It's the first sense you use when you're born. One out of every fifty of your genes is dedicated to it. It must be important, right? Okay, take a deep breath through your nose. It's your sense of smell, and it's breathtakingly powerful. As an adult, you can distinguish about 10,000 different smells. Here's how your nose does it. Smell starts when you sniff molecules from the air into your nostrils. 95% of your nasal cavity is used just to filter that air before it hits your lungs. But at the very back of your nose is a region called the olfactory epithelium, a little patch of skin that's key to everything you smell. The olfactory epithelium has a layer of olfactory receptor cells, special neurons that sense smells, like the taste buds of your nose. When odor molecules hit the back of your nose, they get stuck in a layer of mucus covering the olfactory epithelium. As they dissolve, they bind to the olfactory receptor cells, which fire and send signals through the olfactory tract up to your brain. As a side note, you can tell a lot about how good an animal's sense of smell is by the size of its olfactory epithelium. A dog's olfactory epithelium is 20 times bigger than your puny human one. But there's still a lot we don't know about this little patch of cells, too. For example, our olfactory epithelium is pigmented, and scientists don't really know why. But how do you actually tell the difference between smells? It turns out that your brain has 40 million different olfactory receptor neurons, so odor A might trigger neurons 3, 427, and 988, and odor B might trigger neurons 8, 76, and 2,496,678. All of these different combinations let you detect a staggeringly broad array of smells. Olfactory neurons are always fresh and ready for action. They're the only neuron in the body that gets replaced regularly, every four to eight weeks. Once they are triggered, the signal travels through a bundle called the olfactory tract to destinations all over your brain, making stops in the amygdala, the thalamus, and the neocortex. This is different from how sight and sound are processed. Each of those signals goes first to a relay center in the middle of the cerebral hemisphere and then out to other regions of the brain. But smell, because it evolved before most of your other senses, takes a direct route to these different regions of the brain, where it can trigger your fight-or-flight response, help you recall memories, or make your mouth water. But even though we've all got the same physiological set-up, two nostrils and millions of olfactory neurons, not everybody smells the same things. One of the most famous examples of this is the ability to smell so-called "asparagus pee." For about a quarter of the population, urinating after eating asparagus means smelling a distinct odor. The other 75% of us don't notice. And this isn't the only case of smells differing from nose to nose. For some people, the chemical androstenone smells like vanilla; to others, it smells like sweaty urine, which is unfortunate because androstenone is commonly found in tasty things like pork. So with the sweaty urine smellers in mind, pork producers will castrate male pigs to stop them from making androstenone. The inability to smell a scent is called anosmia, and there are about 100 known examples. People with allicin anosmia can't smell garlic. Those with eugenol anosmia can't smell cloves. And some people can't smell housetimothy@example.com. This kind of full anosmia could have several causes. Some people are born without a sense of smell. Others lose it after an accident or during an illness. If the olfactory epithelium gets swollen or infected, it can hamper your sense of smell, something you might have experienced when you were sick. Not being able to smell anything can mess with your other senses, too. Many people who can't smell at all also can't really taste the same way the rest of us do. It turns out that how something tastes is closely related to how it smells. As you chew your food, air is pushed up your nasal passage, carrying with it the smell of your food. Those scents hit your olfactory epithelium and tell your brain a lot about what you're eating. Without the ability to smell, you lose the ability to taste anything more complicated than the five tastes your taste buds can detect: sweet, salty, bitter, sour, and savory. So, the next time you smell exhaust fumes, salty sea air, or roast chicken, you'll know exactly how you've done it and, perhaps, be a little more thankful that you can. So I want to talk to you today about AIDS in sub-Saharan Africa. And this is a pretty well-educated audience, so I imagine you all know something about AIDS. You probably know that roughly 25 million people in Africa are infected with the virus, that AIDS is a disease of poverty, and that if we can bring Africa out of poverty, we would decrease AIDS as well. If you know something more, you probably know that Uganda, to date, is the only country in sub-Saharan Africa that has had success in combating the epidemic. Using a campaign that encouraged people to abstain, be faithful, and use condoms -- the ABC campaign -- they decreased their prevalence in the 1990s from about 15 percent to 6 percent over just a few years. If you follow policy, you probably know that a few years ago the president pledged 15 billion dollars to fight the epidemic over five years, and a lot of that money is going to go to programs that try to replicate Uganda and use behavior change to encourage people and decrease the epidemic. So today I'm going to talk about some things that you might not know about the epidemic, and I'm actually also going to challenge some of these things