Election interference, Mpox, and A lost city

Intro

0:00This BBC podcast is supported by ads outside the UK.

0:05102 miles ago, the oil light came on. 100 miles ago, you noticed. Now, it's time to head to Take 5. This oil change, fall in love with your car all over again. In just 10 minutes, your dream technician will check your tyre pressure, top off fluids, change your oil, and verify with Carfax exactly what your car really needs, all while keeping you in the driver's seat. Take 5, the stay-in-your-car 10-minute oil change. Save up to 30% on your next oil change to Take 5. $15 value, valid to participating locations, terms and conditions apply.

0:39BBC Sounds, music, radio, podcasts.

MPOX Variant

0:44Hello, welcome to this week's 5 Live Science. I'm Chris Smith from The Naked Scientist. Coming up, the UK detects its first case of the new MPOX variant. Some are saying what took us so long. Also, the discovery of a lost city beneath the jungle canopy in Mexico. And a bit later on... Elections have always been subject to attempts at interference from the outside. It usually didn't make much difference, and it used to involve newspapers and radio and television and so on. The difference now is the degree to which somebody outside can find out exactly who you are,

1:20what you like, what you dislike, what really motivates you, what makes you angry, and they can play on that. Could technology swing the outcome of the US presidential race? The Naked Scientists on 5 Live.

MPOX Outbreak

1:33First this week, a case of MPOX caused by an outbreak of the monkeypox virus variant in Central Africa has now been detected in the UK. The World Health Organisation declared MPOX a global health emergency back in the summer. We produced a special programme on the virus at the time, and one of our contributors was Michael Marks, who's Professor of Medicine at the London School of Hygiene and Tropical Medicine. I asked him to bring us up to speed on what's been happening. There are sort of two families of this virus,

2:05one that circulates in West Africa and one that circulates in Central Africa, and this is a virus that normally lives in animals. Actually, it doesn't live in monkeys, despite the name, and it probably lives in rodents.

Virus Transmission

2:17And from time to time, the virus goes from being in animals to getting into the human population, and in humans, it causes an illness where you may have fever and headache and muscle pains, and most classically, people will develop a rash on one part or many parts of the body. And what do we know about the case that has been reported in the UK just now? We know that, as I mentioned, there are these sort of two families of the virus, and clade 1, which is normally thought to be the more severe virus,

2:52is predominantly spread in Central Africa. So although we've had many cases of MPOX in the UK before, those have all been clade 2 virus. And what's now been described is a case of clade 1, in fact, clade 1B, which is the first time this clade has been reported in the UK.

Case Details

3:11We don't have very many details. Obviously, we need to protect the confidentiality of the individual involved, but we understand that they have returned from Africa, from a part of the world where there is a lot of transmission at the moment of this clade 1 virus. And we have seen similar episodes in a number of other countries around the world, for example, Sweden. In relation to this large outbreak in Africa, what we're seeing is small numbers of cases then being imported to other countries around the world.

3:41And based on what we are seeing in humans who are part of this outbreak, we can anticipate probably our case will have similar sorts of symptoms. What will they likely be? Illness is normally characterised by what we call a prodrome, or that's a sort of illness that arises before the main symptoms. So the prodrome is a bit like having flu. So you might have fever, sore throat, headache and muscle aches. And then individuals will develop a rash. And that rash can be localised to the part of the body where you came into contact with the virus,

4:16or the virus can spread around the body through the blood and other parts. And the rash can then be all over the body. Most individuals have a relatively mild and self-limiting illness from which they make a complete recovery. A small subset of individuals may develop more severe disease, where the rash can be very extensive with hundreds of lesions all over the body.

Case Management

4:39How should they be managed, these cases, then? And I don't just mean the individual, because this is an infectious disease, so presumably a component of the management must also be consideration of who else they may have given it to or got it from. That's correct. So if we think about the individual, at the moment we don't have any specific drugs to treat MPOX. There are a number of drugs that are in studies, but there are none that we know for certain work. So management of the individual is really what we call supportive care. So that's analgesia, treating any additional infections,

5:12making sure that they're not dehydrated, making sure that they're generally looked after. And then there are the public health interventions, and they can broadly be thought of in two sections. So there's isolation of the case, so that they don't lead to further transmission, and tracing of that individual's contacts, so people that that individual has had close contact with, who might be at risk, so that they can be monitored. And if they do develop symptoms, they can be picked up very early. So that's sort of reducing the risk of onward transmission,

5:43and follow-up of the contacts. And then the second strategy is vaccination. So there are vaccines that are effective. And for example, they can either be given to contacts after they've had exposure of a case. We call that post-exposure vaccination. It's effective, but it's not the best strategy. And it's more effective to give vaccine in advance to groups of the population who we know are at the highest risk. So that's pre-exposure vaccination.

