catherine? I think that's very fair to say. And what you said earlier actually struck me because I think what a lot of people have been noticing recently is that dip in antibodies, which has made a lot of people concerned about, oh, no, what's happening to our antibodies, what's happening to our B cells. But what's important to keep in mind is that even if

the weapons themselves disappear and here I'm referring to those antibodies that can maybe block the virus from entering a cell, what's important is that the body may have the ability to retain the potential to produce those antibodies again. It's like checking this if the weapons factory is still working and not keeping as much track of the weapons themselves. I'll also point out that it's pretty easy, you know, at least relatively speaking, to measure antibodies in the blood. You really just have to take a blood sample and look for those proteins. When you're talking about B cells and T cells, it becomes a whole other ballgame. You're dealing with live cells that can be kind of finicky if you want to grow them up in the lab and see what

they recognize. That involves all kinds of tricky scientific tools. And, really, really specially trained personnel. Also, some cells hide out in tissues or in the bone marrow, and those are not really easy places to look. Well, then how much should we depend on counting the antibodies that are left in our blood as a sign that, you know, we have an immunity? Well, I think for research purposes, certainly, I think what we want to do is get a range of outcomes across the different population, right? Because it'll instruct, you know, how often would we need to get a booster vaccine. When do we need to start worrying about new epidemics?

Those are kinds of things that I think that we need to be doing some sampling. Does every single person need to do that? No, absolutely not. I think we'll be able to get some trends from sampling and research and, you know, and getting some idea as to how long the typical response is and then getting a range around those as to how long we can expect any given person to be immune. This week, researchers published what looks like confirmation that at least sometimes a person, might be infected a second time by SARS-CoV-2 or at least a slightly different strain.

Is this bad news about our immune memory for coronavirus? Catherine? I do not think this is bad news. I actually think this is somewhat expected news. And depending on how you look at it, I could even cast this as good news. Considering how many millions of infections we've already seen from this virus, and that's just confirmed infections, having one confirmed reinfections, having one confirmed reinvest. infection so far, that's pretty impressive. But what's really important to note here is that it looks

like his body was kind of doing its job, actually. This is not evidence to me so far that people are doomed to suffer repeat bouts of really severe disease over and over. It seems like the first time this man was infected, he experienced mild symptoms, probably evidence that his body was fighting the virus off. He recovered. And then several months later, he was infected again by a very similar-looking virus, but this time he didn't have any symptoms. Being infected a second time and having significantly reduced symptoms or no symptoms at all, that's a huge win. That could still be really good news for immunity and evidence that his body was doing what it's supposed to do. And I think we will need many, many, many more cases that have some similarities to this to start noticing actual trends.

The next person who has a confirmed reinfection may look extremely different from this. And there are many, many different directions that a second immune response to the same virus can take. This week, the FDA gave an emergency use authorization for convalescent plasma using antibodies from people who have already recovered from the virus. But in the process, the FDA vastly overstated the known effectiveness of this treatment. What can we say at this point about this approach, DeepTA? I mean, antibodies are really best if they're already there. If you give the antibodies or convalescent plasma early, it can be somewhat effective. If you give it later, it's much less so because then the issues are a little bit different.

Then it's damage from the virus itself. It's damage from the immune response to your organs. And then antibodies really not so useful anymore. I think this is then one of the challenges is that we really haven't had a control trial in a way that would allow us to measure when is it effective, what types of plasma are the most useful, how many antibodies need to be in the donor's plasma for it to be effective. and we just haven't gotten any of those answers. And so, you know, I think that convalescent plasma was a fine option based on what we've learned from decades of viral immunology at the beginning.

But this isn't really a permanent solution. And it was really meant to be a stopgap. I don't think any of us felt that this was like a B-N solution. And in fact, there are many better, I think, more uniform treatments that are heading into trials now called monoclonal antibodies, where it just put in one type of antibody, you know exactly what it does, you know, that it prevents the virus from getting into. cells. And there's a number of companies that are really struggling to actually enroll proper numbers of people in those trials for a therapy that I think is frankly much more likely to work consistently than convalescent plasma. And so I think the thing that I worry about the most is that

convalescent plasma emergency use authorization will just open the floodgates. Everyone who use this as a frontline therapy, it's sort of middling in its effects. And then perhaps most damagingly, it really impairs the ability to run those monoclonal antibody therapy trials. Oh, so it could get in the way of understanding what's really happening. Yeah, absolutely. Not only because the EUA disincentivizes running a proper trial, but it also essentially would make someone ineligible to enroll in part of the monoclon antibody therapy trial