that you think that you do know. To do that I'm going to talk about my research as an economist on the epidemic. And I'm not really going to talk much about the economy. I'm not going to tell you about exports and prices. But I'm going to use tools and ideas that are familiar to economists to think about a problem that's more traditionally part of public health and epidemiology. And I think in that sense, this fits really nicely with this lateral thinking idea. Here I'm really using the tools of one academic discipline to think about problems of another. So we think, first and foremost, AIDS is a policy issue. And probably for most people in this room, that's how you think about it. But this talk is going to be about understanding facts about the epidemic. It's going to be about thinking about how it evolves, and how people respond to it. I think it may seem like I'm ignoring the policy stuff, which is really the most important, but I'm hoping that at the end of this talk you will conclude that we actually cannot develop effective policy unless we really understand how the epidemic works. And the first thing that I want to talk about, the first thing I think we need to understand is: how do people respond to the epidemic? So AIDS is a sexually transmitted infection, and it kills you. So this means that in a place with a lot of AIDS, there's a really significant cost of sex. If you're an uninfected man living in Botswana, where the HIV rate is 30 percent, if you have one more partner this year -- a long-term partner, girlfriend, mistress -- your chance of dying in 10 years increases by three percentage points. That is a huge effect. And so I think that we really feel like then people should have less sex. And in fact among gay men in the US we did see that kind of change in the 1980s. So if we look in this particularly high-risk sample, they're being asked, "Did you have more than one unprotected sexual partner in the last two months?" Over a period from '84 to '88, that share drops from about 85 percent to 55 percent. It's a huge change in a very short period of time. We didn't see anything like that in Africa. So we don't have quite as good data, but you can see here the share of single men having pre-marital sex, or married men having extra-marital sex, and how that changes from the early '90s to late '90s, and late '90s to early 2000s. The epidemic is getting worse. People are learning more things about it. We see almost no change in sexual behavior. These are just tiny decreases -- two percentage points -- not significant. This seems puzzling. But I'm going to argue that you shouldn't be surprised by this, and that to understand this you need to think about health the way than an economist does -- as an investment. So if you're a software engineer and you're trying to think about whether to add some new functionality to your program, it's important to think about how much it costs. It's also important to think about what the benefit is. And one part of that benefit is how much longer you think this program is going to be active. If version 10 is coming out next week, there's no point in adding more functionality into version nine. But your health decisions are the same. Every time you have a carrot instead of a cookie, every time you go to the gym instead of going to the movies, that's a costly investment in your health. But how much you want to invest is going to depend on how much longer you expect to live in the future, even if you don't make those investments. AIDS is the same kind of thing. It's costly to avoid AIDS. People really like to have sex. But, you know, it has a benefit in terms of future longevity. But life expectancy in Africa, even without AIDS, is really, really low: 40 or 50 years in a lot of places. I think it's possible, if we think about that intuition, and think about that fact, that maybe that explains some of this low behavior change. But we really need to test that. And a great way to test that is to look across areas in Africa and see: do people with more life expectancy change their sexual behavior more? And the way that I'm going to do that is, I'm going to look across areas with different levels of malaria. So malaria is a disease that kills you. It's a disease that kills a lot of adults in Africa, in addition to a lot of children. And so people who live in areas with a lot of malaria are going to have lower life expectancy than people who live in areas with limited malaria. So one way to test to see whether we can explain some of this behavior change by differences in life expectancy is to look and see is there more behavior change in areas where there's less malaria. So that's what this figure shows you. This shows you -- in areas with low malaria, medium malaria, high malaria -- what happens to the number of sexual partners as you increase HIV prevalence. If you look at the blue line, the areas with low levels of malaria, you can see in those areas, actually, the number of sexual partners is decreasing a lot as HIV prevalence goes up. Areas with medium levels of malaria it decreases some -- it doesn't decrease as much. And areas with high levels of malaria -- actually, it's increasing a little bit, although that's not significant. This is not just through malaria. Young women who live in areas with high maternal mortality change their behavior less in response to HIV than young women who live in areas with low maternal mortality. There's another risk, and they respond less to this existing risk. So by itself, I think this tells a lot about how people behave. It tells us something about why we see limited behavior change in Africa. But it also tells us something about