Hi and welcome back. This is week six of the Epidemics MOOC. This week we've been talking about various different measures or various different types of control for Epidemics. Last week, we've talked about vaccination and now we've talked about a variety of different other, both social and behavioral controls, as well as other connectives pharmaceutical controls. And we're going to just a number of questions related to that this week. We also introduced a video this week from our guest Maria Sparks. Who works, is a faculty member here at Penn State and works on Herpes viruses. And I'll let you introduce yourself quickly and then we're going to deal with some questions from the audience about Herpes viruses. >> Excellent. Well, my name is Maria Sparks and I did my PhD at Berkeley and my post-doc at Princeton before starting my lab here just about a year and a half ago. And we're studying Herpes simplex viruses at the molecular and genomic in cellular level. >> All right, so Herpes viruses are something that a lot of people have heard about. And one of the, sort of fascinating things about these viruses is that you can get infected, you can, you can, that you can have disease symptoms, it can go away, it can come back again. And I think that's one of the things that people ask a lot of questions about, both all the various Herpes viruses, both general herpes, Varicella. People ask a lot of questions about Shingles. And so one of the questions that's come up is, how much do we know about both. How and why these viruses go through these cycles of quiescence, and when they're not certain, they look like, they seem like they're hiding from the body is in fact that is it, is that what they're really doing? Is they're hiding from the body at those times? >> I would say yes, they are. I mean, it's a very useful strategy. It's different from the strategies of a lot of other viruses and pathogens, but to have the ability to establish latency or a quiescent form of infection, is a really good way to allow that host to operate at the normal level, move around, and potential escape again. And I think one of the most exciting things that we've learned in the field of Herpes Virology in the last few years, is that people shed Herpes simplex virus without lesions. So there was one concept that we used to have, maybe a decade or more ago, that people were initially infected, latency was established, and then when they had a visible lesion, they were shedding and were infectious. And now we realize the the virus, actually has lower level reactivations that go mostly, unknown. You don't feel them, you don't see them, and yet you're transmitting virus to your partners or to others. Now that is a really impressive strategy on the viruses part, to move around and infect other members of the population. >> So when it's all being done with lesions and withheld and how's the bar then shooting? In saliva or what? >> Yep, just from skin. So some of the best studies were done at University of Washington and the Fred Hutchinson Cancer Research Institute, and they're just swabbing the skin in the genital region. They were looking for HSV-2, initially. >> Mm-hm. >> And- >> Mm-hm. >> Then later, this was redone in HSV-1, and that is present in saliva. But, these initial studies were done with genital shedding and it's very impressive. The levels can be reasonably, high with no observed phenotype. >> Hm,. >> And no pain felt. So, that makes transmission a. A very different risk than if you thought you were only infectious at the time you had lesions. >> So where is the virus, when it shifts from the skin? Is it in nervous tissue? Or where is it coming from? >> That's a great question. I mean, the initial site of latency, and the site therefore the initial activation, is in neurons. But those nerve endings come very close to the skin surface. And so what we presume is happening is not that the virus. Can miraculously pass through the epithelial skin and get out. But that it must be infecting just a small number of epithelial cells. >> Mm-hm. >> Enough to replicate itself and shed particles on the order of thousands or tens of thousands, maybe even 100,000. But not at a level that the immune system comes in and, and detects that with its surveillance mechanisms to create the whole cycle of inflammation. Painful responses. >> So, is it doing sometimes active to hide or avoid detection by the immune system or is it just staying at really low levels such you know, sort of flying under the radar? >> That I don't think we know the answer to, yet. These new data about the fact, that people showed asymptomatically have come out just within the last five to ten years. >> Mm-hm. >> So, I think people are now asking. Well, what's different? Why do we get a lesion this time and not that time? And that question is actively, being answered with new data coming out of each conference, I would say every year, but there's no set answer. >> Mm-hm. . >> It may be about the