Episode 17: Rae Lambert on Vaccines, Immunology, and the Horror of Organic Corporeality

Transmission electron micrograph of SARS-CoV-2 virus particles

Image: “Transmission electron micrograph of SARS-CoV-2 virus particles, isolated from a patient. Image captured and color-enhanced at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland.” (Source: National Institute of Allergy and Infectious Diseases, NIH – Flickr)

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Transcript

Charles: Hello, this is Assigned Scientist at Bachelor’s, I’m Charles and I’m an entomologist.

Tessa: And I’m Tessa and I’m an astrobiologist.

Charles: And today we have have on as a guest Rae Lambert. Rae is a research virologist at Jefferson University, where they received their MS in microbiology and immunology, and are anxiously awaiting word back from PhD programs. Right now, they are working on a SARS-CoV-2 rabies based vaccine and in their off hours, they drink fancy coffee and eagerly wait for their circus school to reopen. Rae, Welcome to the show.

Rae: Thank you.

Charles: Generally, we begin the show by asking people how they got interested in science, how they got started in science.

Rae: Cool, all right. So up until about 17, the general plan was to go to a conservatory for opera. However, I was currently attending a math and science academy in upstate Illinois, outside of Chicago, in Aurora. And I took this class called microbiology and disease, and it was the only class that I had ever actually cared about before.

And so I went from never cracking a book to spending about 10 hours on this one class outside of school hours, meeting with the professor every, uh, every week to discuss all the key points and make sure that all of my notes were correct. So from there I completely changed course and didn’t necessarily drop music, but decided to focus more on science and applied to microbiology and immunology programs.

And then I got into the University of Rochester. Had a horrible time, almost failed out several times, took a couple of years off, pulled all of my shit together and then, uh, got into grad school in the same degree, at a different location and have been doing fantastically since then.

Charles: So what are you working on now? I mean, obviously we know… vaccines. But more specifically than that.

Rae: Okay. So I can’t get too specific because we have not published data yet. But what I can say is that we have a vaccine prototype. We have an adjuvant that we are using for our formulation, and we are currently doing safety testing and animal testing.

Tessa: You may want to explain for our listener what an adjuvant is and why they’re important for immunization.

Rae: Oh, of course. So I do want to preface this by saying, from what I’ve seen, the current vaccines going out are adjuvant-less, which is totally fine and probably better for a first haul. But what an adjuvant that does is, it takes your body’s reaction to the vaccine and it amplifies it.

So generally speaking, an adjuvant is any chemical compound that you put into it and it kind of like wakes up your body’s immune response. Adjuvants are really important to pick correctly because they can kind of skew your response towards something like an intracellular reaction, like anything to do with a virus, or an extra cellular reaction like with bacteria.

So you have to be really careful about which adjuvant that you choose, which is why I’m kind of glad that what I’m seeing is that these current vaccines are on events, defensive because the most popular attribute is. Alan and Alan biases, body responses towards an extra cellular response, which is the exact opposite of what you want for a virus.

Charles: Mm. Hmm. Wait. So are there vaccines against bacteria?  

Rae: There are some vaccines that are against certain proteins on the surface of bacteria that your body can create antibody responses to. I’m not sure if any of them are in production, but I know several groups who are working on them. So… you can create a vaccine for anything that I know of that. Your body mounts a response to it, it just might take a different approach.

For example, the vaccines that we are seeing come out against SARS-CoV-2 [also known as COVID-19] right now are mRNA vaccines. I work primarily with viral vector vaccines, so inactive whole virus, that is put into a person and then your body sees the proteins on the surface of the dead virus and mounts a response to that, but the virus that we put into you cannot replicate. So it cannot, it cannot cause sickness.

Charles: Why specifically combine a rabies vaccine and a SARS-CoV-2 vaccine?

Rae: Rabies is very well-studied. It creates a very long lived immune response and so we’re hoping that by inducing a response to SARS-CoV-2 and rabies together that SARS-CoV-2 will also have a lasting immune response because they were, um, they were introduced in tandem to influence the kind of B cells that are going to be created at the site of your SARS-CoV-2 spike protein.