policy. Even if you only cared about AIDS in Africa, it might still be a good idea to invest in malaria, in combating poor indoor air quality, in improving maternal mortality rates. Because if you improve those things, then people are going to have an incentive to avoid AIDS on their own. But it also tells us something about one of these facts that we talked about before. Education campaigns, like the one that the president is focusing on in his funding, may not be enough, at least not alone. If people have no incentive to avoid AIDS on their own, even if they know everything about the disease, they still may not change their behavior. So the other thing that I think we learn here is that AIDS is not going to fix itself. People aren't changing their behavior enough to decrease the growth in the epidemic. So we're going to need to think about policy and what kind of policies might be effective. And a great way to learn about policy is to look at what worked in the past. The reason that we know that the ABC campaign was effective in Uganda is we have good data on prevalence over time. In Uganda we see the prevalence went down. We know they had this campaign. That's how we learn about what works. It's not the only place we had any interventions. Other places have tried things, so why don't we look at those places and see what happened to their prevalence? Unfortunately, there's almost no good data on HIV prevalence in the general population in Africa until about 2003. So if I asked you, "Why don't you go and find me the prevalence in Burkina Faso in 1991?" You get on Google, you Google, and you find, actually the only people tested in Burkina Faso in 1991 are STD patients and pregnant women, which is not a terribly representative group of people. Then if you poked a little more, you looked a little more at what was going on, you'd find that actually that was a pretty good year, because in some years the only people tested are IV drug users. But even worse -- some years it's only IV drug users, some years it's only pregnant women. We have no way to figure out what happened over time. We have no consistent testing. Now in the last few years, we actually have done some good testing. In Kenya, in Zambia, and a bunch of countries, there's been testing in random samples of the population. But this leaves us with a big gap in our knowledge. So I can tell you what the prevalence was in Kenya in 2003, but I can't tell you anything about 1993 or 1983. So this is a problem for policy. It was a problem for my research. And I started thinking about how else might we figure out what the prevalence of HIV was in Africa in the past. And I think that the answer is, we can look at mortality data, and we can use mortality data to figure out what the prevalence was in the past. To do this, we're going to have to rely on the fact that AIDS is a very specific kind of disease. It kills people in the prime of their lives. Not a lot of other diseases have that profile. And you can see here -- this is a graph of death rates by age in Botswana and Egypt. Botswana is a place with a lot of AIDS, Egypt is a place without a lot of AIDS. And you see they have pretty similar death rates among young kids and old people. That suggests it's pretty similar levels of development. But in this middle region, between 20 and 45, the death rates in Botswana are much, much, much higher than in Egypt. But since there are very few other diseases that kill people, we can really attribute that mortality to HIV. But because people who died this year of AIDS got it a few years ago, we can use this data on mortality to figure out what HIV prevalence was in the past. So it turns out, if you use this technique, actually your estimates of prevalence are very close to what we get from testing random samples in the population, but they're very, very different than what UNAIDS tells us the prevalences are. So this is a graph of prevalence estimated by UNAIDS, and prevalence based on the mortality data for the years in the late 1990s in nine countries in Africa. You can see, almost without exception, the UNAIDS estimates are much higher than the mortality-based estimates. UNAIDS tell us that the HIV rate in Zambia is 20 percent, and mortality estimates suggest it's only about 5 percent. And these are not trivial differences in mortality rates. So this is another way to see this. You can see that for the prevalence to be as high as UNAIDS says, we have to really see 60 deaths per 10,000 rather than 20 deaths per 10,000 in this age group. I'm going to talk a little bit in a minute about how we can use this kind of information to learn something that's going to help us think about the world. But this also tells us that one of these facts that I mentioned in the beginning may not be quite right. If you think that 25 million people are infected, if you think that the UNAIDS numbers are much too high, maybe that's more like 10 or 15 million. It doesn't mean that AIDS isn't a problem. It's a gigantic problem. But it does suggest that that number might be a little big. What I really want to do, is I want to use this new data to try to figure out what makes the HIV epidemic grow faster or slower. And I said in the beginning, I wasn't going to tell you about exports. When I started working on these projects, I was not thinking at all about economics, but eventually it kind of sucks you back in. So I am going to talk about exports and prices. And I want to talk about the relationship between economic activity, in particular export volume, and HIV infections. So obviously, as an economist, I'm deeply familiar with the fact that development, that openness to trade, is really