because it just gets in the way, and antinpoints get in the way. This is Science Friday. I'm Iroflato. In case you're just joining us, we're talking about COVID-19 and our immune systems with New York Times reporter Catherine J. Wu and University of Arizona immunobiologist Deep Tavadacharya. Catherine, this is a point that we've seen hammered in over and over again. How complicated the immune system is. It's clear we're going to be seeing more headlines, maybe some appearing to conflict about the immune system

as the fight against this virus continues. What are the most important things to keep in mind as we proceed forward? What an easy question to answer. I'm totally like. Oh, gosh. All right. So a few takeaways from me so far. I think one thing to really keep in mind, immunity is not a binary phenomenon. We're really talking about a spectrum of responses here. A lot of times when we talk about immunity in a more colloquial sense, we talk about it as I am fully protected from X, Y, or Z. And I want to make sure that people understand that there's a lot in between being fully protected against a virus so that you'll

never be infected by it again and being completely vulnerable to suffer the same disease over and over. Chances are that we are going to see SARS-CoB-2 occupying something in the middle there. We don't know exactly where it's going to land, but I want people to set their expectations and also make room for some heterogeneity in responses. Some people are going to react differently to this virus and with so many people who have been infected so far with likely some more to come, we are going to see a wide range of responses. And we're going to see a lot of that range filled out. So people should not be worried when they see reports about reinfection. People should not be worried if they see differences in levels of things like antibodies or T cells, how your body reacts

will be different from how my body reacts. And that's still all okay. Having an immune response, that confers even a degree of protection is far better than having no protection at all. Another thing to keep in mind is that, you know, the immune system can work for us, but it can also work against us, whether that's because the virus is kind of messing with the immune system or because the immune system gets confused by something it is seeing that is brand new and is seeing for the absolute first time. Obviously, our immune system has evolved to protect us from disease, But as this virus has so clearly reminded us, there are a lot of ways in which that response can go awry. And maybe in the future, as we keep dealing with this virus, we're going to keep developing

treatment that will help us kind of temper those overreactive responses or revap responses that might not be reacting soon enough or well enough. But it's really a complex process. I think one thing to keep in mind is that as we're exploring treatments and vaccines, there are certain parts of the immune system that might be better dialed up and others that that might be better dialed down. And we don't have to paint the immune system with a single brush. TEPTA, very interesting summation.

What can you add to that? You know, what we're learning is that it's very possible to generate a protective immune response against, in fact, almost everyone does. And so that is almost always one of the hallmarks of something that is susceptible to immunization and vaccination. And so I think that the early immune correlates that I'm seeing from the vaccines, the Immunological behaviors that I'm seeing from people who have recovered from the virus

make me think that this is something that it's very possible to immunize our way out. And so it won't happen immediately. There's a lot of logistical things. But as long as we set our expectations, as Catherine mentioned, is that what we're really trying to do is to limit the severity of disease, make this not so much of an issue.

I think that's a very achievable goal. And I think that a lot of the behaviors of how our immune system has been responding to this virus may make me quite optimistic about that aspect. One other thing that I will add is the immune response that is produced to a vaccine will not necessarily look exactly like the immune response produced by a natural infection by the virus itself. That could actually be a really good thing in this case. As we've seen, there is such a wide range of responses to this virus from the standpoint of the immune system

in different people with different conditions, with different backgrounds, but maybe being able to tailor and administer a vaccine that looks pretty much the same to everyone will really work in our favor. It may also remove parts of the virus that might be deliberately messing with the immune system to make it easier for the virus to gain a foothold. So we have a lot of power here by sort of observing these things from two standpoints from natural infection as well as the vaccine. We can do some compare and contrast. And if things look different, people shouldn't necessarily be alarmed. This may be a really good opportunity for scientists to really produce an optimal vaccine that will produce a lot of protection and continue to tinker with those formulations

as new generations of vaccines come in the future. And we have run out of time. I'd like to thank my guests. Dr. Catherine J. Wu covers science and health for the New York Times. She holds a PhD in microbiology. Thank you, Catherine. Thank you. It was great to be here. And Dr. Deepta Badacharia, Associate Professor of Immunobiology at the University of Arizona in Tucson. Thanks for having me, We're going to take a break, and afterwards we're going to come back to talk about stuff that you asked for, and we are answering all your questions about cephalopods. Stay tuned. This is Science Friday.

