The Hot War - EWTS #016

Joe: Hello and welcome to another episode of Enough with the Science. I’m Joe.

Senan: And I am Senan. And Joe, why am I here?

Joe: Well, are you going to explain to me what a virus is?

Senan: That’s why I’m here. Really? I thought I was here to host a science podcast. That was my segue to allow you to tell us why we’re here.

Joe: That’s a very profound question, you see Senan. So basically, this is a little podcast where we explain complex scientific topics. Well, Senan explains them and I just refuse to understand them. That’s essentially it.

Senan: Joe challenges me to reduce them to simple concepts that Joe can understand.

Joe: Yeah. He has failed, singularly. So we were hoping today is the podcast where this changes.

Senan: But before we get into the subject matter of today’s podcast, we have a really important announcement. It is the first podcast of 2026 and new for this year we have our own website at enoughwiththescience.com.

Joe: Wow. We’re just going to be super famous now, aren’t we?

Senan: We are going to be totally, absolutely famous. So anyway, you can get all our old episodes there. For each episode you can get a transcript and you can get links to other interesting information that supports the topic of each episode. So check out the website.

Joe: And don't forget our shop. Merchandise.

Senan: Enough with the merchandise. That’s next year. That’s 2027. [laughter]

Joe: Have we not got merchandising mugs and pens and t-shirts?

Senan: No. Right. I have a question for you, Joe.

Joe: I knew. I knew it was coming. There always is.

Senan: War. What is it good for?

Joe: Well, I tell you; not for Greenland. That’s for sure.

Senan: You missed your Frankie Goes to Hollywood cue.

Joe: Absolutely nothing; say it again. There you go.

Senan: Correct. And we are here today to talk about probably the most pervasive war on this planet. It’s been going on for millions of years.

Joe: The battle of the sexes?

Senan: It’s happening in every… no well, no, cause it happens with creatures that don’t have different genders. It’s happening everywhere; it’s happening in this room right now and it is the battle that our immune system fights. So we’re going to try and tackle the ridiculously complicated subject of the human immune system.

Joe: Brilliant. I’m not understanding it already.

Senan: So, microbes; what are they? Microbes is a collective name for bacteria, viruses, funguses that are so small we can’t see them. Millions of them around us every day; there is an uncountable number on top of the skin on the back of your hand right now.

Joe: Okay.

Senan: Most of them don’t cause disease. Most of them are indifferent to us; they’re paddling their own canoe.

Joe: They don’t care. They don’t care about us.

Senan: None of them care about us; other than the ones that rely on us to stay alive. Viruses. But there is a subset of microbes which can cause disease and we call them pathogens.

Joe: Ah, so a pathogen is essentially a dangerous microbe.

Senan: A thing you can’t see that can kill you.

Joe: Right. Wow, like a ninja.

Senan: Yeah, a bit of a ninja. And we have this incredibly complicated but also incredibly effective system of many different layers to protect us. And nobody designed it that way. It just evolved over millions of years.

Joe: Of course, if anybody wants to believe that there was a prime mover who designed it specifically to do this job, that’s completely up to you.

Senan: This is not the podcast for them. You are on the wrong station. Evolution just keeps trying new things. Mutations happen in DNA and that means evolution tries something new and that is how our immune system has evolved. The things that worked, the things that protected us became part of us; the things that didn’t work probably didn’t become part of us because the creatures that had those mutations didn’t survive long enough to have children.

Joe: I see a flaw in this.

Senan: Go ahead.

Joe: Because probably the pathogens are evolving too, aren't they?

Senan: The pathogens are evolving too, which is one of the key aspects of our immune system and that makes it really cool; it’s able to evolve to deal with new threats it never saw before. We’re going to cover all that in obnoxious detail as time goes along. It’s a two-parter because the system is so complicated that we just cannot cover it all in one episode. So let’s just talk about what are the components of it.

Joe: Okay, what are the components of it?

Senan: Four main pieces. You’ve got the external barrier ... and I’m going to go into all of them in detail now so I’m going to quickly…

Joe: So just list them now. You're not summarizing, you're just listing; just list the names.

Senan: We’ve got the external barrier. We’ve got an unfriendly environment in our orifices.