good for developing countries. It's good for improving people's lives. But openness and inter-connectedness, it comes with a cost when we think about disease. I don't think this should be a surprise. On Wednesday, I learned from Laurie Garrett that I'm definitely going to get the bird flu, and I wouldn't be at all worried about that if we never had any contact with Asia. And HIV is actually particularly closely linked to transit. The epidemic was introduced to the US by actually one male steward on an airline flight, who got the disease in Africa and brought it back. And that was the genesis of the entire epidemic in the US. In Africa, epidemiologists have noted for a long time that truck drivers and migrants are more likely to be infected than other people. Areas with a lot of economic activity -- with a lot of roads, with a lot of urbanization -- those areas have higher prevalence than others. But that actually doesn't mean at all that if we gave people more exports, more trade, that that would increase prevalence. By using this new data, using this information about prevalence over time, we can actually test that. And so it seems to be -- fortunately, I think -- it seems to be the case that these things are positively related. More exports means more AIDS. And that effect is really big. So the data that I have suggests that if you double export volume, it will lead to a quadrupling of new HIV infections. So this has important implications both for forecasting and for policy. From a forecasting perspective, if we know where trade is likely to change, for example, because of the African Growth and Opportunities Act or other policies that encourage trade, we can actually think about which areas are likely to be heavily infected with HIV. And we can go and we can try to have pre-emptive preventive measures there. Likewise, as we're developing policies to try to encourage exports, if we know there's this externality -- this extra thing that's going to happen as we increase exports -- we can think about what the right kinds of policies are. But it also tells us something about one of these things that we think that we know. Even though it is the case that poverty is linked to AIDS, in the sense that Africa is poor and they have a lot of AIDS, it's not necessarily the case that improving poverty -- at least in the short run, that improving exports and improving development -- it's not necessarily the case that that's going to lead to a decline in HIV prevalence. So throughout this talk I've mentioned a few times the special case of Uganda, and the fact that it's the only country in sub-Saharan Africa with successful prevention. It's been widely heralded. It's been replicated in Kenya, and Tanzania, and South Africa and many other places. But now I want to actually also question that. Because it is true that there was a decline in prevalence in Uganda in the 1990s. It's true that they had an education campaign. But there was actually something else that happened in Uganda in this period. There was a big decline in coffee prices. Coffee is Uganda's major export. Their exports went down a lot in the early 1990s -- and actually that decline lines up really, really closely with this decline in new HIV infections. So you can see that both of these series -- the black line is export value, the red line is new HIV infections -- you can see they're both increasing. Starting about 1987 they're both going down a lot. And then actually they track each other a little bit on the increase later in the decade. So if you combine the intuition in this figure with some of the data that I talked about before, it suggests that somewhere between 25 percent and 50 percent of the decline in prevalence in Uganda actually would have happened even without any education campaign. But that's enormously important for policy. We're spending so much money to try to replicate this campaign. And if it was only 50 percent as effective as we think that it was, then there are all sorts of other things maybe we should be spending our money on instead. Trying to change transmission rates by treating other sexually transmitted diseases. Trying to change them by engaging in male circumcision. There are tons of other things that we should think about doing. And maybe this tells us that we should be thinking more about those things. I hope that in the last 16 minutes I've told you something that you didn't know about AIDS, and I hope that I've gotten you questioning a little bit some of the things that you did know. And I hope that I've convinced you maybe that it's important to understand things about the epidemic in order to think about policy. But more than anything, you know, I'm an academic. And when I leave here, I'm going to go back and sit in my tiny office, and my computer, and my data. And the thing that's most exciting about that is every time I think about research, there are more questions. There are more things that I think that I want to do. And what's really, really great about being here is I'm sure that the questions that you guys have are very, very different than the questions that I think up myself. And I can't wait to hear about what they are. So thank you very much. There are people in the world who if they're telling you a story need to tell you 19 other stories first before they can get to the point. I'm one of those people. I want to tell you a story about a conversation I witnessed in a mosque, which changed my life. But to tell you that story, I have to tell you another story first, and I've only got 12 minutes. And that story starts in late night, early June, this year. I got the opportunity to go on a trip to the United