Teen SciCafe: Virulent Viruses with Kishana Taylor

Title slide: TEEN SCICAFE, Virulent Viruses.

On screen text: Kishana Taylor, Microbiologist, Rutgers University.

KISHANA TAYLOR: Thank you very much for attending this Science Cafe today and I feel very honored to be invited to be able to do the first one of the year, or I guess of the semester, depending on how you think of it. And so I wanted to start off by giving you an introduction to who I am. I am the President of the Black Microbiology Association and I am also a microbiologist.

Slide: Logo of Black Microbiologist Association (Viral Epidemiology, Ecology and Evolution and Social Equity in STEM)

KISHANA TAYLOR:  More specifically, a Virologist. So I study viruses, and I am really interested in viral epidemiology, ecology, and evolution. And essentially what that means is that I'm really interested in how viruses evolve to become pathogenic in humans and animals, and then how they then subsequently spread throughout the human and animal populations. And so, basically, you can see that my research interests have coincided with real-life events pretty well in the last year and a half.

And so, in addition to what I do in the science, I also am really interested in promoting equity and social justice within the science fields, specifically as it pertains to other microbiologists. And so this is kind of where the Black Microbiologist Association comes in. Next slide, please.

Slide Title: What are viruses?

Graphic: 3D model of a protein (Credit Flickr/Naina Nair)

On Screen Text:

• Proteins and nucleic acid (sometimes lipid membranes)
• Not alive
  • Require living cells to survive
  • Typically target a particular cell type (Tropism)
• Not bacteria
  • Antibiotics

KISHANA TAYLOR:  So I'm going to start the presentation today by giving you an overview of what viruses are, and then, as it pertains to the pandemic, kind of an overview of the virology and the science behind vaccinations, answering some common questions that I get about vaccines. And then I also wanted to talk to you a little bit about how to manage your information and where it's coming from, and whether or not you have good sources.

So we can start off with, "what are viruses?" So when we think about microorganisms and when we think about things that make us sick, a lot of people tend to mix up bacteria and viruses. So bacteria are living cells, they can reproduce on their own, they don't use, necessarily, host machinery to do so. Viruses are a little different in that they're not alive that we know of, or that we can prove. They're basically just a composite of proteins and nucleic acids–so things like DNA and RNA–and sometimes they also have what we call a lipid membrane, which is basically just a layer of fat surrounding the cell. And so the key difference here is that viruses are obligate parasites, they cannot replicate if they are not inside of a living cell. And they typically tend to target a certain kind of cell. Next slide, please.

Slide: Types of viruses

Diagram of Helical, Polyhedral, Spherical, and complex viruses. (Credit – Adapted from CNX OpenStax)

On Screen Text:

• Many Shapes and sizes
  • Helical, polyhedral
  • Spherical
  • Complex
• DNA
  • Double stranded
  • Single stranded
  • Circular
• RNA
  • Double stranded
  • Single stranded
  • Segmented

KISHANA TAYLOR: There are many different kinds of viruses. So viruses can be classified based on a few things, including their shape and then very often their nucleic acid. And so, when we think about shapes, the different shapes of viruses are helical, polyhedral, spherical, and complex. So you might see people classifying viruses, they'll say it's a single-stranded RNA virus with polyhedral capsid.

And so the shape is kind of important, but what genetic material is inside the virus is actually super, super important for classification. So you can have DNA viruses that are double-stranded DNA, single-stranded DNA, or circular DNA. And then you can have RNA viruses that are double-stranded RNA, single-stranded RNA, and you can also have segmented RNA both double-stranded and single-stranded. Next slide.

Slide: RNA Vs. DNA 

• Difference in amino acids
  • Thymine vs. Uracil
  • Stores Genetic info vs. store protein structure
  • DNA is typically double stranded
  • RNA is typically single stranded

KISHANA TAYLOR:  I wanted then be able to break down to you the difference between RNA and DNA. When we think about DNA we think about ourselves, we think about humans. And so we know that humans have DNA, and DNA is essentially the genetic code for what makes up you, or what makes up me. And so DNA and RNA are related but a little bit different. So DNA is exactly that genetic code, and it has specific amino acids that then are used to make that code. So DNA has a thymine amino acid. 

RNA is basically the next step. So once you unravel the DNA, unravel that code, RNA is like a downstream product that then is used to make proteins from that DNA sequence. And so RNA, instead of a thymine has a uracil and so that's oftentimes how you can tell the difference. And so we say that DNA stores genetic information, and RNA stores protein structure. And so when the different enzymes in your body are processing DNA it's to get genetic information, and when the different enzymes and structures in your body are processing RNA it's to create protein. And so that's a really big difference. And then, in general in humans, DNA is typically double-stranded and then RNA is typically single-stranded. And any time that the body detects a difference in either non-double-stranded DNA or double-stranded RNA then that's usually an indicator that there's some type of foreign body within your body. Next slide.