Joe: Right, you're going to change… What did we say? Portals. Portals from the external world.

Senan: The portals from the external world into the inside of our body. Then we’ve got the main topic of today’s discussion which is called the innate system. They’re kind of general purpose defenders that are always on patrol inside in our body. Crucially, for reasons we’ll find out next week, they have no memory. And finally, we have the real magic which happens in something called the adaptive system. That’ll be the topic of next week’s show cause it’s a big topic on its own.

Joe: But you should stay listening to this show because you're probably going to need some of the words when we talk next week.

Senan: You totally will. And you need to understand that if you just get next week’s show, you will be missing out on a big part of the picture. Anyway, the adaptive system; it’s able to target specific types of invaders which the innate system that we’re going to talk about today cannot. And it’s also able to; the real magic with it; is that it remembers. So if it saw a particular type of invader before, even years ago, it’s able to remember how to quickly deal with that invader the next time it sees it.

Joe: It's like a sniper with a photographic memory.

Senan: That kind of thing, yeah. So that’s the end of the list. Let’s talk about what do you start out your life with in terms of an immune system. In other words, when you're a wet, wrinkled up, screaming little red baby that’s just come into the world, what do you have? Well the fact is your immune system is immature at that point; it’s not fit for purpose yet. So luckily, your mother bequeaths you a legacy of her immune system. So when you're still in the uterus, some of her antibodies; which are one of the components of the immune system; some of her antibodies pass through the placenta into your bloodstream and you're able to make use of those to help fight off infections.

Joe: Okay. So you've learnt from her? Your immune system has learnt from her?

Senan: You haven't really learnt from her. You've just got bits of her immune system that will act on your behalf. But they aren't teaching your body anything really. Right. And then the other thing is to a lesser extent if you're being breastfed as a baby, you're getting some of her antibodies through the breast milk as well. But I think majority of it is coming through the placenta before you're born.

Joe: Mammies are great.

Senan: Mammies are the world’s best. And Irish mammies are the best of all.

Joe: No argument here.

Senan: So the problem of course is that those antibodies, because your body isn't making them itself just yet, because your poor old baby immune system isn't up to that yet, they fade out after a few months. So there is a period of vulnerability until you're about a year old when your own immune system is fully active.

Joe: So kind of from about six months to a year, you're sort of… there's a gap?

Senan: Yeah even less, maybe four months to a year, but so like… it is important that babies are kept in a clean environment and protected from getting too cold or getting wet or whatever for that first year until their own immune system gets going. Right. Let’s start talking about your actual immune system. The primary protection, the front line is your skin. So if you were a medieval castle with a big stone wall all around the outside of the castle to keep invaders out, that’s what your skin is. It’s like a tough impenetrable barrier that these pathogens cannot get through.

Joe: Usually.

Senan: Usually. And it’s remarkably effective; it keeps out most of them. And the other thing is some pathogens will manage to cling onto the outside layer of your skin. But the fact is you're constantly shedding dead skin cells from the top layer.

Joe: Is the word sloughing? Is that the word? Sloughing?

Senan: Sloughing. Yeah, I think that’s it, yeah. Isn't it a place in England too, I think?

Joe: Name of a place. And the Irish Sloughing Championship? No, wait a minute.

Senan: No, that’s ploughing. That’s men in muddy fields digging holes.

Joe: Okay.

Senan: And there are women too, I shouldn't say it's a man only pursuit. Ploughing is by the way what I'm referring to.

Joe: Speaking of digging holes.

Senan: So most of them can't… most viruses and bacteria just bounce off your skin, gone, can't get in. However, of course, we do have the aforementioned portals like your mouth, your nose, your eyes, your ears and other places further south. And those of course are not covered in skin so nasty things can get inside. So the inner areas like your throat, your lungs, your nostrils, your eyes, they have mucus membranes. So you remember we did that fantastic show about mucus and snot a few months ago.

Joe: Who could forget? Who could forget all the goo?

Senan: So there is this thick layer of this goo on the inside of your lungs and your throat and so on and the bugs get bogged down; they get stuck in this stuff. And then underneath that on the surface of the lining of your throat and your lungs, is these tiny microscopic hairs, a field full of them like a field of wheat and they're beating over and back in a rhythm. And that’s like a conveyor belt that gradually moves that mucus up and out of your body.