Tessa: What are the advantages and disadvantages of using an MRI vaccine versus the sort of whole virus approach that you’re using?

Rae: I have to preface this with, I am not an mRNA vaccinologist. This is not my area of expertise. I can just tell you a little bit more about what I do and give you a couple of hypotheses, but I’m not going to say anything necessarily negative because I don’t think that that’s what’s best for the current climate. [With] mRNA vaccines, you shoot genetic material into the patients. And then the host, so your own cells, make the spike protein and the spike protein is on the outside of SARS-CoV-2, which is kind of like a ball shaped virus with little spikes all around. So your body will make the spike protein and then your body will also create a response against the spike protein.

What I do with whole viruses, is that we use rabies as a vector. Now, rabies has been studied extensively. We have several rabies vaccines in effect. So what we do is we put the protein of the disease that we’re trying to protect against into the rabies virus, so that we grow a virus that is the rabies bullet shape, but with another protein on the outside, for example, the vaccine that we’re working with right now has both rabies proteins and the SARS-CoV-2 spike proteins.

So really the only difference between these two vaccine techniques is that in mRNA vaccines, your body’s making the spike protein, but in the killed virus vaccines, that spike protein is already made. So either way, you’re mounting the same reaction to the same protein. It’s just where this protein is made is different.

Tessa: Since you’re using sort of a rabies virus as sort of a carrier, would this vaccine potentially confer some immunity to rabies as well?

Rae: Yes. So the vaccine that I’m working on is a bi-valent vaccine. So you would be immunized against rabies and SARS-CoV-2. Now, the important thing about this is that rabies might not be a big deal in developed countries like the USA, but in developing countries, such as anywhere in Western Africa and even in Eastern Europe, rabies is still pretty much uncontrolled and rabies related diseases are a big issue.

So if we can get a vaccine that protects against rabies, which is a problem, and SARS-CoV-2, which is a huge problem, we can kill two birds with one stone.

Tessa: That’s really clever. I like that.

Rae: My boss likes it too, which is why it was all his idea. I work under a Dr. Matthias Schnell and being in his lab was actually the entire reason that I wanted to come to Jefferson, which is where I was.

Tessa: I’m glad you’re working on that admittedly for very selfish reasons. Also in that, um, my wife is a veterinarian. And apparently it’s expensive to get a rabies vaccine in the U S and as a result, her company has been very prickly about actually paying for it despite her being in probably one of the few demographics in the US that’s actually at risk. So, you know, if we can get her immune to it, great.

Rae: We have a virus lab that you cannot enter without being rabies vaccinated, which is a whole big problem because not all of the, uh, not all of the workers in the university have been rabies vaccinated. So we can’t even get things fixed unless they’re by specific subset of people.

But luckily our health insurance covers the rabies vaccine because we literally can’t do our work without it. Not that there’s a huge risk because we do work with inactive virus, but you can never be too sure.

Tessa: Right.

Charles: As a very anxious person…

Rae: As is my partner, he’s like, please do not bring your work home.

Charles: No, I honestly, I’m not sure that I could date somebody who was in immunology.

Rae: Totally fair. I am probably your worst nightmare then romantically, because my entire goal is to work in a biosafety level four with the viruses that have no treatment or vaccine. So right now, solidly a BSL three, where there are some treatments, but the viruses are still dangerous. And I want to get to that next level.

Tessa: Is there any particular virus or class of viruses that you’d be interested in working with something in the, um, Oh, I can’t remember the exact name, but the family that has Ebola in it, for example.

Rae: Actually a great segue because hemorrhagic fevers is my niche interest and the entire reason that I am in Dr. Schnell’s lab is because I wanted to work on his Ebola vaccine project. So I am already working on hemorrhagic fevers and I would like to continue doing so this time at a perhaps higher danger threshold. So yes, you hit the nail right on the head. I am very interested in working with Ebola. I would love to do further work, uh, there, and that is the entire reason I’m in the lab that I’m in.