Slide: Viral Life Cycle

Diagram of the viral life cycle (Credit – Created with BioRender.com – Mohamed et al. 2021. Frontiers in Physics)

KISHANA TAYLOR:  And so it's also really important when we think about viruses, we think about their genetic material, we think about their shape, we also then need to think about their life cycle. And so their life cycle is going to be dictated by their genetic material. So in general, when a virus infects a cell, it uses cell receptors. So every cell in your body has receptors that are used to communicate with each other or have a specific function, and viruses basically exploit this and use these receptors to get into your cell.

If the virus is made out of DNA, it's going to travel to this area here, which is called the nucleus, and that's where your cellular DNA is being held. If you are infected by an RNA virus, because it's considered already translated, it's going to stay in the cytosol, it does not go anywhere near your DNA, and then uses cell machinery to then replicate itself, and then will make proteins. Those proteins and then additional copies of that genetic material will then be packaged into new viruses, and then those viruses will be released from the cell. You can do the next click.

Diagram of the Coronavirus with arrows pointing to specific features. Virus replicates and generate mRNA, Viral mRNA processing and protein production, Newly synthesized proteins are packaged together, new virus. (Credit – created with BioRender.com)

KISHANA TAYLOR: Specifically as it pertains to Coronavirus, which has been pretty much on everybody's mind these days, Coronavirus specifically starts CO-V-2, the pandemic virus, is an RNA virus. And so it's not going to enter your nucleus, it's going to stay in the cytosol, and it's going to replicate there and then send its translated RNA into the ER, and then make additional proteins, so then reproduce itself, and make new viruses.

And so I think a common thing that I've heard over the course of the pandemic is that it's going to alter your DNA. That's not accurate. The virus doesn't go anywhere near your DNA, because it’s not a DNA virus. Next slide, please.

Slide:  Mechanisms of Evolution

Mechanisms of Evolution – Mutation, Recombination, Reassortment.

Two diagrams of Viral Recombination and evolution.

(Credit – Adapted from the International Genetically Engineered Machine (iGEM) Foundation) Vijaykrishna et al. 2015. PLOS Pathogens.

KISHANA TAYLOR:  And so, because I am interested in viral evolution, I thought that it was really important to then bring that into the conversation, especially as we start to talk about virus variance and the changes that we see with each viral variant. And so there are three main mechanisms of evolution within viruses. Regardless of genetic material, all viruses mutate. The difference is going to be the speed at which they mutate. So because DNA viruses have similar structure to our DNA, they usually have a proofreading mechanism, and so their rate of mutation tends to be slower than those of RNA viruses, because there is no mechanism that checks to make sure that they're copying the code from whatever virus infected your cell first. 

And so typically we see that RNA viruses have a higher rate of mutation, and then depending on which RNA virus, the rates of mutation will vary even more. So there are two additional ways that we can see virus evolution. And we consider these dramatic forms of evolution. So mutation is very slow, you have to have a certain number of mutations to accumulate before you see changes, and so we call that genetic drift. So as you drift along, eventually you'll see some changes that then change some of the mechanisms within the virus.

With recombination and reassortment, it's a very dramatic and almost instantaneous change, and so we call that genetic shift. And so both recombination and reassortment occur while the virus is replicating and making new copies of itself. I like to think of recombination [as] if you have two copies of the same book, but the inside of the book [starts] on different pages. So one book starts on page five, and one book starts on page ten. And you then take each matching–like the next page, so you take page five from the first book and page 11 from the second book, you can still basically get a complete story, but the numbers are not going to match, so you get this combination or this recombinant genetic material that then can give the virus a new advantage or give it new characteristics that it didn't have before. And then also gives the virus the ability, sometimes, to evade the immune system.

And then reassortment is an even more finicky process in that only happens in segmented viruses. And so the virus that we see reassortment in the most is influenza virus. So it's one of the reasons why we have to get vaccinated with influenza every year, because the virus both has a high mutation rate and has the ability to undergo reassortment. And so it has a lot of viral diversity every year. And, basically, what happens with reassortment is that you have two different viruses that are replicating at the same time, and because their genetic segments are segmented, they can be mixed up during viral packaging before it leaves the cell.

And so when we see reassortment, sometimes we see very dramatic changes, sometimes we see slight changes, but usually it allows a virus to evolve enough to evade the immune system. And then, again, that's why we have to get flu shots every year. Next slide.

Slide: SARS –CoV2

3D model of the corona virus.