Joe: Snot.

Senan: Snot, yeah. And it carries the stuck bugs with it. So it’s like a conveyor belt of fly paper. So that’s how the orifices… then of course there's another orifice somewhere else that leads into…

Joe: Portal. External portal.

Senan: Portal, portal, yes. That leads into your gut. And inside in your gut there are an awful lot of pathogens. Like it’s mostly pathogens in there.

Joe: But all of those have come in from the outside originally?

Senan: Oh yeah, they got in from the outside and got established. It’s a lovely environment for them in there. Like there's loads of food, it's nice and warm, it's nice and moist. So yeah, they reproduce like mad in there. And a lot of them are useful; they're not all pathogens. A lot of the microbiome as it's known is useful to your body and it’s not likely to make us sick. But there are some things like E. coli in there that could make us sick. So the lining of your gut is a bit like your skin; it’s really dense tightly packed cells that the pathogens can't get in through and it’s covered in a thick layer of mucus. And the other thing is that a bit like your skin, it’s constantly shedding dead cells off its top layer the whole time. So even if some bugs do manage to latch onto it, they fall off when the dead cells are being shed. So you've got this great system inside too.

Joe: Then you excrete them.

Senan: Yeah, you excrete them, yeah, eventually. But I mean the percentage… I can't remember the percentage but there is a significant percentage, like could be 30 or 40% of the bulk of your feces are dead bacteria. It’s shocking.

Joe: And only you know that.

Senan: Well no, there are other people that know it too. But not many! Tears and saliva, another form of defense; they're not just water. They contain enzymes that actively attack bacteria.

Joe: I love this idea. Tears. You're lost, you're hacking through the middle of the Amazonian rainforest and someone accidentally hacks into your leg with a machete and you're miles from a hospital. And all you gotta do is cry into your own wound.

Senan: Well you'll be crying, that's for sure. So you might as well have the presence of mind to let it drip into the wound and see what happens.

Joe: Or cry at will. You could do that… Like actors can.

Senan: Actors, yeah, like Joey from Friends.

Joe: Remember what he used to do? He used to cut the bottoms of the pockets of his trousers and pull out one of his hairs from that nether region when he was called upon to cry. So if you could do that for mankind to help people's wounds.

Senan: I really wish you would not put that picture into my head. So yeah, and there's other stuff like antibodies in your tears and saliva that attack things. We'll be talking about antibodies next week; they're part of the adaptive system. All right. What happens if the barrier does get breached? What do the early stages of an infection look like? So initially we won't notice the infection has taken place because typically when something gets inside you that shouldn't be there, only a small amount of it gets in and it’s not enough yet to make you sick. And in its early stages the infection is actively replicating itself, building its army. Just making more of itself and more and more of itself until it has enough to actually attack.

Joe: So essentially this could come in… this could be in food, this could be standing on a rusty nail, it could be the bite of a wild rabid dog.

Senan: Yeah, or you inhaled a virus.

Joe: Okay. Yeah. Somebody sprays a virus into your face. Right.

Senan: That kind of thing.

Joe: Novichok type situation.

Senan: Novichok is not a virus.

Joe: Right. This is why I need this. This is why I need this podcast.

Senan: It’s a poisonous chemical. Anyway, some of them are actually quite good at hiding from your immune system in the early stages to give themselves a breathing space to replicate to build up their army. Some of them actually hide inside our own cells. Some of them jam our immune system’s radio. So our immune system has a way of signaling that reinforcements are required; it’s like chemicals are released that form a signal, but we'll call it a radio.

Joe: So these guys blow up the radio tower.

Senan: So some of the pathogens are able to jam those signals to stop the immune system calling in for reinforcements. And some of them are able to build little protein shields above themselves that protect them from being attacked. So they've all these different strategies for giving themselves a breathing space to get established. However, our innate immune system; which is the subject of today's podcast; is always there waiting and it does kick into action fairly quickly, within hours of invaders coming in. And lots of invaders will never survive that initial period because our innate immune system; we're going to talk about the details of it now in a moment; just swings into action so fast that it kills them before they can build up their army. And in that case usually we are never aware that we had an illness.