Charles: I mean, this attitude towards danger is… it makes a lot of sense that you are also into aerial [aerial arts and circus arts include apparatuses like silks, trapeze, and lyra, which are suspended in the air].  

Rae: I mean, I think they do definitely go hand in hand.

Charles: I am interested in what got you so interested in hemorrhagic diseases.

Rae: Alright, here’s the real answer. You know, that book…

Charles and Tessa, simultaneously: The Hot Zone?

Rae: Yeah, that’s it. That’s the whole answer. I’ve read everything Richard Preston and Michael Creighton has put forth onto this earth because I love them so much. Between The Hot Zone and The Demon in the Freezer, I was like, that’s it. That’s what I want to do. And then that movie Contagion came out and it was just, I had to, I had to keep going.

Charles: This is actually a really perfect encapsulation of the difference between you and me. Because I had to read The Hot Zone for school, in middle school. And I hated it, and then I had recurring nightmares for like months, but I mean, within The Hot Zone, what is it about Ebola that made it so engaging?

Rae: So, yeah, I don’t know. I think it was just like, it’s one of those things where… if you would put me as like a 13 year old, and you’re like, what’s the grossest, you know, when you, when you think that you’re a fan fiction writer and you write all of a bunch of weird shit, like what’s the grossest disease that you can make up? It would be something like Ebola.

So the fact that that’s like a thing and around and is killing people, I would like for that to no longer be a thing that’s around and killing people, it’s more like it’s… it’s so… it’s gross. It’s gross and interesting. And I want to know just everything about it.

Charles: See, this sort of fixation on the grotesque I can plug into as an entomologist and as somebody who loves aliens, because when you look at a lot of insects, it’s like, well, we don’t need to go to space for those – they’re right here.

Rae: Yeah. Ooh. I just had this conversation with my partner yesterday about the experiments where they put spiders into space.

Charles: I don’t know about this. Please continue.

Rae: Oh, okay. So very, very briefly. And mind you, this is all like third hand, but basically a bunch of kids were like, Hey NASA, let’s send some spiders to space. NASA is like, sure. Let’s do that. So the whole experiment was to see the effect of the lack of gravity on spiders’ webs, because a spider’s web has irregularities due to the effects of gravity and they always sit at the top facing down. So scientists wanted to see what would happen if you took, uh, spiders into space where there is no gravity.

So like as expected the, um, the webs got much more regular and symmetrical, but due to the light set, spiders were still at the, at the top of the web facing down away from the light, which is weird because even cave spiders that don’t even know what light is, are at the top of the web and facing down. So it looks like it’s a backup system that spiders and use either light or gravity or both, both to make webs and nowhere to sit to hunt for food.

Tessa: Fascinating. Good to know that spiders are prepared if for some reason gravity fails.

Charles: Well…

Rae: Yeah, spiders are ready for some shit.  

Charles: Orb weavers are ready… but probably some other spiders are too.  

Rae: Oh, well fair, not all spiders spin webs.  

Charles: Well, cause it’s interesting… because a lot of spi… cause orb weavers are sort of the classic ones that we see, like, you know, the symmetrical webs that we imagine and we put in picture books and Charlotte and whatever, but there are a lot of other spiders… because spiders in general produce silk, but the silk is not always used to make webs and there are different kinds of webs too. So there are the orb weavers that make the various geometric webs that we’re used to seeing, and then there are like funnel web spiders that make sort of nests that they retreat into. And then there are some, I think fishing spiders might be among them, that make sort of nets that they hold in their feet, in their little spider feet, and then they use those basically like as a net that they then trap stuff in.

Rae: Fascinating.

Charles: Spiders are pretty good. Not as good as insects, unfortunately. Sorry, arachnologists.