On Screen Text:

• Coronaviruses
  • Common Cold
• Wuhan, China Nov. 2019
• First US Case, January 202
• Pandemic, March 2020 - Present

KISHANA TAYLOR:  And so, of course, in the last year and a half, last two years, Coronavirus, SARS-CoV-2 has been on everyone's minds, and this is really how I have started doing events like these, because people have more questions about viruses. And so what we do know about SARS-CoV-2 is that it's in the family of Corona Viruses and before SARS-2 or even SARS-1, popped up, we had Coronavirus, and we have other Corona viruses in the form of the common cold.

And then we know that sometime in November of 2019, we saw the first cases of Coronavirus in Wuhan, China. And then by January 2020 we had seen the first cases in the U.S. And by March 2020 we had been declared in a pandemic, and we are still in the pandemic and it is not quite over yet. Next slide.

Slide: COVID Vaccines

Image of an mRNA covid-19 vaccine. (Credit SpencerBDavis)

On-Screen Text: What’s Different about COVID vaccine? Why is a vaccine necessary? How was it made so fast? Is it safe?

KISHANA TAYLOR:  And so, because we are in a pandemic, and because it is a virus, usually one of the best ways to help to temper disease spread is vaccines. And so there's been a lot of controversy over the COVID vaccine specifically, because it has used what can be considered a newer technology in comparison to some of the traditional methods of vaccination. And so when we think about traditional vaccines, most of the time it's a virus that has been what we call attenuated, so it's been weakened so that it doesn't cause as extreme disease. Or it's inactivated, so it's been killed, so it's a dead virus and we are injected with those things and then our body responds to them, and we have an immune response.

And so the reason why the COVID vaccine is different is because it's MRNA. And so, when RNA is translated it makes messenger RNA, and that's what's then sent off to additional cell structure, so then produce the protein. So MRNA is essentially the code for protein. And so this is different because we are essentially exploiting virus biology to then prime our bodies against a virus infection. And so some of the questions that have come up about COVID vaccines are, does this virus alter your DNA? Which we've already been over, no, because the virus is an RNA virus, it doesn't go anywhere near your nucleus, it doesn't go anywhere your DNA.

How was it mean so fast? I'll get into that a little bit more in the next slide, but essentially we had a vested interest in this vaccine being produced so quickly, because so many people were dying and because we had reached pandemic and it was spreading all over the world. Is it safe? Yes, it's safe. While this is considered a newer form of technology for vaccinations, it is not new. It wasn't just produced in the last year. People have been using MRNA technology for 10, 15 years. This just happens to be the first vaccine where it worked, and where we had concerted effort behind us to do the research to get things done. Next slide.

Slide: Vaccine Production

On Screen Text: What is a vaccine? How do they make vaccines? What is in a vaccine?

Logo: Operation Warp Speed – Accelerated Vaccine Process. Mission: Deliver 300 million doses of safe and effective vaccine by January 2021. Visual diagram of Operation Warp Speed, demonstrating the typical vaccine process, compared to the accelerated process, typical time to completion 73 months, accelerated time to completion 14 months.

Phases: R&D – Preclinical Trials

Phases I, II, and III clinical trials, manufacturing, distribution.

KISHANA TAYLOR:  And so, when we think about vaccine production, the main question is, how is it made so fast? So we don't have vaccines for some other really important viruses, but we managed to get a vaccine for COVID, right? And so How did we do that? So any vaccine, any type of medication, requires research. And research is really expensive. And so oftentimes one of the main things is having funding to then do the research to make a vaccine or medication. And then the other issue is that you need to then have people to be able to participate in the trials to make sure that the vaccine or the medication is safe right.

And so because we were in a pandemic, where all of the world's governments were interested in getting a vaccine to protect their citizens, and because it was a pandemic, there were lots and lots and lots of people who could be entered into these trials, we were able to kind of rocket through some of the processes that usually would take years. And then on top of that, thanks to academic research, so usually research done by the NIH or by universities, we already had a vaccine candidate picked out in that the protein that was used was for the original SARS outbreak in 2003, until once we were able to get the RNA sequence for SARS-CoV-2, we were just able to swap out the protein sequences and pop them in.

And so all of these things together has made it a much faster process to then go through vaccine creation, and then vaccine emergency use authorization, and then finally, approval, which just happened–full approval, which happened a couple of weeks ago.

And so the other question we always get is, what's in the vaccines? So the Covid-19 MRNA vaccines are actually a bit cleaner than our traditional vaccine, because it's only The MRNA, the lipid nanoparticle that encapsulates the RNA, and then basically a solution to make sure that the particle survives while it's being injected. Whereas traditionally in order to attenuate a virus, and really to grow a virus in general, they're often grown and chicken eggs. And so then you have to go through the methods of cleaning out the chicken proteins, and the residual chicken egg stuff, before you can then give it to people. Next slide.