Joe: So this is probably happening all the time. Just right now.

Senan: Right now. Yeah. We're never aware and it just all goes away. Or the other thing that can happen is the adaptive system we're going to talk about next week is able to remember how it dealt with specific problems before. And if that particular problem arises again, it's able to swing into action pretty quickly. So also the adaptive system may kill stuff before it gets to be a problem. And really we only start to feel sick when either the invader has built a big enough army that he has spread around your body and is starting to cause problems, or your immune system has ramped up its own response so strongly that the actual side effect of your immune response is starting to make you feel sick.

Joe: So the symptoms are from your own response to the invader?

Senan: Or the invader's large scale activity. Yeah, one or the other or both. Right, so what are the components of this innate system? So there's five of them. We'll just list them off quickly now and then we'll go through them in detail, right? So there's phagocytes. Those are cells that basically eat invaders.

Joe: Pac-Men for pathogens.

Senan: Correct. There are… there's something called the inflammatory response, which is the hot red swelling thing that you often experience. There are what's called complementary proteins in your blood which help the immune system on its way. There's the wonderfully named Natural Killer cells, believe it or not.

Joe: Looking forward to them.

Senan: That's the official name, believe it or not. And then there's my personal favorite name, cause I like things that sound science-y; there's the interferon proteins, which basically are like warnings.

Joe: That's Doctor Who. That's a Doctor Who science-y made up name. Interferons.

Senan: Interferons. We'll find out later why they're called that. Right, let's go back to the first one, the phagocytes, the eating cells. There’s two kinds of course because nothing is simple with the immune system. So one kind is the neutrophils. They're the most numerous type of phagocyte, the most numerous type of eating cell. They only live for a day or two these things, so they naturally break down in your system if they haven't kicked into action within that day or two. So your system is continuously making thousands and thousands of these things, like a deluge of them in your system the whole time. They are the front line infantry; they're like kamikaze fighters. When a neutrophil kills a bacteria for example, the neutrophil dies as well. So they're like one shot wonder, but they're…

Joe: It’s like you've only given them a grenade. That's it. That's all they've got. You've got a grenade, you've got to use it, that's it.

Senan: So if you get a cut that gets infected and you notice pus coming out of it, a large proportion of what's in that pus is dead neutrophils because they're the front line attackers. And they're white, so if the pus is very pale colored, it's almost all neutrophils and the other stuff that's in it typically would be dead invaders, like dead bacteria or dead fungi or something.

Joe: But if it's green, you've got gangrene and you should go to the hospital.

Senan: Yeah, I mean it's obviously an indicator that a cut is infected if pus is coming out of it, but it's also an indicator that your immune system is fighting. The other kind of phagocyte: macrophages. So those guys are less… they're not the front line but they're the next line and…

Joe: Second line.

Senan: They're tougher. They don't die when they kill something. So each macrophage…

Joe: Oh, they're harder. They're harder those fellows. They don't even feel it. They just kill people, they go off, they have a sandwich, they come back, kill again.

Senan: Yeah, yep, they're constantly like… one macrophage could kill 20 or 30 bacteria. Like they're…

Joe: Just for fun. They wouldn't even think about it.

Senan: And they're only getting warmed up. So they're constantly on patrol, patrol, patrol.

Joe: Petrol. They’re on petrol.

Senan: Looking for things. They do have a secondary role which we'll be talking about next week in that they do help train our adaptive immune system. We'll put a pin in that until next week. So how do these phagocytes, you know these macrophages and neutrophils, how do they identify targets? I mean we don't want them…

Joe: Excuse me. Are you a pathogen?

Senan: Because we all know that all pathogens are pathologically incapable of lying.

Joe: Right. That's where the word pathologically comes from, isn't it?

Senan: I don't know if you've seen Pluribus, but the infected citizens of the hive mind are incapable of lying, which is one of the key aspects of the plot of the show. Anyway, I digressed a bit there.

Joe: Yeah, absolutely. Got to reel you back in now.