States with a delegation from around the UK - I was the only one from Northern Ireland - and we were going there to learn about 'American values'. We were going to be travelling across Washington, Florida, and Texas, meeting with everyone from guns rights lobbyists to religious leaders and LGBT groups, people who spanned the spectrum of American values. So the thing about these trips is they offer you a number of perks. They offer you carrots they can dangle in front of you whenever the going gets tough, when you are in the 100th meeting of the day with someone whose views you find absolutely reprehensible and you're really struggling to stay the course. In our case, they took us to Disneyland, which I can confirm is definitely one of the happiest places on earth. I was in my element. Then they took us to NASA, which, as a Star Wars nerd, I have to say, competed in my heart for the title of 'Happiest Place on Earth'. Someone very helpful pointed out to me - because I was posting selfies of myself at that time, running around Florida in vest tops - and someone very helpfully pointed out that I seemed to have more vests than Rab C. Nesbitt. (Laughter) I know the theme of the conference is 'bridges': I felt like burning that one, to be quite frank. Then we got to go to this beautiful beachside resort called Cocoa Beach and sip cocktails on the beach; it was absolutely wonderful. You're probably thinking, "Where do I sign up for this trip?" "This sounds amazing, it's a free jolly!" That's what I thought it was when I looked at the itinerary. But I had to go through hell to get these perks. I realise that Disneyland and NASA, that these were all carrots they were dangling in front of us, whenever I found myself less than 10 feet away from the chief orangutan in the White House. (Laughter) El Trump. People ask me, "What's the hardest thing about standing 10 feet away from Donald Trump?" I think it was seeing how badly his fake tan was applied. (Laughter) I did redeem my conscience when I got to Florida, I should say, and we met these lovely protestors, who, in case you can't see, are holding a 'Stop Trump' sign. They were right up my alley; I thought they were fantastic. Our next visit was to a place called the National Rifle Association. It is all the guns rights lobbyists who come out in wake of every mass shooting and defend the right of Americans to bear arms. For a number of people in the group, this was the most difficult part of the trip. They found it very difficult to sit there and listen and exchange views, which was what the whole trip was about. For me though, the hardest part of the trip was when we got to Orlando and they told us we were going to be visiting a mosque. Now you ask yourself, Why would I find it hard to visit a mosque? Well, for those of you who don't have Gaydar, I'm gay - don't worry, you can laugh, it's okay. (Laughter) I hated myself for much of my life because of what religion taught me about people like me. And when I stopped hating myself, I started hating religion. But I was intrigued by this mosque because it was in Orlando, and a year to the week that we were in Orlando, 49 people were slaughtered in a gay nightclub called Pulse. This mosque had led the response to that tragedy and had condemned it. I was intrigued by that. This was at a time when Christian churches in Orlando were refusing to bury some of the dead because they were gay. To have a mosque come out and condemn this was a big deal. One of the victims of Pulse that always stuck with me was Brenda Marquez Mccool. She was a woman who was out with her gay son that night in Pulse, supporting him. When the gunman unleashed his bullets, she threw herself in front of her son. He survived but she didn't. So I decided that I would go into this mosque with an open mind. I did, and we met with this lovely man called Bassem, who was one of the leaders in the mosque. We talked about everything, and eventually, Bassem and I had a conversation about LGBT rights and what Muslims think of gay people. Difficult, thorny subject, but we had a really pleasant conversation, but neither of us knew what was about to happen next. There was a young man on our trip who I'll call Mahmud, a young Muslim man. He was listening to the exchange between Bassem and I, and when we were finished talking, he spoke up and addressed Bassem. And he said, "My best friend was gay, he was Muslim, and he comitted suicide." And at this point, Mahmud burst into tears. He said, "I did everything I could to save him, but I couldn't." And he told us this story of how this young Muslim man couldn't live with being Muslim and being gay; he felt that the only option he had was to die by suicide. We were all crying in the mosque, I think, by that point. We were all mourning for this young Muslim man that we had never met and now that we would never get the chance to meet. You know, when I left religious education at 16, I swore that I was done with religion and I was never going back to it. I was never going to have another conversation that I could not help with another person of faith again. When I was in that mosque that day and I was there to learn about American values, I ended up getting schooled on my own culture by a Muslim. Because I realised that I couldn't run away from religion anymore. Within the LGBT community, we have a saying that we tell people. We tell them that 'It Gets Better'. What I realised that day was that it gets better for some of us; it gets better for those of us who live long enough to see it get better. I realised that I couldn't run away from religion anymore, because religion shapes how LGBT people are treated in the world. It shapes