6:14In the UK, the previous outbreaks of MPOX have been very strongly amongst gay, bisexual men who have sex with men, and therefore they are the group who have been predominantly offered pre-exposure vaccination. How will the staff who look after this person, while they're presumably highly infectious because they're at the peak of their symptoms, how will they be kept safe? So again, there are sort of two broad strategies. The patient is being managed by a specialist infectious diseases unit

6:45with a lot of expertise in this particular disease and similar diseases. So there are what we call universal precautions. So as I mentioned, most transmission is really thought to occur by direct contact with the rash. So that can be managed through use of gloves and other protective equipment and sensible interactions with the patient. You don't, we think, catch MPOX simply from being stood in the same room five metres away from someone. So the basic universal precautions that we can take.

7:15And then secondly, as I mentioned, there is vaccination available. And because of the 2022 outbreak of MPOX in the UK, many specialist healthcare workers, those individuals working in infectious diseases units, have been offered vaccination. So again, we have two strategies, broad principles of infection control and then vaccination for staff managing these patients. And what do you feel the threat is, if any, for the wider public in countries in the West, like the UK, like Sweden? I think that the risk is relatively low, very low.

7:48In fact, you'll have seen that there was a lot of publicity when there was a case in Sweden, but there hasn't been subsequent publicity saying, well, there's now a large outbreak in Sweden. And the same is in fact true for most of the other countries where clade 1B has been exported outside of Africa. Michael Marks there from the London School of Hygiene and Tropical Medicine.

Antimicrobial Resistance

8:10Antimicrobial resistance is a natural process that occurs when microorganisms that cause disease become resistant to antibiotic drugs. It's a growing problem, one which former England Chief Medical Officer Dame Sally Davies described as posing a bigger threat than terrorism. One microbe in particular that's proving extremely troublesome, although you may well not have heard of it, is called Acinetobacter baumannii. And it isn't just resistant to one drug, it's effectively resistant to everything we have,

8:41to the extent that patients need special isolation precautions in hospital to prevent them passing it on to anyone else. The mortality rate is up to 50%. But necessity being the mother of invention, two teams have been working recently on a solution. One, based in Hungary, and whom we'll hear from in just a minute, is looking at the century-old approach of using bacteriophages, those are viruses that attack bacteria. But first, closer to home, Steve Baker at the University of Cambridge has developed a way to mass-produce antibodies

9:13which can neutralise and prevent infection with the agent, the danger post by which he's absolutely emphatic about. It's a problem that we hear a lot about, but it's really difficult to emphasise how important it is. There's a real chance that all the antibiotics that we have come to use and rely on are no longer going to be effective. So, therefore, we're desperate, really, for new solutions. The reason that we don't have any, or there's nothing that's forthcoming at the moment, is because it's been largely neglected for other things in recent years

9:46because pharmacy-dooker companies are less interested in it. And also, we've really gone through the whole kind of spectrum of different drugs we think that can kill bacteria, and therefore we really need new kind of alternative solutions. What's been your approach instead? So, what we've done then is think about how we can do things in a slightly different way and work out whether we can kill microorganisms with a different approach. So, rather than using small molecules, such as antibiotics, we have worked on an approach to try and develop antibodies.

10:19So, these are naturally occurring, but we can manufacture them to target specific components of the out of a bacteria to try and trigger the immune system to try and do something to kill the bacteria instead. That we've got sort of form in this area, haven't we? Because over COVID, for example, when you and I saw each other quite a bit, we were making antibodies that would attack the coronavirus and do, I presume, something quite similar. Right. So, this is then the reason we really wanted to try it, because this approach, so monoclonal antibodies, has been used for a whole host of different things,

10:51including cancer, but also is becoming more receptive for infectious diseases and particularly against viruses. However, it hasn't really been developed or scaled against bacteria, so we're one of the first kind of groups to try and do this and see whether we can identify things that we can hit with antibody on the outside of the bug. Which bacteria have you gone after, then? The bacteria we were interested in is a bacterium called Acinetobacter baumannii, and it causes really aggressive respiratory tract and bloodstream infections, and particularly people that are hospitalised.

