In the vein of making videos about interesting stuff I come across, the other day I stumbled across the story behind these five dots:
Not much to look at – but! – these dots, which are known as the EURion constellation, are interesting because if they exist on a piece of paper you’d like to scan or photocopy, the machine will refuse to copy the paper.
This is useful for two things:
Preventing the copying of banknotes for money counterfeiting
In fact, the EURion constellation is very popular on banknotes! Here is a happy citizen, gazing with love at a shiny new £10 UK note, and sure enough, there’s a bunch of orange EURion dots on the left of the note:
I guess I’m pretty naive about how money is designed. Unless it’s something like the Euro 1, I assumed that every country designed everything that went on to their banknotes. Wrong – because the EURion constellation crops up on a few other notes.
From the Wikipedia, these include the Armenian dram, Aruban florin, Austrian schilling, Australian dollar, Belgian franc, Bosnia and Herzegovina convertible mark, Bulgarian lev, Canadian dollar, CFA franc, Chilean peso, Chinese yuan, Comorian franc, Croatian kuna, Czech koruna, Danish krone, Djiboutian franc, Dutch guilder, Egyptian pound, Euro, Faroese króna, French franc, German mark, Hungarian forint, Indian rupee, Indonesian rupiah, Japanese yen, Kyrgyzstani som, Kuwaiti dinar, Macanese pataca, Malagasy ariary, Mexican peso, Moroccan dirham, Namibian dollar, Netherlands Antillean gulden, Norwegian krone, Polish złoty, Romanian leu, Saudi riyal, Singapore dollar, South African rand, South Korean won, Slovak koruna, Surinamese dollar, Swazi lilangeni, Swedish krona, Swiss franc, Thai baht, Tunisian dinar, Turkish lira, Ugandan shilling, United Arab Emirates dirham, United States dollar and Zimbabwean bond notes.
So why am I not making a video about this? Weeeeeell, here’s the common sense.
What I wanted to do was make a video in which I would essentially have a slideshow of bank notes, zooming in to the constellations and highlighting five dots, possibly to the beat of something like Take Five, for any watching music nerds.
This would be cool because a) I could show you just how widespread this semi-secret symbol is, b) how some countries nicely use the constellation in their design, rather than the obvious “here are some dots” approach on the current UK notes, and c) it’d probably be more engaging than something like, say, a blog post.
The thing is – as I’d been thinking about, at length – governments across the world do not want you to make digital copies their notes.
They would like it if you didn’t include all, or even parts of, their notes in your projects. They even used things like, oh I don’t know, the EURion constellation to help to prevent people spreading pictures of banknotes.
The Bank of England has a whole page dedicated to the digital use of their notes, as well as a handy list of approved images which you can use without going to prison. You can also contact various countries’ banks asking for permission, but… that was never going to happen.
So in future, before embarking on a project, collecting the highest resolution images of as many of the world’s banknotes as I can find, scoping out free-use music in 5/4 timing and typing “counterfeiting banknotes” into Google enough times to get added to a watchlist, I will try to ask myself “is there any reason I shouldn’t make this?”.
From which the EURion constellation gets its name: a) because it looks a bit like the Orion constellation and b) because it was discovered on Euros – that’s right – discovered. This anti-fraud device was invented, quietly rolled out across the world and it seems like we only know about them because somebody noticed. ↩︎
The reason we call nasty computer programmes ‘viruses’ is because their behaviour mimics the real thing – spread between individuals, make more copies of yourself and repeat. So it’s kind of glorious that we can flip this around and learn about the viruses that make us sick by studying their digital analogues.
Here a team from London, Oxford and Changsha (in China) looked at the role of ‘hybrid spreading’ – a phenomenon shared by HIV infection and computer malware such as the Conficker worm. These viruses both spread over long-distances (bloodstream / the internet) and between close contacts (between cells / between computers on a local network). And both are also extremely difficult to get rid of once the infection is fully established because local ‘pockets’ of virus can be difficult to eliminate1.
The computer model the research team have developed suggests that to combat HIV infection in people, we need treatments that work effectively against both means of spread, and we need to treat earlier than we currently do. The team’s model may also provide a way of testing whether drugs are effective at stopping cell-to-cell spread; a measurement that is otherwise difficult to study.
During an infection, the cellular ranks of our immune system army fall into two different squads: Rhinos and Elephants. While the Rhinos’ orders are to charge headlong at the invader (on the double!), the Elephants have a more subtle objective: remember this enemy.
If you win the battle against the maraudering microbe, the brave and knackered fighters of Rhino squad are rewarded with “early retirement”1, but the Elephants (actually called ‘Memory Cells’) live on and await a repeat encounter with the enemy. Should the bug come back, the memory cells rapidly turn Rhino and destroy the germ before it can so much as dig a trench.
The problem with vaccines is that they are difficult2 and time-consuming to develop. When a brand new virus species causes an outbreak in the future, we will need another strategy to stop its spread in the short-term: vaccines are for old foes, not the new disease on the block.
But an interesting project underway at the Defense Advance Research Projects Agency (DARPA) is aiming to give us rapid vaccine-like powers by transferring the immunological memory from a single person to everybody else.
To understand how it works we have to return to the memory cell squad of our army. Just like a regular army, the memory cells comprise separate units which attack at short or long-range. It is the long-range attackers, called B-cells, that are the focus of the DARPA project.