Slide: Viral mRNA: Infection vs. Vaccination

Two Diagrams of the coronavirus (Credit – created with biorender.com)

KISHANA TAYLOR:  And so, basically I've made the slide to kind of give you an understanding of what natural infection with Coronavirus looks like in comparison to vaccination. And so if you're naturally infected with Coronavirus, the virus is going to enter your whole cell through the receptors which we talked about earlier. It's going to uncoat its RNA sequence, it's going to then use host machinery to produce new viral proteins, and it's going to use its own polymerases, so its own proteins, to then produce more RNA.

And then those proteins and that RNA are going to be packaged together, and then new viruses are going to be sent out into your body, and then those new viruses are going to infect new noninfected cells. And so basically over time, so if you get infected on Monday, depending on which strain of device you're infected with, within four or five days you have so much virus in your body that you are able to then test positive for COVID if you get a test, and then also get people sick because you're excreting large amounts of virus.

In contrast,  you use the MRNA vaccines, you are getting that nanoparticle which basically mimics viral proteins on the outside that allow it to enter into the cell. And then that lipid particle becomes part of the membrane and then the MRNA is released into the cytoplasm. And so because the MRNA sequence that's used in these vaccines is only for one protein, the spike protein on the virus, so the entry protein, so this is the protein that the Coronavirus uses to get into the cell, it then only produces that one protein. So it doesn't produce any new RNA, it doesn't produce any of the other viral proteins, and so you don't have a complete virus when you're using the MRNA vaccine in comparison to what you would have if you were infected with a real, a whole coronavirus.

And so your body, then, is able to detect those spike proteins and mount an immune response to it and then your body remembers that it has seen the spike protein before. And so then, as a vaccinated person, when you come into contact with actual Coronavirus from, you know, some event that you went to, or school perhaps, or the grocery store, or your cousin or whomever, whatever, your body goes, hey we've seen this by protein before, we know that this is something that we want to get rid of. And so this is how you then are able to fight off infection faster, how you are potentially able to be asymptomatic if you do get infected, and how you avoid hospitalization and potentially death, in comparison with natural infection. Next slide, please.

Slide: Vaccine Mediated Immunity

Diagram showing the impact of vaccine-mediated immunity on the cellular level (Credit – created with bioredner.com)

KISHANA TAYLOR:  And so, this kind of just gives you a better, or more detailed understanding, of what happens in terms of immunity. It says "vaccine-mediated" but even if you were infected with actual Coronavirus the process is similar. So essentially your cell, which thinks it's infected with this spike protein, is then going to present the protein to both your T cells and your antibodies, and your memory immune response is basically made up of these T cells and these antibodies, all of which, over time, become more specific and have a stronger reaction to this protein.

And so, if you are vaccinated you know, a couple of months before you then get infected with a virus you're more likely to have a stronger immune response to the secondary infection because your body has had time to produce these really strong antibodies and T cells, and that's why it takes about two weeks post-second-vaccination with MRNA vaccines for you to be completing immune. Next slide.

Slide: How to validate information

Image of a woman reading a book by a window. (Credit – Pexels / Thought Catalogue)

On Screen text (strike through style): Memes, Youtube videos, the rumor mill.

On Screen Text: (Normal style) CDC.gov, ASM.org, Coronavirus.jhu.edu.

KISHANA TAYLOR:  And so, now that we kind of understand how vaccines work, I also then wanted to talk to you about how to validate information. And so one of the other things that I've seen a ton over the last year and a half is people who, you know, want more information about the vaccines or want more information around the science who, you know, are getting things from TikTok, or YouTube, or their cousin's best friend's sister, or memes that you see on Facebook, etc.

And so it's not to say that any of these things cannot be factual, it's just harder to validate that information. And so when you want information that is backed up by scientific evidence, it's better to go to sites like the CDC.gov, ASM, so the American Society for Microbiology has a really good COVID site, and then also Johns Hopkins University, which is a university down in Baltimore, have all done really good jobs of correlating things like the number of cases of Coronavirus we've seen over time, the difference in cases between vaccinated and unvaccinated people. They will give you facts about either the coronavirus or the vaccine based off of scientific research that you can find in scientific journals, and those sorts of things.

And so the difference between those sites and maybe YouTube or Facebook or wherever else you might see some type of information is that it usually provides you with the sources of the information that they're getting it from. And so usually it will link you to the study that it's quoting or will collate some of the studies for you so you'll have like a mass link of all the different studies that they're getting this information from. 

And that makes it a little bit easier to validate the information because you see, okay, they're telling me this, and then they're showing their work, essentially. They're showing where they're getting this information from. And so that makes it a little bit easier to kind of separate through some of the things that we're seeing and hearing on the Internet. Next slide.