Rae: I actually was just talking about how I can never be an entomologist because that’s not the right kind of weird for me. Oozing blood coming out of your pores? All over it. Things with more than two legs? Eh, I don’t know.

Charles: I mean, to be fair… insects don’t have blood in the way that we typically think of it, nor do they have pores. They have holes in their cuticle, in the outer layer, but… Well, cause I don’t know if you know this, but insects, the way that insects respire is through holes in the like exoskeleton, the outer cuticle, called spiracles.

There’s like a rel… I’m not, I don’t want to misspeak because I’m not a physiologist, you know, but air goes through these holes and then it gets taken into the body. They don’t have a central respiratory system like we do. And so similarly with blood, they don’t have like, a liquid that goes through veins that takes oxygen through the body, it sort of passively moves through the body in a substance called hemolymph. So if you squish them a blood-like substance will come out, but it’s, it’s not like the dramatic red.

Rae: Gross. What’s your favorite bug?

Charles: I mean… what a question, you know? How to pick a favorite star in the sky or a favorite child, you know what I mean? But in general, my favorite groups of insects are a clade called, which has mantises, cockroaches, and termites. And then within those cockroaches, and then within cockroaches, my favorite genus is one called Gyna. And I claim these as the gayest cockroaches in the most positive way in the world, because they’re gorgeous. They’re just beautiful and so elegant. They’re just wonderful. Tessa, what’s your favorite insect?

Tessa: Um, Hmm.

Charles: Or I guess a more, because you know, we’re going around the circle saying our favorites from our study groups. What’s your favorite space thing?

Tessa: I would probably have to say at least… the favorite organism that I have studied in the course of my career has to be, they found this fungi growing in the ruins of the Chernobyl reactor that instead of using chlorophyll to perform photosynthesis, because it doesn’t have chlorophyll because it’s fungi, produces melanin, which it then derives energy from it, getting the inter um… the bonds in the melanin being broken by the high energy gamma radiation that the reactor core is emitting. So basically it eats radiation, or… uses it like plants use sunlight.

Rae: Okay. So when you say eat, does it, does it use the radiation in such a way that it absorbs it and there’s less radiation?

Tessa: No, unfortunately it does not do that, but it does live off of it. There are microbes that can, they don’t make it less radioactive, but they do reduce it to like a form that is less mobile in the environment. But as far as I know there isn’t aren’t any that like take it and make it like less radioactive period.

Charles: Ummmmmmmm… science. Why… it is easier or harder to develop vaccines for different kinds of viruses and diseases?

Rae: I haven’t been seeing a lot of pushback against this idea that this vaccine came out in what, what are we at eight or nine months. So why hasn’t there been a, an equal response towards things like cancer? Is that kind of the direction you were thinking of?

Charles: Kind of, yeah. I mean HIV is the first thing that comes up to the top of my mind.

Rae: Oh yes. So I have, I have an answer that kind of touches on both of those types of things. Again, we’ll do the same preface. HIV and cancer are not my bag. It was very interesting entire departments devoted to them.

I am not that I can touch on. Why I’m not that. So for a disease like cancer, and similarly for HIV, you’re not looking at one disease. You’re not looking at one virus. You’re not looking at one protein. You’re not looking at one type of cell. There are some proteins that are similar in many malignant tumors.

However, the hallmarks of cancer are, are the mutations, right? On the surface of all of these cells that make up a tumor, they’re not presenting the same proteins. Right. So it’s it, it’s impossible to make one vaccine that will target all the parts of the cancer. So maybe you can make one vaccine that looks at one protein.

You can kill off, maybe if you’re very lucky, half of the cells in a tumor, but that’s not helpful because the other half that are still alive and flourishing will continue to create a tumor that now you have no, because like mutated, I assume. Right? Exactly. Because the cells that survived will continue to reproduce things in their image and will have different proteins.

Charles: Well, I imagine it’s similar to the phenomenon of superbugs and the idea of bacteria that get killed by certain antibiotics die and then the ones that are resistant to them multiply a lot more.