quantity, it might be about coincident other infections, or other stresses, but I don't think we have a solid single reason why. >> Mm-hm. Mm-hm. >> So in a related question, you think that the lesions are just to speculate our, the ideal strategy for the virus or perhaps the ideal strategy is to go under the radar and have that low level release. What do you, what do you think? >> I would have to say I've, I've been influenced by what Rachael has talked about with Social stigma and people's behavioral responses >> Yeah. >> And I would guess that the virus can spread more effectively, when it's flying under the radar with these It's the amount of infections. >> You mean, people are avoiding the lesions. >> I would've know. >> People are avoiding individuals with lesions. >> Right. >> Yeah, I mean that's something that we've, we've talked about in terms of what other species do, and it looks like humans in particular really attend to visual cues, especially those that our, our species thinks of as disgusting. And the lesions do evoke disgust. >> Yeah, your. And so we attend to them quickly. We orient to them. We remember them for a long period of time. You always remind me that we were just lobsters [LAUGH] that we would pay attention to smells or other cues that may actually be much more diagnostic. But yeah, for a species that orients to visual cues, wow, how smart on the virus's part to go under the radar. >> And I think there's a sense of personal. More responsibility too when you have people in partnered relationships. That a person who is aware, and senses that they have a lesion >> Yeah. >> Or feels an infection coming on. >> Mm-hm. >> Might behave differently of their own choosing, in addition to how others respond to them. >> And the public health campaigning has actually fed into that. >> Mm-hm. >> Where, when you're supposed to take therapy it's when you may or may not have a symptom. That you're supposed to be changing your behavior when you have symptoms. >> Mm. >> So there's actually. Actually, been messaging around this as well- >> Mm-hm. >> That, for better or for worse, we're going to have to undo. [LAUGH] >> Right. >> So that people really that this is something that they won't just have a trigger and then change behavior. They'll have to change their behavior in a more systematic fashion. >> Yeah. Tim? >> And so it, has this understanding changed the direction of how therapeutics are being developed? So are, what therapeutics were, very often the past- >> Mm-hm. >> Does, you know, targeted towards. People that were towards minimising lesions and to, you know, oftentimes people were only using them when they had flare-ups. Is there, are, you know, are, are there new therapeutics that are being designed for long-term use or for, or to, to effect this shedding in the asymptomatic phase? >> Yes. Yes, and I think it changes how we have to think about them. All right so that there were already things in the pipeline that were designed to deal with. What we call therapeutic vaccines. So, ones that would just reduce a person's- >> Mm-hm. >> Symptoms and make that person feel better. Make that person not have lesions. [CROSSTALK]. >> So, just, just to clarify, what, what, what, what's, what's the distinction, what's a therapeutic vaccine as opposed to a, just a drug? >> Okay. That's a great question. So, a therapeutic, we distinguish vaccines in multiple categories. Released a couple that are as a preventative vaccine versus a therapeutic vaccine, and then audits of the drug part. >> Mm-hm. >> So a preventative vaccine would prevent you from getting the infection, and a therapeutic vaccine says,' You already have this infection. We're going to make your symptoms more tolerable, or aim to make them more tolerable. Then, having a drug, again you would presume that you already have an infection and you're trying to treat it and mitigate the symptoms. >> Mm-hm. >> A cure would be fine too and it's own drugs can effect a cure. But you can also have ones that just reduce symptoms and let you live on with this. [CROSSTALK]. >> I'm sorry, so the Shingles vaccine. That would be an example of a, of a current therapeutic vaccine, is that right or? >> The Shingles one, yes. Would be. >> But not the Chicken pox one. You know, it's a bit of a, that is a difficult one actually to categorize >> Mm-hm. >> Into the two. [NOISE] When, when it's used as a Chicken pox vaccine, the idea is that children would not then get the normal infection. They have antibodies to prevent infection. But the Shingles vaccine is often given in both cases. It's given to people, who don't yet have it. To help, to hope that you'll prevent infection. >> Mm-hm. >> But it might also be given to someone who had Chicken pox as a youngster. Perhaps I'll take. This Shingles vaccine someday since, I had Chicken pox in the hopes that I will be able to stop my own reactivation, when I'm 60 or, or 70 years old. So it's, it's used both ways. That's a tricky one. >> Fantastic