Slide: Teen SciCafe Virulent Viruses with Kishana Taylor PhD. Thanks for joining!

Logo: 150 years – American Museum of Natural History.

Background Illustrations of the coronavirus.

 On Screen Text: Created with the support of the city of New York Department of Health and Mental Hygiene. Copywrite City of New York.

KISHANA TAYLOR:  And so, if you have been interested in anything, and then I talked about today, and you want to hear more.

Multi View conversation format beings with presenters on screen: Presenters are Kristina Taylor – Jaileen Jaquez – Nick Martinez (He/Him)

KISHANA TAYLOR:  And that's all that I have to present for you today, and so I am really excited to hear some of your questions and have some conversations, thank you.

NICK MARTINEZ: Thank you, Dr. Taylor, this was amazing. I have a few questions of my own and then we'll jump right into some of the questions that were thrown into the chat. So my first question is actually where did viruses even come from if they're not living things? Is that known yet? Like how they sort of first formed and emerge?

KISHANA TAYLOR:  That is a big evolutionary question that we do not necessarily have an answer to yet. [LAUGHTER] We know that they're really old, we've found some really ancient viruses and even those viruses have evolved over time. But I don't think that we have an exact idea of where they came from. But the assumption, I believe, at this point is that they are a precursor to bacterial cells and stuff like that.

NICK MARTINEZ: Oh, thank you. So we had a question from Ethan, what's your favorite thing about being a microbiologist?

KISHANA TAYLOR: That's a good question. I think my favorite thing about being a microbiologist is being able to do the lab work, the experiments, and then seeing the results. And so I, as someone who does what we called benchmarks, as someone who actually works in the lab, I get to work with actual viruses, I get to do evolutionary experiments. If I let this virus grow in cells, for you know X amount of time, what happens to the virus, how does it change, and then how does that affect whether or not it makes you sick, or how does that affect how it functions? And I think it's just really cool to see this kind of stuff happen in real time. People who do evolutionary experiments with animals, it moves so much slower, but because various move so much faster, and they produce so many offspring, it's like watching evolution, but much faster in real-time so it's really cool.

NICK MARTINEZ: And kind of a follow up to that, what got you into Microbiology?

KISHANA TAYLOR:  So, I was not into Microbiology at all, I really wanted to be a dolphin trainer. That was my career goal in high school.  [LAUGHTER] And I went to college and was studying marine biology, that was my major, and realized that marine biology has a lot of chemistry. And chemistry is not my favorite subject, I actually really, really hate chemistry. And so I was like, how can I be with the dolphins, but not do a lot of chemistry? That was my next question. And so from there, I decided I was going to be a vet, I was gonna be a marine-mammal veterinarian. 

And veterinary school is actually way more competitive than medical school because there's less veterinary schools in the country, and so they encourage you to do all these things to make yourself attractive to vet schools. And I inadvertently got involved in avian influenza research on campus. And so when I got to the lab, I was like, oh, this is really cool, I think I actually like this better than poking animals with needles. So I basically changed my career trajectory at that point.

JAILEEN JAQUEZ: Thank you, Dr. Taylor, we also have another follow-up question. People are really interested about your career as a microbiologist, what was your coolest experience as a microbiologist?

KISHANA TAYLOR: Coolest? They're all so different. Okay, so I'll give you two different ones, because one was working with bacteria and one working with viruses. So when I got my Masters, I was doing a project where we were looking to see whether or not there was a difference in environmental E-coli and their resistance to antibiotics, based on whether or not the watershed, the river or the stream, had high-production agriculture, because at the time, there was a lot of use of antibiotics in agriculture, and so we were wondering like what the effects of that were.

And so it was really cool because I could go out and drive on the eastern shore of Maryland, and just hang out on these streams, and basically take water samples, and be outside all day, and I actually really enjoyed fieldwork. So that was really cool. And then being able to see the results of that, and so seeing that there was a little bit of a difference. 

And then I would say that the other thing working with viruses that's been really cool is that for my PhD I got to work with a vector-borne virus, so a virus that’s spread by insects of deer. And so I got to see some experiments with deer, but then I got to work with mice. And so getting to work with animals, but then also basically coming up with a new animal model for this virus that I was working on was really cool. So basically either way, being able to have a question, and investigate the question, and come up with real, tangible answers that have an effect on science, has been probably the best part about being a biologist.

NICK MARTINEZ: And we had a question, is a virus able to maintain homeostasis?

KISHANA TAYLOR: No. Homeostasis implies that it is living and functioning. And a virus does not function on its own, it has the ability to alter homeostasis within our cells, but it doesn't have any cellular machinery, really, so it can't really maintain homeostasis. Which is why it requires a cell to live and replicate.