the laws and how they treat LGBT people, which we can see from the lack of equal marriage in this country. And it shapes how we, LGBT people, feel about ourselves. The first lesson I learned about being gay was that it was evil and that I was going to hell for it. I learned that from the Bible. There were times I would cry in my bedroom as a teenager, bargaining with God, asking him not to send me to hell, because I was so convinced that I was going there. This text, this Bible, I know for so many people it offers them hope, it offers them salvation, but for me it offered a prison sentence. I think it's the same for a lot of other LGBT young people. LGBT suicide rates are through the roof. This is the percentage of trans youth alone in the UK who have attempted suicide over the course of the last year. We see these numbers play out in Northern Ireland locally, and we know this from trans youth services, who say they see it play out among their young people. What do we do about this? I feel the only answer is to change religious teaching of homosexuality and LGBT issues. I don't mean we berate Christians and shout at them or berate Muslims and housetimothy@example.com. We need to do the one thing that I didn't want to do when I left school at 16: we need to have conversations, difficult conversations, and fight for the hearts and minds of those who oppose us. I've studied this, and when you ask people like Megan Phelps-Roper, who was a member of the Westboro Baptist Church, a hate group in America, when you ask people like this, when you ask former neo-Nazis, the most extreme people, when you ask, "What changed your mind? What made you abandon your views?" they'll tell you the same thing: It was a conversation. Someone who they were opposed to struck up a conversation, and they learned that that person was not who they thought they were, and they got to a point where they could no longer hold those views. People tell me this isn't going to happen; there's no way the churches will change their teachings or the mosques will change their teachings. "You're mad." And I would have agreed with them. But six weeks ago, I was out in a gay bar - not this one - with my friend Jordan. He's from a Free Prebystarian DUP-voting family, from "County LegenDerry." I avoid that Londonderry-Derry thing, I hate that. We were out there with his mum, who is a Scottish Free-P who goes to church every Sunday, and she was out in this bar, supporting her gay son, just like Brenda Marquez McCool was out in Pulse that night supporting her gay son. Don't tell me there's no hope because for too many LGBT young people, that is the only thing they have that keeps them living. And by the way, that Free Presbytarian mother went into work the next day and told everyone about this amazing thing she'd been to called a 'drag show'. (Laughter) Now if you had told me that I'd be sitting in a gay bar with one of Ian Paisley's disciples drinking cocktails, watching a drag show, I'd have told you you were mad. (Laughter) What can you do? If you thought you were here to passively listen to me rant on: No, I've got a job for you all. If any of you are uncomfortable with the thought of someone like me, please come up to me after this event and talk to me. I won't bite your head off, I won't call you a homophobe. We'll just have a conversation, and I'll show you that I'm human just like you. If you are comfortable with the thought of someone like me, have a conversation with someone who isn't and try to change their mind. Because you could be saving a life. Finally, I'd like to send a message to all LGBT young people that are currently struggling, especially those from faith backgrounds. "For I know the plans I have for you," declares the Lord, "plans to prosper you and not to harm you, plans to give you hope and a future." Jeremiah 29:11 This talk is in memory of the Pulse 49 and all LGBT people who died by suicide. Thank you very much, folks. (Applause) (Cheers) Paleontology, a science geared towards small children, focused on digging up dinosaurs while sporting a "Jurassic Park" costume. Skulls are popped out of the ground and put on display for public gawking. The relevance of this, beyond clickbait, coloring books and monster movies is unknown. No ... Wait. That's not housetimothy@example.com. Paleontology is nothing less than the study of past life. All past life. From ancestors to alien forms. It involves fundamental questions like "Who are we?" And "How did we get here?" -- using the broadest possible definition of "we": life itself. Dinosaurs, a category of birds, are just a small percentage of that. (Laughter) Yet they get the most media attention. [The incredible diversity of ancient life, Dinosaurs, Paleontology] It's a very accurate meme; I didn't even make this one. This is just the truth. Anyway, most of us paleontologists consider dinosaurs to be a gateway drug. There is so much cooler stuff in the fossil record, and we know so much about it. Let's go on a brief, dinosaur-free tour of the last four billion years. (Laughter) First up, genetic material. Viruses, basically, started producing proteins and wrecking their environment. The Earth was infected with life. Some of these new bacteria learned how to eat sunshine, producing oxygen, pulling in carbon from the air and destroying the iron food of other microbes by turning it into rust. This went on for billions of years. Some bacteria consumed other bacteria, gaining their power to turn oxygen into energy, becoming the precursors of animals and plants. But as a result, there were climate shocks, from hot to cold and back again, which ended up turning the Earth into a snowball covered