I'm Ira Flato. One group of animals seems to universally unite people. No matter whom they are, I'm talking about cephalopods. Everyone has a favorite cephalopod. From the color-changing octopus to the multi-chambered nautilus, Everyone has a question about these smart, colorful undersea creatures. How do they move? How do they change shape and color? How intelligent are they? How do researchers study these animals? So we decided to devote some special time to dive into your squid and cuddlefish questions and talk about some of the latest Ceph Research.

It's time for Ask a Cephalopod Scientist. And our guide through this cephalopod celebration is Dr. Sarah McAnulty. She's a squid biologist and an assistant research professor at the University of Connecticut in Stores. She's also executive director of Skype a scientist and a tireless tweeter about her favorite friends. Welcome to Science Friday. Thank you so much. And we have an audience listening in via Zoom. We want you to ask your question.

So please don't be shy. Now, I know that you recently graduated from your PhD program. Congratulations. How did you be coming? interested in researching cephalopods to begin with? I have been interested in biology broadly since I was a little kid. I first started as being interested in dinosaurs. And then I went to the library with my mom all the time when I was young in Ben Salem, Pennsylvania.

And one day, we checked out a videotape all about the ocean. And about halfway through, Twilight Zone music started playing. And they introduced the cuttlefish. And they were doing this really amazing behavior called Passing Cloud. I didn't know that was what it was called at the time. But effectively, it looks like a hypnotic wheel is passing over the Cuddlefish's body. And I thought that was the wildest thing I had ever seen. And I was pretty much hooked on cephalopods from that moment on.

You study the Hawaiian bobtail squid. Why focus on that squid? The Hawaiian bobtail squid is really phenomenal, specifically for studying how animals and bacteria have these beneficial relationships with each other, these successful communications that we have in our body too. So we have, of course, bacteria on our skin and our gut, and they're totally essential for our health. The nice thing about the bobtail squid is that they have just one species of bacteria

in these specialized organs on their underside called the light organ. And so those bacteria produce light that allow the squid to camouflage with moonlight coming down from above. Now, my work covers basically how the immune system can tell the difference between beneficial bacteria and all the other bacteria that squid may encounter in the seawater. That's cool. What are some of the big questions that you have still left over? You've been studying these bobtail squid for quite a while.

What don't you know yet that you got to know? One of the things we really want to know, specifically with the female bobtail squid, is how they can pick out the consortium of bacteria that they'll eventually have as an adult in what's called an A-N-G, that's short for accessory nidimental gland. And now this is a super cool organ, also associated with bacteria. Imagine like a pile of spaghetti, and each spaghetti strand has a different species of bacteria inside of it. When the female squid go to lay her eggs, she'll wrap the baby squid in coats of jelly, that if you cut it in half, looks like that. If you cut it in half, a lot like an onion. And so each jelly layer has a bunch of bacteria all in that jelly. And so she'll lay

her eggs. And unlike an octopus that constantly cleans her eggs, she'll just leave them under a coral bit or a rock and go swim away to lay another clutch another day. So the bacteria in the egg protect the baby squid from bacteria, fungus, and potentially other things in the water as well. And so we want to know basically what compounds or what chemicals are the bacteria creating to protect the squid? And how does the female squid, when she's first developing as a little baby squid, how does she pick out the right bacteria? Because there may be like a hundred different species in there, but there's way more than 100 species in her environment.

So how the heck is she picking the right stuff? We have calls. We have viewers coming in who have some questions. Let's go to our first question. Let's go to Terry Kirby Hathaway in Outer Banks, North Carolina. Has a question for you. I do. Thank you for calling on me.

I love your Twitter feed. I'm one of your followers on Twitter, so I was excited to see you on here. My question is about your bobtail squid. Is the bacteria that produces the light for the bobtail squid? Is it the same as the bacteria that produces the light and flashlight dishes? That's a great question. Yes. The bacteria that we're talking about is bribriofisher.

sure eye. And it shows up in a lot of different places in the lore of anglerfish in pine cone fish in those little under eye areas. So yeah, it shows up in a lot of different animals. It's a slightly different strain. So if you took the bacteria out of the pine cone fish and you tried to put it in a squid, it doesn't go so well. If you took the anglerfish bacteria out, it again, it doesn't really jive with the squid, but it's the same species. Great answer. Thank you. Thanks for calling. You're the first person on our Zoom call ever. We'll put a little bit of trivia on our website about that. There's another question that came up earlier that I'm glad you're on because I really wanted to know the answer to this. Earlier this month, scientists used CRISPR to make the first genetic