NICK MARTINEZ: And we have a question, what's the difference between the Pfizer Covid vaccine and the like one-shot Johnson and Johnson vaccine?

KISHANA TAYLOR:  So any of the vaccines that require two shots are MRNA, so kind of what I talked about in the talk. The one-shot vaccine is what we call a vector vaccine, and so they basically have taken the spike protein and inserted it inside of another virus. And then they deliver that to you. And so, because it's not MRNA, it's like an actual virus, it works a little bit differently so that's why they were able to give one shot versus two shots.

NICK MARTINEZ: And we had a question about the sort of immune response. So, how does an mRNA vaccine prime our bodies against the infection, could you sort of elaborate on that process, a little bit?

KISHANA TAYLOR:  So I teach a whole immunology class to undergraduates, and so this is like a whole semester's worth of question. But essentially the vaccine is mimicking infection, so your immune system doesn’t know the difference between a live infection versus a vaccine infection. And so it's going to respond the same way it would if you were actually infected with a natural, we call it a wild-type, virus compared to a vaccinated virus, or in this case mRNA.

And so basically if we use the COVID vaccine as the example, once your cells have made this spike protein, it will present the spike protein on the outside of the cell, using a different set of receptors, and it'll push the protein out into the environment. And so your immune system can then pick up these proteins, and that basically starts the immune response. And so basically it starts a cascade of responses within the immune system. 

And so ultimately, some cells are called memory cells, specifically, and so they just continually float in your body, over time. And so the next time you're introduced to whatever pathogen you've been vaccinated against, those memory cells are activated and they respond faster the second time than the first time. So if you were to actually get sick, it would take one to two weeks for you to fight off, whatever the infection is, but once you have that memory response it hits immediately and so you're able to fight it off faster. I hope that answers your question without giving you a whole semester of immunology. 

NICK MARTINEZ: It seems to definitely be helpful. And sort of tangential to that, there were some questions about booster shots, and is there a difference between the original shots, the original vaccine, and what's in the booster shot? Or sort of how the booster shot changes the immune response?

KISHANA TAYLOR: To my knowledge, they have not changed the mRNA sequence in the booster shot. Yet. I don't know if that's coming, but as of right now it's exactly the same as the original vaccines that a person would get. Basically the underlying thought process, and we see this with common-cold Coronaviruses, is the immune response, for whatever reason is not as long-lasting, and so you start to have a waning and immunity. And so it's basically saying to your body, hey remember this thing, you should still fight this thing. And it basically reminds your body and boosts the immune response that way. What was the second part of question?

NICK MARTINEZ: Oh, how does your immune system respond, does it respond differently, after the booster shot?

KISHANA TAYLOR: Theoretically, yes. So for the people who have been approved to get a booster shot, it responds the same way, it's in the name, it just boosts the response.

JAILEEN JAQUEZ: Dr. Taylor, we have a question, how does the shape of a virus determine how it replicates?

KISHANA TAYLOR:  It doesn’t. It usually just determines the mechanism it uses to get into the cell. So if we think about the complex virus shape, that's considered a phage, and so phages only infect bacteria. And because of the structure, it's just easier to infect bacteria that way. So usually it has something to do with infection, but less so about the replication. Because once the virus gets into the cell, the structure uncoats itself and it's just the genetic material, so it doesn't matter at that point.

JAILEEN JAQUEZ: And then, a similar question about bacteria phages, why can't we use them as antibiotics?

KISHANA TAYLOR:  Who says we can't use them as antibiotics? People use them. They're used in usually antibiotic-resistant infections. The problem is that bacteria phages are very specific, and so you have to find a phage that infects the specific bacteria that you're infected with, and so, for some bacteria, we just haven't found it yet. But they are absolutely using some infections.

NICK MARTINEZ: We had a question about, does the immune system perform better when you had COVID previously or by just being vaccinated. So is there a difference in the way the immune system responds?

KISHANA TAYLOR: Yes, so we are actually seeing a stronger immune response with vaccination and that is not uncommon with viruses so basically when you are infected with not like wild type coded your body has to respond to all the different viral proteins, as opposed to just the spike protein but the spike protein is how the virus gets into the cell and so, if you can mount a really strong immune response to different pieces of the spike protein the virus doesn't get into your cell it doesn't replicate and it doesn't then, like mount a bigger infection and so because it's a more targeted response as opposed to a more broad response it's a P it's showing to be more effective than natural infection.

NICK MARTINEZ: We had a really interesting question from my soon I'll knock. The question is, there are oncogene genomic viruses that cause cancer so example like HPV. And we have vaccines against some of them, but why not against all of those types of viruses?