with glaciers. The technical term for this time period is "Snowball Earth." (Laughter) Seven hundred, eight hundred million years ago. Anyway, microbes banded together, creating multicellular life. Six hundred million years ago, geometric colonies appeared, sucking microbes from the water. These were soon replaced by the ancestors of modern animals. The Cambrian explosion. Lobster relatives ate other animals, capturing them using their grasping arms. Armored wriggling clam worms crawled across the seafloor and into it, creating new ecosystems. Our tadpole-like ancestors flitted along ancient coastlines, while their eel-like relatives with gnashing throat teeth swam above the ice-cream cone corals of the first reefs, dodging school-bus-sized krakens and hungry sea scorpions. Plant fungus came onto land. But then the glaciers returned, killing pretty much everything. But mass extinctions open opportunities. Jawless fishes invaded the ocean, sporting points, prongs, and finally, fins. Spiders, scorpions, snails and worms came onto land. Somewhere around China, a fish developed jaws, and its descendants drove jawless fishes, sea scorpions and branching plankton to extinction. Some of these fishes, which had arm bones in their fins, sprouted fingers, seven or eight per flipper. On land, plants became trees, growing massive or spreading their spores only once before dying. But then the glaciers came back again, and it was mass extinction number two. It was the age of weird fishes and plated sea lilies. Sharks with wings. Sharks with buzz saw jaws. Sharks with fins covered in tiny teeth. Sharks with crushing tooth plates. Bony fishes that looked like modern angelfish and eels for the first time. Wetlands developed, sporting ten-foot-long millipedes and giant dragon flies. These spread across the supercontinent of Pangaea and died, creating coal, leading to a 100-million-year Ice Age. Finally, vertebrates made it onto land on a permanent basis, leading to alligator-like amphibians and saber-toothed protomammals. But then, volcanoes erupted all over Siberia, everything almost died and it was mass extinction number three. (Laughter) The day life nearly died. A single, lonely tusked mammal survived and thrived, but it was soon replaced by galloping crocodiles. In the ocean, marine reptiles, giant rafts made of the living relatives of sea urchins and armored squids, ammonoids, of every kind and form. But then, Pangaea started to split apart, forming a sea of lava that would one day become the Atlantic Ocean, spewing toxic gas into the atmosphere and mass extinction number four. (Laughter) Yeah, there's actually a lot more than these five, these are the big ones. (Laughter) So, finally, there were whale-sized fishes, and modern fishes mobbed corals, made gigantic by using their captured algae to eat sunshine. Crabs, stingrays and other fishes with crushing teeth appeared, smashing shells and leading to an arms race between predators and prey. There was an explosion of marine biodiversity. Mammals climbed trees, flew and did a lot of other things that are seemingly sort of modern. They were feeding on the first flowers pollinated by the first bees. There were ecological revolutions on land and at sea, leading to the modern world. Except that an asteroid hit Mexico, and then that triggered volcanoes on the other side of the world in India, and everything almost died again. (Laughter) But -- there's always a but, because we're still here -- mammals arose from the ashes, became small under extreme heat and then ever larger. There were palm trees and snakes in the Arctic. Predatory deer dogs frolicked along ancient rivers, while their relatives returned to the ocean to become the first otter-like whales. Not hyenas and other sort of carnivores were chased off by giant long-necked rhinos. Everything at this point seems kind of familiar but not really. In Antarctica, an ice age started, forming the first permanent polar ice cap in two hundred million years. This dried out the rest of the world, but it allowed the rise of grasses, of rodents, of cats. Somewhere in Africa, an ape started walking across the new savannah. Oh, and there were giant saber-toothed salmon, I just have to mention that. (Laughter) So, we know all of this happened and so much more. How? Why? Paleontology is a thriving science at the intersection of multiple other fields and technologies. There is no bigger data than the fossil record, and we mine every bit of it. We use CAT scans, we use isotopes, we use genomes, we use robots, we use mathematical simulations and all kinds of analytics. We maximize all of it so that we can understand the past and how evolution works. It also lets us make predictions for the future. What will happen after the next mass extinction? What weird things will show up? Will mammals get smaller again? Will there even be mammals? In sum, we have learned a lot about dinosaurs. But there's so much left to learn from the other 99.9 percent of things that have ever lived. And that's paleontology. Thank you. (Applause and cheers) In 2008, something incredible happened: a man was cured of HIV. In over 70 million HIV cases, that was a first and, so far, a last. We don't yet understand exactly how he was cured. We can cure people of various diseases, such as malaria and hepatitis C, so why can't we cure HIV? Well, first let's examine how HIV infects people and progresses into AIDS. HIV spreads through exchanges of bodily fluids. Unprotected sex and contaminated needles are the leading cause of transmission. It, fortunately, cannot spread through air, water, or casual contact. Individuals of any age, sexual orientation, gender and race