Senan: Right. How do they identify their targets so that they don't start killing the good guys? So it's all about chemical binding. So all of these little beasties that are running around in our body have particular chemical structure on the outside. It’s like, think of it as a signature. And it's like a key going into a lock; the phagocytes have certain structures on them that are able to fit onto or stick to…

Joe: Velcro. The two sides of velcro.

Senan: Yeah.

Joe: So have you got the right type of velcro or the wrong type of velcro?

Senan: That’s it, yeah. When you've got the right type of velcro your macrophage sticks to that and kills that thing. Right. So that's the surface of the bacteria or fungi or whatever. But the other thing is viruses have particular DNA patterns that these phagocytes can identify also. So there are common DNA patterns that would be in a virus that wouldn't be in a healthy cell that they can identify and sometimes latch onto viruses. There's also a different process we'll talk about in a minute in the immune system that can tag invaders. So they don't kill the invaders initially; they put a tag on them saying "he's a bad guy."

Joe: This is Mission Impossible again. You spray the stuff onto your hair and wear special glasses and you see the purple hair going up the stairs, that's the guy you want.

Senan: That's the suspect. Yeah. So the macrophages are able to identify the tagged ones and use the tag as a way of finding things to kill. Crucially, they have a cancer prevention role as well because our healthy cells have a like a passport, like a "this is me" signature on the outside. And often cancer cells or other cells that are damaged and maybe are going to start doing things we don't want them to do; our own cells I'm talking about now; don't have this passport. They don't have this signature on the outside and the macrophages will then latch onto them and kill them as well.

Joe: Where's your ID? I don't have it. Okay. Poof.

Senan: So it's great, we have this system for killing cancer cells before they start to spread and cause problems. And if we didn't have that we'd be in serious trouble because cancer actually occurs in our bodies far more often than we realize, but it just gets wiped out.

Joe: Or want to think about. Or keep talking about.

Senan: Well, yeah, but fine, we move on to the next thing. Damaged cells release alarm signals, chemicals, and the macrophages are able to detect those and it draws more of them into the area around the damaged cells. How do they eat the invaders? So they extend what are known as pseudopods…

Joe: You just love this bit. This is Doctor Who stuff again.

Senan: Basically tentacles. And they surround the thing they want to eat in tentacles until it's completely encapsulated and they draw it inside their body in a kind of a container or a capsule. And then they flood the capsule with acid and bleach and it just basically dissolves the invader.

Joe: I love the bleach. Where do they get the bleach from?

Senan: Yeah, so…

Joe: The acid… Was the acid not enough? No, obviously not. Put in some bleach there.

Senan: Yeah, yeah. I suppose different creatures need different chemicals to dissolve them. So that’s how they kill them. Right. Let's move on to the inflammatory response. So some people think it's like a side effect. You know, being sick. That you get swollen and red and maybe hot and all that. But actually it's a fundamental component of the immune system response.

Joe: So the symptoms are from trying to fix the problem a lot of the time.

Senan: Yeah, oh yeah, that aspect of the symptoms are. Yeah, yeah, they are. So if we take the case of, you know, a cut that gets infected. The damaged cells release chemicals into the bloodstream called cytokines. And those are essentially what triggers this inflammatory response. They have a couple of roles. Number one, they're like a distress signal. So they travel out through the bloodstream away from the area that's damaged and they essentially notify the immune system; like the macrophages we spoke about a moment ago and the neutrophils; to come to this area. So they're like an alarm bell going off drawing in the troops. But the other thing they do, which is more connected with the inflammatory response, is they cause the blood vessels in the area around the infection to widen. So it's like, say the blood vessel is normally a two lane motorway; well they turn it into a four lane motorway so that the army, the defending army can get there quicker.

Joe: Right.

Senan: So and the problem with that of course is when the defending army comes along on the motorway, when they reach the area where the infection is, they need to be able to find an exit off the motorway so they can start fighting. And that's the other thing that these cytokine chemicals do; they make the blood vessels leaky in the area of the infection. So fluid leaks out and kind of floods the area around the cells that are infected. And that's what causes the swelling, but that also is what allows the neutrophils and the macrophages to escape from the bloodstream into the infected area and attack the invaders.

Joe: Right.