Rae: Exactly the same mechanism. And that’s the same thing that you see in HIV. HIV is known for a high mutation rate, so you might be able to wipe out a sub-population, right, that presents with one type of surface protein, but you’re leaving all of the other subpopulations that don’t look like that. So in order for you to mount a good response to something like HIV, there’s one method, which has, if I remember correctly, we have cured like one baby.

I’m not talking about the more recent, uh, Berlin patient and the second patient who were cured by, um, the bone marrow transplant, I’m speaking specifically to vaccines. What took care of something like HIV? You have to catch it early and you have to hit it with absolutely everything that you have so that nothing can have survived.

It, the problem is that there’s no way to know that you’ve killed everything. And so if you even leave one replicating virus that is different from everything that you’ve hit it with, then all of a sudden that virus is what’s repopulating your entire body and you have a virus that, you have nothing that works against it.

Charles: Mm I’ve said it before, and I’ll say it again, but living inside a human body is just a constant, it’s just like just, just a real nightmare.

Rae: They are gross and it just get grosser as you age.

Charles: Sometimes people in a very like, body positivity kind of way, assert that the human body is art and it’s, you know, it’s just, they’re all beautiful. I take the radically different approach of extreme body negativity, but because we’re all equally gross.

Rae: Yeah. I think it’s just like the kind of art that you like. See, I like, the super not kind of fun to look at, like needs a paper to describe what you’re looking at, kind of art. And that’s how I imagine the human body to be. Like, not everybody likes modern art that you need a degree to dissect, which is very much the same as the human body. But I think like you got a taste for what you have a taste for it that, or…

Tessa: You’re an HR Geiger fan…  

Charles: See, I like both… I like weird stuff in art and I like weird stuff in science fiction. I think it’s the inescapability of my own human body that, that prevents me from appreciating the human body in the same way.

Rae: That makes sense. Like, especially on this podcast, like the inescapable reality of your personhood, like, I hate this, like, you know, when you get those days when you’re like, everything is uncomfortable, I don’t want to think about this.

And then that’s easier to think about, all right, well, like what are the cells inside of me doing rather than how is my human experience affecting me on a day-to-day basis.

Charles: Yeah. What actually goes into the production and the testing of a vaccine?

Rae: A lot of waiting, honestly. Huge regulations. The things that take the most time about vaccines are not related to the vaccine at all. It’s all finding funding and having the right people sign the right paperwork. So basically what happens is, um, years and years of research about a specific, let’s… let’s say virus 1, about a specific virus and you have focused on one, we’ll say protein, and you’re like, this protein – if we can create enough of this type of antibody, because what’s important in a vaccine, isn’t even antibodies in general, it’s neutralizing antibodies.

In your immune response, this is an entire orchestrated movement in two acts. Alright. First there is, there’s the innate immune system and the adaptive immune system. Now, the innate immune system is anything that’s non-specific that your body does on instinct. So anytime you get sick, you get the same stuff. You get a fever, you get the aches and chills, you get a headache. Alright, that’s your innate system, they’re like –  we have a set of protocols, and the set of protocols, it doesn’t change from, from virus to virus.

And then about two weeks later, your adaptive immune system kicks in. Now this has your T cells and your B cells. This is the stuff that kills specific viruses or bugs or whatever you’re ill with.

And even within that, in your adaptive immune system, in your B cells, your B cells are cranking out antibodies and there are multiple types of antibodies. So in a vaccine program, what you’re most worried about are neutralizing antibodies. What an antibody is, is a Y shape, or it can be a star depending on what type of antibody… it’s a Y shaped protein that sticks on the surface of whatever bug you’re fighting.

So I’m going to talk about viruses because that’s what I know best. So you have a Y shaped protein that sticks to the protein on the surface of a virus. What you really want is an antibody that sticks to the right protein on the surface of a virus. These are called neutralizing antibodies. And if you have a virus that’s coding and neutralizing antibodies, the virus cannot attach to the host cells and continue its life cycle.