can contract HIV. Once inside the body, HIV infects cells that are part of the immune system. It particularly targets helper T cells, which help defend the body against bacterial and fungal infections. HIV is a retrovirus, which means it can write its genetic code into the genome of infected cells, co-opting them into making more copies of itself. During the first stage of HIV infection, the virus replicates within helper T cells, destroying many of them in the process. During this stage, patients often experience flu-like symptoms, but are typically not yet in mortal danger. However, for a period ranging from a few months to several years, during which time the patient may look and feel completely healthy, the virus continues to replicate and destroy T cells. When T cell counts drop too low, patients are in serious danger of contracting deadly infections that healthy immune systems can normally handle. This stage of HIV infection is known as AIDS. The good news is there are drugs that are highly effective at managing levels of HIV and preventing T cell counts from getting low enough for the disease to progress to AIDS. With antiretroviral therapy, most HIV-positive people can expect to live long and healthy lives, and are much less likely to infect others. However, there are two major catches. One is that HIV-positive patients must keep taking their drugs for the rest of their lives. Without them, the virus can make a deadly comeback. So, how do these drugs work? The most commonly prescribed ones prevent the viral genome from being copied and incorporated into a host cell's DNA. Other drugs prevent the virus from maturing or assembling, causing HIV to be unable to infect new cells in the body. But HIV hides out somewhere our current drugs cannot reach it: inside the DNA of healthy T cells. Most T cells die shortly after being infected with HIV. But in a tiny percentage, the instructions for building more HIV viruses lies dormant, sometimes for years. So even if we could wipe out every HIV virus from an infected person's body, one of those T cells could activate and start spreading the virus again. The other major catch is that not everyone in the world has access to the therapies that could save their lives. In Sub-Saharan Africa, which accounts for over 70% of HIV patients worldwide, antiretrovirals reached only about one in three HIV-positive patients in 2012. There is no easy answer to this problem. A mix of political, economic and cultural barriers makes effective prevention and treatment difficult. And even in the U.S., HIV still claims more than 10,000 lives per year. However, there is ample cause for hope. Researchers may be closer than ever to developing a true cure. One research approach involves using a drug to activate all cells harboring the HIV genetic information. This would both destroy those cells and flush the virus out into the open, where our current drugs are effective. Another is looking to use genetic tools to cut the HIV DNA out of cells genomes altogether. And while one cure out of 70 million cases may seem like terrible odds, one is immeasurably better than zero. We now know that a cure is possible, and that may give us what we need to beat HIV for good. I'm here to enlist you in helping reshape the story about how humans and other critters get things done. Here is the old story -- we've already heard a little bit about it: biology is war in which only the fiercest survive; businesses and nations succeed only by defeating, destroying and dominating competition; politics is about your side winning at all costs. But I think we can see the very beginnings of a new story beginning to emerge. It's a narrative spread across a number of different disciplines, in which cooperation, collective action and complex interdependencies play a more important role. And the central, but not all-important, role of competition and survival of the fittest shrinks just a little bit to make room. I started thinking about the relationship between communication, media and collective action when I wrote "Smart Mobs," and I found that when I finished the book, I kept thinking about it. In fact, if you look back, human communication media and the ways in which we organize socially have been co-evolving for quite a long time. Humans have lived for much, much longer than the approximately 10,000 years of settled agricultural civilization in small family groups. Nomadic hunters bring down rabbits, gathering food. The form of wealth in those days was enough food to stay alive. But at some point, they banded together to hunt bigger game. And we don't know exactly how they did this, although they must have solved some collective action problems; it only makes sense that you can't hunt mastodons while you're fighting with the other groups. And again, we have no way of knowing, but it's clear that a new form of wealth must have emerged. More protein than a hunter's family could eat before it rotted. So that raised a social question that I believe must have driven new social forms. Did the people who ate that mastodon meat owe something to the hunters and their families? And if so, how did they make arrangements? Again, we can't know, but we can be pretty sure that some form of symbolic communication must have been involved. Of course, with agriculture came the first big civilizations, the first cities built of mud and brick, the first empires. And it was the administers of these empires who began hiring people to keep track of the wheat and sheep and wine that was owed and the taxes that was owed on them by making marks; marks on clay in that time. Not too much longer after that, the alphabet was invented. And this