Senan: So yeah, it's pretty cool that that inflammatory response is facilitating the defenders to get to where they need to be. However, it's like a lot of these things, a double edged sword; there's no… you know, you can get too much of a good thing. And if the inflammatory response becomes hyperactive and just everything gets super inflamed, it can actually stop the normal processes of your body from functioning properly. And that was one of the hallmarks of COVID. A lot of the people who died or got seriously ill from COVID, it was because the inflammatory response caused by the COVID just ran away. Just became ridiculously over the top and stopped their own body from working properly. So it's a double-edged sword.

Joe: And that was… but that was because of what COVID was. Obviously it didn't know… like it overreacted to the specific…

Senan: Oh yeah. Yeah, whatever. There was some aspect of COVID, of the way COVID acted inside our bodies that made our inflammatory system just go into overdrive. But it didn't happen to everybody.

Joe: No.

Senan: That was one of the weird things about COVID is that like, you know, some people had a very mild, relatively mild infection and other people like really made them terribly sick. So yeah, didn't happen to everybody. So that's the inflammatory response. Right, the next piece of the innate immune system is what we call the complementary system. So this is a group of about 30 proteins that are always present in our blood.

Joe: 30 types?

Senan: 30 types of, yes. 30 types, not 30 cells. 30 types. That are just…

Joe: Really big proteins. They're the size of a tennis ball.

Senan: Yeah, now I should correct myself there because a protein is not a cell. It's just a complicated folded up, squished up chemical. But yeah, 30 different types are floating around in our blood all of the time usually just doing nothing. But then they're able to; a bit like the way the macrophages I mentioned earlier work; they're able to identify a bacteria based on latching onto a certain structure on its outside, detecting a certain structure exists. And when that happens, it causes a cascade of activating stuff. One of these proteins latches onto a bacteria; it essentially cascades the reaction out to the other proteins and activates them and suddenly they start taking an active role. They do stuff like punching holes in the cell walls of bacteria. They do a cool thing called opsonization, which is a very complicated word for tagging.

Joe: Okay. They tag them, yeah.

Senan: They tag the invaders so that the macrophages we spoke about earlier can identify them and come along and eat them. And they also have a role in triggering some more inflammation which helps more immune cells to reach the infected area. Right, onto the cool Natural Killer cells.

Joe: This really is though, I mean you can see that it was in the lab, it was like five to five on a Friday evening of a holiday weekend and someone says "We need a name for these. What's the Latin for whatever?" He goes "No. Not doing it. Natural Killer cells. That's going to do. The NK cells."

Senan: Yeah, they didn't put a whole pile of thought into it in fairness. I would have preferred if they had some really cool long scientific name.

Joe: But somebody would love to have them named after them, surely? The "Senan cells." Oh yeah, they're the mean ones. Oh yeah. Special Ops.

Senan: The Smith and Jones cells. Anyway, they're called Natural Killer cells because most of the other components of the immune system need some kind of a triggering action to activate them. They're kind of semi-dormant until something triggers them. Not these fellows.

Joe: These are the psychopaths.

Senan: Yes, absolutely.

Joe: They're just walking around looking for a fight all the time. "Are you… you looking at me?"

Senan: These guys are walking around with an AK-47 in one hand and a machete in the other.

Joe: "You looking at me? Come on. You?"

Senan: So they don't need any priming. As soon as they find something that they regard as a target, that's it. It's over. So, how do they identify their targets? So I think I alluded to this earlier. Healthy cells in our body have this kind of passport, this signature on the outside that says "This is me. Don't kill me." And basically if one of these Natural Killer or NK cells, they're sometimes called; if one of these NK cells finds another cell which does not have the signature, that's it.

Joe: Sorry, your passport's out of date. Boom.

Senan: Yeah. So they could be… they also have a role obviously in killing cancerous cells but a lot of what they kill would be invaders, bacteria and the likes. How do they kill? So they basically tell the cell to kill itself.

Joe: "I'm not even going to hurt you. You're going to hurt yourself."

Senan: Yeah.

Joe: "I'm going to talk to you and you're going to do stuff to yourself."

Senan: Another fantastic scientific word: Apoptosis.

Joe: Okay.