So through all of this research that you’ve done on your particular virus of interest, you’re looking at which part of this virus creates the highest neutralizing antibody response. Alright, and that’s the part you focus on. So for the case of SARS-CoV-2, it’s the spike protein, the spike protein is what you need to be able to attach to the host cell and then get inside the cells and start replicating. And on the spike protein, there’s a little part of a couple of amino acids called the receptor binding domain. And that’s the part that the that’s the most important part on the most important protein of the virus you’re looking at. What antibody is that specifically attached to your most important part of the most important protein on the most important virus that’s in your system right now? So you have mountains and mountains of work. And so what you’re trying to do is create a scenario in which your body will pump out the right kind of antibodies.

So for what we’re seeing right now, the vaccines that are being done – Moderna and Pfizer – So what they do is they create the mRNA, which is like a ticket order for your, for your cell. And your cell reads the ticket and then makes the protein. And then this protein is seen by your adaptive immune system.

And your adaptive immune system will make a buttload of antibodies, just antibodies for every single part of this virus, but not all of the antibodies are created equal and not all of the antibodies are even helpful. The antibodies that you want are the ones that are against the receptor binding domain.

So what you see with a lot of viral illnesses is like part one is the vaccine, which creates the most important part of the virus of interest, but you also see different antibody treatments, for example, rabies. Tessa? Okay, so like your partner, if she is bitten by a dog, the first thing that she gets is the post exposure prophylaxis, so another rabies shot.

The next thing that she get is RIG, which is a high dose of rabies specific immunoglobulins. The most important part for both the vaccine and the future treatments are the specific kinds of antibodies, also called immunoglobulins. And so far, the neutralizing antibodies that we’ve seen are IgG, which are Y shaped.

They have a specific linker protein, with specific protein-protein interactions. What you’re looking for in the perfect vaccine is the perfect antibody response to the perfect part of the protein. That is the most important part of the virus of interest. So it’s all very, very specific, but we got really lucky in that on the outside of SARS-CoV-2, it’s mostly just spike proteins. And we immediately saw that the part of the virus that was binding to host cells is the spike protein. So we knew that we had to look at that part specifically, and if you’re making the entire protein, you don’t have to worry about whether or not you have the receptor binding domain because it’s going to be made altogether.

So mRNA is just kind of like, here is the entire, most important protein, which also has the receptor binding domain. So we’re going to kick a whole bunch of it into yourselves and your body’s going to make as many antibodies as possible. And within the antibody population, we’re going to have neutralized the antibiotics and that is what’s going to stop the infection that comes up in your body if you are infected with the actual replicating part.

Charles: So just to summarize. I think cause I’m imagining, well, basically I’m imagining my dad listening to this cause I know that he does listen.

Rae: Aww.

Charles: But basically the whole process of, of what we’re thinking about – viruses get into the body and they can attach to cells and then use those cells to recreate themselves and spread throughout the body.

And the way the vaccines work, the way ideally vaccines would work is by identifying the protein on the outside of the virus that antibodies would most be able to attach to and sort of neutralize that virus.

Rae: Yes.

Charles: Okay. So the way a vaccine generally would work then is, it is engineered so that researchers figure out which antibody you most want the body to produce, to neutralize the virus, and then they create a vaccine either using mRNA itself or, or like a deactivated version of the virus, and put that in the body so that the body can recognize it and then start producing those antibodies like preemptively in defense against it.

Rae: Right. And so then when the virus actually enters your body, you have all of these pre-made neutralizing antibodies that sees the virus that has just come in, attaches, and renders it useless.

Charles: Hmm. So why do some vaccines last longer than others? Like why do some, you need a booster for every year or every 10 years and others, you can get them once and you’re basically gravy.

Rae: There are, there are two scenarios. The first scenario is the flu vaccine, which I just want to reiterate is a different vaccine every year because the flu mutates, so you’re not actually getting boosters.