altered squid. Why is that such a big deal? What is so exciting about being able to do that? This is truly huge because a lot of times in cephalopod research, in the research that I've done and many others have done, we get kind of to this wall of understanding where you really need to start playing with the genetics of the animal that you're studying to really piece out the mechanism of how things are happening. The one challenge with squid is that they're really rubbery, honestly. And so when you're playing with CRISPR, often what you have to do is take a. very, very tiny needle and inject it into a little squid embryo. And so when it comes to some cells, they're very easy to puncture. And with the squid, it's like trying, it's like the needle sometimes would just bend when you would try to poke the squid. And so it was a collection of challenges, including raising the squid in captivity, that have all kind of come together at the marine biological

the laboratory to just overcome these obstacles and make a genetically modified squid happen. And now that we can do it in the market squid up in Massachusetts, we can hopefully do it in a whole bunch of other species as well so that we can understand specifically what genes are playing around with communication of bacteria and animals or other questions as well. Have you in your own laboratory done this needle thing trying to poke? How hard? How hard is that? You break needles,

trying to do it? I broke all kinds of things. It was so hard. Yeah, so I did a workshop with Judith Pungnour, who is another scientist who works on this kind of thing. And she had us basically like taking teeny, teeny, teeny tiny scissors and sniffing part of the egg in order to get the needle. And wow, yeah, it was easier said than done, for sure. Took a very steady hand. Let's go to another question. Greg Miller. Hi. Welcome to Science Friday. Hi, how you doing? Hey there. Go ahead. I think cephalopods are absolutely brilliant, very intelligent, and I just wanted to know how you test cephalopod intelligence.

Another excellent question. So I recommend that everybody read this book called Are We Smart Enough to Know How Smart Animals Are? The answer is barely. So it's really, really hard to compare different animal intelligences because what one animal needs to get by can be very, very different from one another animal needs. So for example, if a squid looked at us and saw that we couldn't change color at all, they might think that we're not very smart at all, even though we can talk to each other with words and they don't hear that well at all.

And so you really have to think about what is intelligence to this animal's lifestyle and how do you compare one animal to another when those lifestyles are so, so different? So we might think that a bacterium, for example, is not particularly intelligent, but they can do things that we could never do. So I'm not just trying to like send the question right back to you. In determining animal intelligence in terms of like a quantitative this animal is smarter than this animal is really tough. But you can test kind of what they're capable of doing in terms of problem solving. You can give them association tests, mazes, trying to recognize themselves. These are common things that animal behaviorists use,

try to figure out what they're capable of. Do they have a brain like we do? You know, some of these fish that don't have them, or some of the animals that live in the ocean don't have these big brains like we do. They do have brains and they're quite large. And also, fun fact, they're donut shaped, which is one of my favorite squid backs of all time. Their esophagus goes through their brain. And so they have to eat very small little bits because if they were to take a huge chunk,

like it would squeeze their brain, which can't be comfortable. But they have one central brain, and then octopuses have ganglion, which are like collections of neurons that are not quite a brain, but still a collection that is capable of doing some stuff. And those are each in the arms. So it's kind of like they have eight or nine rather brains, the central brain and then the eight brains in the arms. Donut brain. That must be the Homer Simpson of cephalopods to have that donut brain. I want to talk more about some of these really interesting species. There's something called the strawberry squid that has two different sized eyes on purpose?

Yeah, the strawberry squid is one of my favorite squid species because it can really show you how different cephalopods can be from one another. Cephalopods have been on Earth for 500 million years. That's longer than trees. That's longer than sharks. They've had a lot of time to evolve these really wild adaptations. And the strawberry squid is a phenomenal example. For those of us in the Zoom call, I've made a doodle of the strawberry squid for today. So that looks great.

We've got two different eyes here that are for two different purposes. So facing toward the surface of the water, the strawberry squid has this big, bulbous yellow eye that you see here. And so while it's looking up, that yellow color is filtering out different. wavelengths or colors. And so it helps the squid differentiate between counter illumination, so animals that are using color or light to kind of disappear among the light coming down from above, which is super, super faint because they're super deep. And so there's really not much light to work with. And you need a huge eye to pick up all the light you can. And then the eye that they tilt downward is much smaller. And it's specifically used for detecting, we think, like,

ioluminescence down where they live. And so maybe the small eye is used to detect food for that night, whereas the bigger eye is looking up to make sure there's no predators coming from above. And on top of that, they also are covered in what's called photophores, which are bioluminescent organs all over what's called their mantle or their body, basically. Let's go out to back out to Zoom to Anne Papa. Hi, welcome to Science Friday. It's Papa, I think.