Senan: It means programmed cell death. So it essentially means it triggers the instructions in the cell for how to kill itself in a nice polite way. So it's a nice clean death, doesn't cause any problems, it just dissolves into its component parts.

Joe: "You have no friends. You have no friends. What are you going to… Go on, kill yourself."

Senan: So it's just these granules it injects that basically triggers this self death thing. And that's actually… all of our cells sooner or later have to die by this programmed cell death; that's just the natural cycle, cells don't last forever. And one of the key attributes of some kinds of cancer is that that mechanism is turned off in those cells. So they don't have the off switch that every other cell should have for the end of its life and they just keep growing or keep multiplying or whatever when they shouldn't. All right. The last component is the Interferons.

Joe: Doctor Who. This is a Doctor Who term.

Senan: What was that kid's toy? Transformers.

Joe: Yes.

Senan: I feel like this could have been one of the Transformers.

Joe: No, this is next Christmas. You could have a whole series of Interferons for sale on our website.

Senan: Branded with Enough with the Science. With our gobs on the front of it. So what are they? They're actually not cells, they're proteins. So now we get to talk about viruses. And what viruses do… how much do you know about viruses, Joe?

Joe: I'm not going down that road again. We had a conversation about viruses earlier on. They're not alive but they just program other people to do the stuff that they want. I don't get it. I just… it's like some weird…

Senan: So a virus is not in my view anyway alive in the way that we regard a bacteria or a fungus to be alive, or a person for that matter. Like they're just a set of instructions for how to make more viruses. That's it. And like an injector mechanism for putting those instructions into one of our cells. So what they basically do is they hijack the machinery we have in our cells for making things to use their program instead of our program to make copies of them. So anyway, interferons; what happens? When one of our cells is injected by a virus; in other words the instructions from a virus are injected into one of our cells; our cell will release these chemicals called interferons. They're called that because they interfere with viruses. So again that was one of those five-to-five names.

Joe: What do we call them? What do they do? They interfere. Hmm.

Senan: Yep. Interferons. So what happens is basically they… when interferons get released, the cells nearby detect the interferon and it causes them to toughen up their cell walls so that it's harder for the virus to inject itself into them. So it's a way of one cell saying "Hey, I've been infected; you guys should probably toughen up the barrier there so you don't."

Joe: It’s kind of like the leprosy bell. Ding, ding, ding. Get away from me.

Senan: Yeah. "Right lads. Come on. Let's get our armour on." So that's the last component of the…

Senan: Well, leprosy bell, not quite because it's not warning the other cells to go away. It's warning the other cells to toughen up because they're going to get attacked.

Joe: Okay.

Joe: So it's like a motivational leprosy bell. "Come on lads, let's get our armour on."

Senan: I'll give you that. So that's kind of the story of the innate immune system. Now the interesting thing about it is it has no way of remembering how it fought a particular battle. So if it successfully defended your body and killed off a particular invader, next week if that invader comes along again, it'll do all the things it did without skipping over the stuff it didn't need to do.

Joe: Right. So go straight to the last thing that worked rather than trying the last thing that worked first.

Senan: Yeah, yeah, yeah. So it has no memory of how it fought battles in the past. So it goes… it takes the hard road all the time. It goes the long road to solving the problem all the time because that's the only way it knows. So it's a general purpose thing and it's able to kind of hold an infection at bay; no, it'll wipe out lots of infections; but the more serious ones, it's able to kind of hold them at bay until your adaptive immune system gets into gear.

Joe: Gets out of bed, basically. Just kind of sitting in bed going "Oh, really?"

Senan: So that's going to be the subject of next week's show.

Joe: That’s it?

Senan: About how that adaptive immune system gets triggered and the fantastic memory that it has and the fact that we can use that memory for vaccines. Vaccines basically use that memory.

Joe: Yeah. Very good.

Senan: So that's the end of this week's show. Don't forget about our website, enoughwiththescience.com.

Joe: Yeah. 50% of the immune system is now down. So the other 50% will be in our next episode. So thanks for listening this time. My name is Joe.

Senan: And I am Senan. And stay healthy.

Joe: Okay. That’s enough with the science this week. Take care.