That’s just a whole separate, the flu is complicated. And every year you have to make a brand new vaccine, but with something like rabies, which generally you only need, once you get it once and then you get the booster and then you’re fine, unless you get it, and then, then you get another one. Some diseases just don’t create a lasting impression on your immune system.

Like they don’t make the long lived B cells or if they do, it’s not the right… it’s not the right B cell, or it’s not a very strong B cell. Right. And so you have all of these populations of these cells that are trying to remember every disease you’ve ever even glanced at. And some of them. Some of them don’t make it.

And there isn’t some diseases like measles, where if you catch measles and you haven’t been vaccinated, measles wipes out your entire immune repertoire, and then all of a sudden your body has no defenses against anything. So different diseases cause different immune responses. And some of them are just not as long lived as authors.

Charles: Hmm. I mean, the answer is basically just that bodies are complicated and everything is complicated.

Rae: Bodies are a nightmare and some things work and some things don’t, yeah.

Charles: Those are all that I have to ask about your specific research. And if you would entertain me, I do have some general vaccine questions. Is there, if you get one vaccine for something, is there any danger in getting a different vaccine for the same thing?

Rae: Ooh. You know how bodies are a nightmare?

Charles: Yes.

Rae: Bodies are a nightmare. It depends on the vaccine. There are some viruses where if you like, say there’s, um, And I’m so sorry. I can’t remember any specifics, but say there’s virus one and it has serotypes A, B and C. There are some viruses, if you protect against one, like type A and then you get infected with Type B, it will produce a bigger response, like a bigger negative response, and you will get very, very ill. For most diseases, where it’s… for which there are not multiple serotypes, it’s totally fine. Like if you get one brand of rabies vaccine, and then you got a different brand of rabies vaccine, it’s still against rabies, you’re good.

But in diseases where there’s a wide variation, there could be potential problems. However, for SARS-CoV-2, the variations that we are seeing in the virus populations are not enough to cause any problems with the vaccines that are currently being produced. The receptor binding domain, the most important part of the most important, uh, protein is still the same.

Charles: Somewhat related question, if viruses don’t give you a disease, then why do people sometimes, after getting a vaccine, have a disease like symptoms?

Rae: There could be a couple of reasons. First off, it depends on what kind of vaccine you’re getting. Like, are you getting a live vaccine? Are you getting an inactive vaccine? But still you have to remember that the entire point of a vaccine is to induce an immune response.

Your body has to think that it’s sick. And remember that there’s two parts of the immune response. There’s, there’s your automatic innate immune response, and then your adaptive immune response. So what’s going to happen first is your innate immune response is gonna kick in. They’re like, Holy cow, this is something that I have not seen before, we need to kill it with fire. And the fire is the fever that you get. So it depends on your body’s reaction to the vaccine that you get. Um, another thing that is tricky, right? Is some people have allergic reactions to the adjuvants. So the stuff that makes your body’s response to vaccines bigger. So it all depends on what kind of vaccine you’re getting and what else they put in it, adjuvant-wise.

Now the stuff that people get the most upset about like the mercury, those are stabilizers and put in such low volumes that your body doesn’t even register. They’re, they’re… the things that are going to cause the reactions are the vaccine itself and the adjuvant. And those, those reactions are mostly fine – like bodies are a nightmare and some people are going to have a bad reaction and I’m very sorry, but those, those things do happen because your body has to think that it’s sick.

Charles: I mean, it is interesting. I think it’s something that people, or at least that I don’t often remember, and then when I do remember, it’s like, Oh yeah, a lot of sickness is not actually caused by whatever pathogenic agent is inside your body. It’s your body responding to that pathogen.

Rae: Exactly.

Charles: And then I have another question which is less about the actual biology of vaccines and more about sort of the regulation of them. Okay. Specifically, let’s go back a couple of years. I am about to turn 26, and I think, well, I should probably get the HPV vaccine because soon I won’t be within the approved age group for it. And then I was thinking specifically with the HPV vaccine, but also in general for a long time, it was like only approved for girls up to age 26 or whatever. This was very confusing to me.