I recently saw a picture of an octopus that was the size of a fingernail. And I was wondering for cuttlefish, what's the smallest cuttlefish and what's the largest cuttlefish? What's the smallest cuttlefish? I know the smallest squid. The biggest cuttlefish without a doubt is the giant Australian cuttlefish. They can be a meter long in mantle length, which is huge. One of my bucket list items is to go to Australia and check out that mating aggregation because it's really apparently stunning. The smallest cuttlefish, I know there's a dwarf cuttlefish, but I guess. I can't promise that it's actually the smallest.

But can I tell you about pygmy squid? No one's going to stop you. Go ahead. Great. Okay. So pygmy squid are super, super tiny. They're about the length of your pinky fingernail. They're like 16 millimeters long.

And they are fantastic and amazing. But we've only really recently realized how cool they are behaviorally. They have the ability to create the sticky substance that's on their back and then stick to a blade of seagrass. And I kind of like to call them the Post-It Notes of the Sea, because they just look like a little goofy squid stuck out of the top to a piece of seagrass. And then they pivot their little faces around to look for food. And it is really cool. And on top of that, they also use their ink in a really peculiar, awesome way.

They will squirt out a little blob of ink and then hide behind that ink from their prey and then quickly jump through the same. ink and attack their prey. So they're basically creating a hunting blind with their ink, which is wild and so cool. Wow, is that cool? In case you're just joining us, I'm Ira Plato. This is Science Friday from WNYC Studios. We're talking with Dr. Sarah McAnulty, newly minted PhD, Dr. McAnulty. She's a squid biologist and the ultimate squid geek, I think. Do you live and breathe squid even when you're not in the laboratory? Yeah. I try to do. to give my personal friends a break from squid just so that I can maintain friendships. But yeah, even my car is called the SquidMobile and it has phone number on the back that you can text

for a Squid fact as long as you're not driving. Oh, wow. Send us a photo of that. We'd like, to spread that around. How has the pandemic affected you and other Cephalopod researchers? Has it had an effect? Yes. It's been tough, but I mean, it's been tough for all scientists. Anybody working with animals is really sort of stuck because if we can't go into the lab every day to take care of them, it sort of creates a problem. The one benefit of working with Hawaiian bobtail squid is that their lifespans aren't all that long. And so for an animal that may only live about five months in the lab, we were luckily right at the end of kind of a squid cohort. So we wrapped up that cohort and then just didn't get any more squid. I was going to go back to Hawaii to collect in June.

But that was unsafe, so we didn't go. I am theoretically supposed to go in January, but I kind of doubt that that's going to happen either. So we have to just cross our fingers that everyone gets healthy again so that we can hit the ground running. What about all the squid and all the cephalopods and everybody's lab during the pandemic? Did they leave them there? Are they okay? What happened? I know the ones at the MBL are being taken care of just as normal.

So because the scientists weren't going into the lab as often, they didn't breed as many cephalopods to be studied. So there's just sort of like a pared down family of cephalopods there. You know, you reminded me of a few years ago there was a new octopus, a cute little octopus called adorable. Oh, my goodness. Yeah. We tried to get it named because it was so adorable. Whatever happened, did it work? That's a good question.

I mean, I know there are a lot of sepulopod researchers who call it Adorabilis still. Think of it as adorable as well. I don't know what the official like names on the book is, but it is cute as hack, yeah. Such a cute little octopus. You know, we have run out of time. I can't believe it. It's gone by so quickly. I want to thank you, Sarah, for taking so much time to be with us today.

Absolutely terrific on our first Zoom meeting. Hopefully we'll have many more of them. Dr. Sarah McEnulty. is a squid biologist and assistant research professor, University of Connecticut in Stores. She's also executive director of Skype a scientist. And you can watch the entire video of this interview and sign up to find out about joining us on future Zoom interviews on our website. It's there at Science Friday.com slash events. Oh, one last thing before we go. Some news from our book club. We've picked the book and we want you to read it. It's called New Sons. It's a collection of short

speculative fiction edited by Nisi Shawl. The club launches later this fall, so stay tuned for more announcements, and check out our website, ScienceFriday.com slash book club. Charles Berkwist is our director. Producers are Alexa Lim, Christy Taylor, Kethe, Kathleen Davis, B.J. Leiterman, composed our theme music, and of course, if you missed any part of this program or you would like to hear it again, subscribe to our podcasts. Have a great and safe weekend. I'm Ira Flato.