KISHANA TAYLOR:  Yeah so it's really about the like the mechanisms that the virus uses to evade the immune response HPV well, so I usually work with RNA virus, so I know a little bit about HPV but it's not my area of expertise, and so I can't answer and like exceeding detail, but essentially HPV is it it's a little bit easier to target than, say. I tried to most we have vaccinations for most for like most of them really harmful DNA viruses or chicken pox of the DNA virus measles DNA virus mumps HPV so I mean we're it's really just knowing enough about each virus and then being able to come up with a vaccination mechanism that's effective until it's going to vary by virus.

So I think I've heard the one I've heard is why don't we have an HIV vaccine, even though we have now a coven vaccine and HIV is a special is a special kind of ice and then it's called a retrovirus and so, even though it's RNA it infects you, and then it transcribes itself into DNA and then it turns itself into your into your DNA and so it's a little bit harder to target right when you have to then like make sure that you're not targeting also your own DNA because that's how you then promote autoimmunity and stuff like that, and so different viruses have different mechanisms which make it easier or harder to then create a vaccine for.

NICK MARTINEZ: So this is a question like going back to sort of the beginning of your career and thinking about what it was like at the beginning, what was it like when you first began a research project, how do you come up with the subject I do want to investigate and that was from miracle St Kitts.

KISHANA TAYLOR:  yeah so um. If you get involved in research as an undergraduate you're less likely to come up with a whole research on your own you usually get put on a research project that's already existing and you help out, and so I did not conceptualize really most of the research, I did as an undergraduate. But once you go to typically you get to have more control over the product that you do you work on our research, when you get to graduate school so that's like either a Masters or a PhD and so basically you come up with a subject to like so I went to School for public health Microbiology for a master is and learned that vector borne viruses are. considered neglected, because we don't really have, which is not even a true statement, but I was taught we don't really have them here. 

And so they're more and what we call the global South and so because they don't affect us here, people are less likely to put money into it, and so we don't do as much research on them, and I was like well that's silly. I want to help all these people I'm going to go to the vector one virus research and so when I got to my PhD program I like sat down, it was like I want to work on this virus, because it affects X amount of people and then just did a bunch of research to then see like what questions there were that could be answered in a project and then kind of what went that way. But typically anytime you start a project you start off with a lot of reading a lot of investigating to find out what is known, and what is not known and then you go from there.

NICK MARTINEZ: And sort of follow up how many years does it did it take you to sort of become a virologist and was it a sort of stressful process to get to where you are?

KISHANA TAYLOR:  Okay, so it's four years of undergrad. I did two years for masters, but you don't always have to do a Masters and then five years for PhD so 611 11 years, which is a long time. um So yes, it can be a little bit just because you're in school forever right your family like did you graduate yet are you done yet way then be finished you just want to be a student forever. You know you're not I mean you're gaining experience and you're like you're learning things but technically, like, no one is going to think that you have a job right they're going to think that your freely, even though, like very much research as a job, your PhD specifically is very much like a job.

And then yeah I mean you're just consistently learning you're taking in all this information, research is hard, a lot of the times, your experiments don't work or your hypothesis is wrong, and you have to start over again, and so you definitely have to be someone who's willing to take chances and be wrong and make mistakes, if you want to go into a career for research.

JAILEEN JAQUEZ: Thank you, and then we have a question from Ian, what's the evolutionary advantage for viruses different shapes if, once they find a wholesale they replicate and their sheep doesn't matter anymore?

KISHANA TAYLOR: That's a good question that I don't know that I have an answer to, to be honest I'm. I can do some research and get back to you, maybe, but I don't have a good answer for you right.

NICK MARTINEZ: No problem um so, how would you suggest, encouraging someone who is vaccine has attend based on misinformation to get you know vaccinated whether the sort of sources that that they should really be looking at to understand the vaccine process?

KISHANA TAYLOR:  Well, I think it also depends on why they're vaccine-hesitant um but if it's really just that they have gotten misinformation from like social media I then usually I will offer to go through some information with them, usually like scientific literature, which can be kind of like really heavy to go through for someone who doesn't have the expertise, or who like doesn't have the training or like I will offer to like have them look up the papers, they want to read and then like translate it for them essentially.

But basically, I just tried to, there's usually an underlying reason so it's like miss trust in the medical system, maybe you're like maybe a fundamental misunderstanding of like how certain things work and so usually if someone is asking me they trust me, and I think that that's the biggest difference is that. I'm someone that they will actually be willing to listen to, right. So the relationship between me and that person usually plays a really important role in whether or not they're going to listen and believe anything that I say. So I will give them a list of different places where I would go that kind of do a good job of translating. So any science journalism article, so The Atlantic has been doing a really good job over the pandemic, The New York Times, and other places like that kind of bridge the gap between what the scientists are saying and what the people really need and want to know.

And then, if they're still curious at that point, then we can jump into the science and I can be that translator for them.