11:22And the reason it's so important is because certainly in many countries in Asia, and also increasingly in Europe and the US, it is now untreatable with every antibiotic that's currently available. So if you're infected with one of these and you don't trigger a natural immune response to recover, then there's a good chance you'll die from it. So therefore, we saw this as a challenge to see, okay, this is a high bar, but can we use this technology to try and come up with something that's a bit different? And just to add to that, we do see cases in countries like our own

11:54when people come back from having been overseas. Do they bring it back with them, don't they? Yeah, right, and that's the case for most drug-resistant bacteria. So I think there's a bit of a, okay, this is a problem of other countries, particularly kind of poorer countries, but like coronavirus, it's bacteria can travel internationally, they don't need passports, and therefore they can end up in hospitals and healthcare systems anywhere in the world. So this is a problem, yeah, everywhere. So how have you got around this? What have you gone for on these A. sunita bugs, these problem bacteria?

12:26And how have you coupled it to what the immune system then does? Yeah, so our approach was working with a colleague of mine. They had this chimeric mice that allowed us to immunize the animal, and the animal then generated a large immune response to whatever we gave it. So rather than assuming we knew what to target, we gave the mouse a cocktail of different components of the bacterial cell and let the immune system decide which one was the most important things

12:57we thought we could target. And once the immune system starts making a response, how do you then get the bit of the immune system that knows how to make that antibody that you want? How do you get that out of the mouse and then turn it into something useful? So this is the clever bit because then there's a whole process to do this. So we could mine the cells. They're called B cells. These are cells that produce antibody. And these mice have a human B cell repertoire, which means they produce human antibody. So there's a mechanism for us to sort those cells. We collect them and then we go through a process

13:29of screening each individual cell that we can harvest to try and work out what they're producing an antibody against. So it's a lot of kind of grunt work to really find the matching combination of which antibody and how and where it's sticking to the bacteria. That gives you a cell that has the genetic know-how for making an antibody. So you can harness that. So you can now make these antibodies at scale. How are they used? So what we did in this experiment, we used it prophylactically. So we used it like a vaccine. The test that we developed was one

14:00where we gave these to mice and then let them develop a short-term response within 24 hours later and then we challenged them with the bacteria. And the idea would be if we were going to use it in people, yeah, we'd either inject it prophylactically or we'd give it intranasally. And then hopefully those people that were vulnerable going into such places where these organisms circulated would then have some degree of instant immunity. The idea long-term probably would develop them into more into therapeutics when if people had these infections, then we could then target the bacteria in the same way

14:31and actually specifically choose the immune system to kill those bacteria. And have you sussed out how these antibodies are achieving the therapeutic effect on the bacteria when they're there? Yeah, so we think that the antibodies stick to the outside of the bacteria and they label it and then they activate certain cell types and that means they get eaten by these macrophages and then they get destroyed. And we think that's a mechanism that these antibodies are performing by and we think that's why we can demonstrate they protect the mice we infect with the bacteria. Very encouraging news. That was Steve Baker

15:03from the University of Cambridge. We're now back to that team I mentioned in Hungary who are also trying to solve this same problem but their approach is a bit different. They first analysed thousands of samples of the Acinetobacter bacteria from around the world to build a map of which subgroups of the bugs tend to circulate where and for how long. And this they use to inform how to assemble suites of bacteriophages viruses that can selectively kill bacteria which are specific for the strains of Acinetobacter

15:33which are active in any given geography. Here's the Biological Research Centre's Balint Kintshesh. So one of the most promising alternatives of antibiotics is phage therapy. Phages are viruses. They are completely harmless to humans but can heal bacteria even the most antibiotic resistant superbugs. So they are very promising alternatives for treatment. However, they also have some drawbacks.

16:04The biggest problem with bacteriophage is that they are very specific. So bacteria change over time and therefore in nature hundreds of different types exist and each require different phages. In other words, each patient requires a different bacteriophage. So we asked the question if this bacterium spreads within hospitals how has it come that each patient

16:35require a different bacteriophage? Wouldn't it be possible to tell in advance which bacterium or which version of the Acinetobacter baumwani is going to cause the next infection if it spreads primarily within the hospital? And how are you trying to do that? To that end, we use genomic surveillance. So we saw that it works brilliantly to track the COVID pandemic and we thought, okay, why don't we use it for bacterial patogen

17:07Acinetobacter baumwani to track the different versions and have phage therapy. Is the approach then that when you suspect a person has this, you'd collect samples from them, do genetic analysis on the infection to work out where it sits in the family tree of this particular group of bacteria and therefore what phage might be best able to manage it? Is that the kind of direction of travel with this?