Cause this is like, (a) why only people the FDA is describing as female, and then, (b) why only up to 26. And so I guess there’s a broader question here of like, what are the principles that guide, like, why not just give everybody the HPV vaccine?

Rae: So a lot of it is insufficient testing for the HPV vaccine. The people who suffer from actual HPV infections are what the FDA describes as women and before 26 is when you’re most likely to get it. That’s the age and the population that they’ve done the most amount of testing on. Do I think that it’s bad for the rest of the population? Probably not, but there’s insufficient evidence to say otherwise.

Charles: So it’s more of trying to decide which groups are sort of highest priority for the vaccine and then getting to the point where you’ve determined. Well, it’s safe for these people and we know it’s safe for them.

Rae: So get it out immediately. Yeah.

Charles: Okay. Well, good for everybody – Gardasil-9 is now approved up to age, like 42. [The FDA approved Gardasil-9 up to age 45 in 2018]

Rae: And if nine, uh, versions of HPV, rather than the three, I think, which was in the vaccine that I got when I was 10 or so, because…

Charles: Well, I got it when I was 25 and I got G-9, so come at me HPV. Just kidding. Don’t cause there are still like 140 other strains..  

Rae: If you’ve ever had sex, the odds that you have a strain of HPV are very high.

Charles: Well, and this is what always so perplexed me because the people who are mostly like getting the cancers caused by those specific strains of HPV are people who have a cervix. But most of the people who have a cervix and are getting these strands of HPV, have to be getting it from somebody.

Rae: Yep. Yeah. So this is my problem with why the human body is a nightmare. Most STDs are like that. People who don’t have a cervix just pass along merrily and people who do have a cervix are suffering

Charles: Well, and that’s why it perplexed me that there wouldn’t be more of an emphasis on vaccinating, both people with a cervix and people without a cervix, because it seemed to me sort of common sense that if you can pass on the virus, then it makes sense to vaccinate you against it so that you are less likely to then become a vector for other people.

Rae: It also makes sense to me to put sex education pressure on people with cervixes as people, without a cervixes, but you don’t see that happening either. So that is a societal failure, not a scientific one.

Charles: Yes. Fair But good news. I think Gardasil-9 is now approved for like everybody up to age 42 [it’s 45]. So go get Gardasil-9, have a party. Go to the CVS minute clinic. Your insurance may cover it.

So our final like podcast segment is asking our guests to weigh in on one of our recurring themes. We’ve got sort of a general rumination on the theme of, is it gay if it’s in space, which can take on any number of meanings. Like, is it gay if we’ve progressed so far into the future of human civilization, that we have many colonies in space or, is it gay if it’s with an alien?

Rae: So like, my answer is kind of more hopeful in that I hope in the future, everything is gay. So yes, I would hope that it’s gay.

Tessa: I like this response.

Charles: It’s a good one. It’s not one that we’ve had before.

Rae: Also my, my hope is the gender and sexuality and gender presentation as the spectra that they are, are then recognized for the spectra that they are. And everyone becomes accepting of the fact that we are all at least a little gay.

Charles: I like this approach of like less, that we’re going to lose the like specialness and the distinction of these experiences and more that they’ll become so normalized that they will be positively incorporated into culture.

Right. Right. You’ve been a great guest. If people want to find out more about you or your research online, where should they look?

Rae: Great question. My LinkedIn is probably the best place and I don’t even know what that is. Just search Rae Lambert and whatever you come up with is fine. But to know more about me as a person, actually, the best place to see me is Twitter, where I lurk. So my handle is @appalledimmuno.

Charles: I’m on Twitter @cockroacharles, and Tessa?

Tessa: I’m on Twitter @spacermase.  

Charles: The show is on Twitter at @ASABpod, and at our website where we post show notes and transcripts for every episode at asabpodcast.com.  

Tessa: And until next time, keep on science-ing.

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