NICK MARTINEZ: And there was a question that was about sort of that there are millions of viruses out there, what makes a virus, particularly harmful to humans, since you know we're probably encountering lots of different pathogens Why are some harmful and others not?

KISHANA TAYLOR:  yeah it is it. It really just depends on it's like its evolutionary mechanisms and whether or not it's had the opportunity to meet humans right. And so the underlying theory around starts to is that, and I mean the evidence points to this is that evolving and jumped from an animal into a human, and so there was an opportunity at some point for this human in this animal to interact and it just so happened that this virus had the right genetic sequence, and then be compatible, to the effect of human and so it's really. When I was in graduate school we called it, the filter theory and so essentially right, you have viruses over here, you know humans over here their own filter until they kind of just float around in the environment. And the virus is evolving and humans are kind of just hanging out we're evolving to, but at a much lower scale.

And then, if we interact with each other then this gives the virus, the opportunity to then evolve in a way that allows it to infect us it doesn't always work. But sometimes it does and then that's why we have some of the virus viral infections that we have and so it's kind of random kind of selection based it's like a combination.

NICK MARTINEZ: And did you have sort of like an inspiration for while you were going into this process of becoming a microbiologist was there, someone that was like a mentor to you or sort of motivated you and in the field?

KISHANA TAYLOR: Um not maybe not like a specific biologist but I've definitely had like mentors who were microbiologists or biologists or whomever who even like not even scientists who were there to encourage me when I got discouraged, or who were able to provide really good advice, so I definitely would not have made it all the way through if I didn't have people on my side who believed in me and who were encouraging for sure, but I think the thing that kept me going was just partially I'm very stubborn and so once I start, something I kind of have to finish it it's like a quirk I have. But also just knowing that at some point, I could be able to do something really good for my Community for the globe for the global population and that's definitely something that keeps that was always running in the background of my head.

NICK MARTINEZ: And there was a question about whether sort of viruses can become extinct or sort of obsolete.

KISHANA TAYLOR:  Absolutely um so we have eradicated to viruses from the face of this planet so far smallpox does not exist in the world anymore, and something called render pets, which is an animal, a remit virus so like cows and so like that have been eradicated through vaccination and through other preventative methods. So essentially because viruses need a live host to replicate if you can basically put a barrier between the virus and alive host then it can't replicate anymore, and it dies out, it goes extinct.

The problem becomes if the virus can you know start to invade some of that vaccine-mediated immunity, then you, you have to like you know change your vaccination strategy or change your other mitigation policies so like in the case of just coming to right it's not just vaccination that's going to get us out of this it's going to have to be wearing your mask and social distancing and all that kind of stuff.

And then there are so, like the other virus that we're really close to eradicating as polio, but essentially what happens is that in countries where there's a lot of like political turmoil and like war and stuff like that vaccine campaigns get interrupted. And so that makes it a little bit harder, because you can't get to the people who need to be vaccinated and then on top of that, polio, it has this really interesting mechanism when the vaccine so polio vaccine is a tip they use the attenuated version so it's a live virus that's been weakened because it spreads you don't have to vaccine so many people it spreads through like fecal contamination, but the attenuated virus sometimes reverts back to its natural state, and then it basically then like spreading regular polio, and so we've had some issues being able to eradicate it but yes, you can have a bias become extinct for sure.

JAILEEN JAQUEZ: Okay, and then our final question. How do you predict that coven 19 might continue to affect us in the years and decades of the future?

KISHANA TAYLOR:  There are so many variables to that question um do we get to a 90% vaccination rate in the population? Do masks become less of a controversial thing to wear and to put on kids and that sort of thing? Do we finally actually get vaccine access to the rest of the globe and not just to be in States and Europe in a couple of other countries? Based off of what I'm seeing now, I think it will be around for a little bit longer. But hopefully we can get it together and it, I mean it has one of three-ish one or three-ish options we can potentially eradicated, but I don't think that's really possible at this point we can what we call eliminate and so that's kind of what's happened with polio has been eliminated, but not eradicated, because it still exists in some places, but not in others.

Or it can become endemic kind of like flu, and then we just see continuous infections of people with coronavirus and hopefully at some point, it becomes a little bit less deadly as it as it evolves with the human population but there's no guarantee, and so I am not smart enough to predict that maybe some other scientists, with some more data, but those are some of the possibilities.

NICK MARTINEZ: Alright, thank you, everybody, for joining us, and thank you, Dr. Taylor, for spending your afternoon with us this is really important and honestly I feel like with all of the questions we could have gone on for like another hour of just questions, so thank you, everybody, and hope you join us at our next one, which will be in late October early November.

KISHANA TAYLOR:  Thank you, everyone. 

NICK MARTINEZ: Bye everybody.