17:38Exactly. So we generated a detailed map of this bacterium. We basically put the different variants onto the map and answer questions. Was the diversity of this bacterium in a given geographic region like Western Europe or Southern Europe? And we found that even though this bacterium exists globally in hundreds of times, in a given geographic region, their number is limited.

18:10On average, we found that 17 versions of this bacterium exist in a given geographic region like Western Europe, which doesn't seem to be a lot. It means that maybe a handful of phages could be enough to target the majority of the infections in a given world region. Do we not have to be careful though? Because in this day and age, the world population is more mobile than it's ever been. And so we've got people turning up in different countries

18:41from the opposite side of the world on a regular basis and they could be bringing these things and therefore their particular type from their world region could be coming to a hospital near you anytime soon. And therefore it might inject additional genetic diversity and forms that won't respond to the phages that you had planned to use. Yes, that's correct. Therefore, we need to monitor these bacterium or actually all bacterium continuously to be able to see

19:13how fast they transmitted from one part of the world to the other. And we found that on average, it takes six years for a given country to change completely the Acinatobacter baumony types. In other words, it means that there is a six-year time window for phages to target the Acinatobacter baumony types of a given country. Do we have

19:44the right cocktails of phages for this though, ready to go? They are definitely not ready for therapeutic application, at least not in our region because currently in our region the legal framework is not ready for phage therapy. But there could be other countries where our phages can immediately be used. So right now I'm looking for partners. This is something that it is very easy

20:14to do with our map. By mapping this bacterium, I can easily pinpoint to the countries where the same types of this bacterium causes the problem. So I can directly contact basically clinicians and scientists who work in these countries and ask if they need our phages to treat patients.

20:45Balint Kinczes there from Hunren, the Biological Research Centre in Hungary.

Lost Mayan City

20:50You're listening to 5 Live Science with me, Chris Smith. Still to come, will technology sway the result of the US election? Before that though, a PhD student called Luke All-Thomas has discovered an impressive lost Mayan city concealed under a jungle canopy in Mexico. The find, dating back over a thousand years, includes pyramids, houses, sports fields and amphitheatres. Elizabeth Graham, Emeritus Professor of Mesoamerican Archaeology at UCL,

21:21told me how Luke and his colleagues did it. He was looking at what are called LIDAR images and LIDAR refers to a way in which laser beams can be shot at the surface of the earth and they reflect the topography like hills and valleys and even caves and that information can then be turned into a map. But the great thing about LIDAR is that it ignores the vegetation, the jungle. So it doesn't give you images of the vegetation,

21:51it just gives you images of the ground surface and this is fantastic for people like us who work in what people here call the jungle. On the ground, you can walk right past some really large structures sometimes because you can't see them because of the thickness of the vegetation. So you can see how much of an advantage something like LIDAR imagery is because it kind of gives us a map of the surface of the land and in this case it shows where people have lived thousands of years ago

22:22through the ruined buildings that are left behind. I gather that the study that produced the initial images was of a totally different kind. It was an environmental study that had nothing to do with archaeology and it was only fortuitous that the author got hold of the LIDAR data and then subjected it to his own analysis. Yes, because most of the LIDAR imagery up to now has been initiated by archaeologists who raised the funding to have LIDAR imagery of their particular site and the immediately

22:52surrounding area. But in this case, Luke had found images that were made in Mexico for an environmental survey and he thought he would take a look. Oh, I'll just, you know, see if through their survey we can recognize any structures and so they took three blocks of areas and lo, and behold, the LIDAR imagery showed structures just about everywhere. They varied in density. I think one block the density would have indicated rural structures but the other two

23:23were really dense. The remains of houses and buildings that were quite dense and one of them even had the remains of a city which they called Bellariana. Did they recognize the significance of what was coming up in these pictures as soon as they saw it or did they initially dismiss this as some other explanation? Oh, no, because by this time most archaeologists are familiar with the kind of imagery that LIDAR produces. You would have noticed quite well the buildings organized around patios and plazas

23:55and things like that just that don't occur naturally. So it was quite recognizable to the researchers that these were the remains of habitations from long ago. It's almost like a Tutankhamen moment isn't it for the discoverers this? Yeah, it's pretty exciting not just because there's been a new major city but also that we have this much in the way of settlement and I suppose a lot of my colleagues are hoping that the city will have inscriptions to tell us dates about rulers and things.

24:27What can you tell us about who the people who built these ruins were? When were they there and where did they go? The earliest dates on some of the sites are about 2000 BC but that has to do with some of the structure so there were people in Mesoamerica from about you know 10,000 but the people we call Maya were actually different groups with related languages but we call we say Maya because at at the time of the period in which some of the biggest cities were built

24:58they did share the rulers at least shared a language in the way they shared Latin in Europe and so that's that's the language that the inscriptions are written in then at about 800-900 AD the dynasties had a collapse and the whole landscape changed people spread out and you developed a lot of small cities so when the Spaniards came the landscape was covered with smaller sized cities smaller populations they weren't centered in these large cities which is evidenced by the site like Valeriana Presumably then

25:28this now opens the door to pointing us towards a rich archaeological seam which hopefully no one has been to previously and we have a chance to see some of this stuff in an undisturbed state There are many sites that have not been excavated this is a newly discovered one but there still are many that remain as ruined temples in the forest That was Elizabeth Graham at UCL Welcome back

US Election

25:55to 5 Live Science with me Chris Smith and today The United States has announced sanctions against some executives of Russia's state-funded news outlet RT and a number of other individuals accusing them of trying to influence the presidential election in November A lot of countries are going to try to manipulate our voters they're going to try to manipulate our elections that's what they do People not knowing where to go to get trustworthy facts The US election between Democratic nominee Kamala Harris

26:25and Republican nominee Donald Trump is going down to the wire Indeed this has been described by many as the closest presidential election ever seen Inevitably with tensions so high on either side the cry of electoral interference is a common one But just how is today's technology being used to sway voter opinion and to what extent? Well that's what we're seeking to uncover on this week's programme beginning with an outline of just how close this election is Scott Lucas is an

26:56expert on US politics at the Clinton Institute University College Dublin and at the University of Birmingham He's also founder and editor-in-chief of EA Worldview which is a leading site for coverage of international affairs So the dramatic change in this year's election was when President Joe Biden stood down and let Kamala Harris run this very very brief but intense campaign to try to hold the White House for the Democrats this time around Because probably those sentiments you've expressed have been reflected

27:27in the polling hitherto haven't they? We can focus on how close it is now in a second but there had been quite a gulf opening up between where Biden sat and Trump now The indicators beyond the polls was that Biden's age was sucking all the oxygen out of the room and so Trump's lead was widening including in the seven states that will decide the election As soon as Harris replaced Biden Trump's advantage in those seven states and indeed nationwide disappeared

27:57and ever since then it has been a 50-50 race and I think it will remain a toss-up all the way to November 5th And is it literally that close at the moment? It's sitting around the centre point 50-50 each way at the moment? So in the seven states that will determine this election in each of the seven the gap between Harris and Trump is less than 2% and in five of the seven states the gap is less than 1% And how do we regard social media in all this? Is that going to be a big player? It seems to be dominating all the headlines who's saying what online?

28:28Well social media has been an influence in US elections all the way back to 2008 when Barack Obama's campaign used that platform very effectively then we've seen as social media and the technology behind it develops and as you have new platforms that come forward that this is the way that people are reached quickly this is the way that not necessarily full discussions of issues but at least soundbites from the candidates are presented so I would say not only that social media has become more important I would say that social media actually is overtaking traditional media

28:59in being the platform for immediacy in terms of seeing the candidates and thus making your decision It's interesting though isn't it because Donald Trump got thrown off Twitter and then Elon Musk spent billions tens of billions buying it and has reinstated him and is also backing him so has Elon Musk basically spent tens of billions in order to help one potential candidate here? Well social media is not necessarily a neutral venue in terms of elections and what we have seen with Elon Musk

29:29takeover of Twitter converting it into effectively a personal platform which tries to propel his beliefs his views and his alliances is that this in effect is an attempt to make that outlet a Donald Trump platform so Musk who has personally given 250 million dollars to Trump you know this is not hidden the fact is is that Musk is now part of a social media environment in which the platform might be one where

29:59everybody can join in but the people running the platform can politicize it and tilt it to make a difference in an election. Indeed are there any rules around any of this because presumably all it would take is some lines of code to get inserted into the algorithm to just tilt the balance a bit and you could very dramatically change what people were exposed to who they were introduced to as possible followers etc and rebalance things in a different direction. The US government and the courts effectively gave up on

30:30regulating balance in media in the 1980s when they removed the fairness doctrine so that's not new. what has been significant is that with this brave new world of the media that we now have is that there's really been no attempt to bring in a regulation. There's no particular federal authorities at least in the United States that can tell Elon Musk you really cannot put up these posts which are flagrant violations of

31:01balance, flagrant violations of fairness and in some cases coming very very close to