B-cells wage war by releasing sticky chemicals that plaster themselves on to specific microbes. When smothered in these chemicals the germ is prevented from going about its business and is painted as a target for destruction. If the chemical, called an antibody, sticks strongly to the right spot on the germ: hasta la vista, buggy.
Each of our B-cells is stuck in their way. When they’re growing up, they rearrange their DNA to try to make antibodies that stick better to incoming germs, and only those that succeed get the job. As the successful will only ever make one version of an antibody, we can look at the cell’s DNA, find the antibody’s genetic code and make it in the lab – no B-cell required. And this is where the DARPA project comes in.
As described in a story published on the website Fusion.net, the idea is to recover B-cells from survivors of disease (for example, people recovering from Ebola) and learn the genetic code for the best antibodies targetting the infection.
So far, so good. But the next step? Inject DNA containing the antibody code into the blood of uninfected people, where it will be taken up by cells in their body, decoded and used to start pumping out the antibody. Should these people then catch the disease, the bug doesn’t just have to worry about the regiments of the immune system, it has to worry about the armed civilian populace.
This plan is audacious, and there are plenty of reasons to be skeptical about its success. Even if you get to the stage where your cells are happily pumping out the antibodies, viruses can throw up a number of problems:
they could mutate; changing shape so the antibody doesn’t bind any more
if they spread directly between cells rather than being released out into the open spaces of your body, antibodies won’t have a chance to bind them (HIV and herpesviruses, for example)
they may already have countermeasures against antibodies (again, herpesviruses)
But even if the plan didn’t work against everything, that doesn’t mean it won’t against any. And if it does work? That would be incredible.
Head over to Fusion for the full story, including much more on the technology of vaccination using DNA and the hurdles standing in the way of the technique’s progress.
So cool. Being able to image where a virus is hiding inside an infected animal or person is a big sci-fi-esque deal. Current bioluminescence imaging techniques, where the glowy-glowy genes of fireflies are engineered into viruses, are an excellent tool for studying virus spread in small animal models of infection. But what if you’re an AIDS researcher relying on larger animal stand-ins to study human disease? In this work, the authors used a system called immunoPET to see where simian immunodeficiency virus (SIV – a simian contemporary of the human virus, HIV) collected and spread inside live macaques. The system works by injecting SIV-specific antibodies into the macaques, which then lock on to the virus particles and stick to them. Cunningly attached to these antibodies are radioactive molecules that can be detected using a PET scanner (PET stands for Positron Emission Tomography, and is a fascinating medical tool). Thus, via the interface of antibodies, virology and PET combine to visualise the location and amount of virus deep inside the body. The work revealed unknown reservoirs of virus infection in the upper respiratory tract and could potentially act as an avenue for studying infection in people, though I’d guess that was some way off. Click through to see some great images of the work and more discussion.
Simply put: the current Ebola-afflicted countries had gotten complacent about Measles vaccination, had realised this and aimed to roll out large-scale vaccination campaigns – and then Ebola hit and ruined everything. The successful vaccination coverage in these countries is now way below where it should be. It’s also important to note that the same is true of other diseases. Western Africa would usually have a full anti-malaria campaign in action, but Ebola has wrecked the pre-existing healthcare infrastructure.
As an aside, this isn’t the first interesting science article I’ve read from Buzzfeed recently. Who knew it wasn’t just about the cats, lists and lists of cats?
A small study has shed some light on the immune response to Ebola infection. The immune responses of four people treated at Emory University Hospital were assessed to understand how the human body combats the virus. Interestingly, the patients had strong T-cell responses to the virus nucleoprotein, which wraps up the virus genome. As our current vaccine attempts are targetted at driving an antibody response to the virus surface glycoprotein, this new information could help us develop a superior treatment against the virus. The big caveat to note is that these infected individuals received novel anti-viral treatment that could have interfered with the normal development of the immune response, and (of course) the sample size here is just four people.
All this talk about stopping Ebola, but has nobody asked the virus what it thinks? No: it’s just another form of discrimination. Whilst this is 99% political parody rather than microbiology, I couldn’t resist – a great article where pox virus stands in for a pox on the UK political landscape. Perfect.
Honeybees toil endlessly to make delicious delicious honey, but just like you and me, they have their off days when they don’t feel the buzz. Mites, microrganisms and viruses are enough to put pupa off their pollen, and a sick hive can suffer reduced honey production to full colony collapse. With our vested interest in their well-being, we’ve swotted up on what blights our bees, but whether the unwelcome critters in our managed hives reflect those that bug bumblebees in the wild is less understood. Things I learned from the linked article: 1) there’s some spillover of viruses from our own workers to wild bee populations, with transmission possibly occurring from sharing the same flowers, 2) bee viruses have excellent names – black queen cell virus, deformed wing virus, acute bee paralysis virus, slow bee paralysis virus and sacbrood virus.
If our bees are propagating viruses that later swarm into the wild, birds provide the opposite flight path when it comes to flu.
I think the headline “Wild birds may spread flu virus” is kind of like saying “water flows downhill”, but the article itself is a useful look into how the H5N8 and H7N7 bird flu viruses are travelling around Europe. For instance, ducks on a farm in Yorkshire in the UK may have contracted H5N8 from migratory birds from Russia. How this happens isn’t clear yet, as poultry are kept inside and wouldn’t have mixed with the wild birds.
The guys at the University of Glasgow Centre for Virus Research interview herpesvirologist Professor Peter O’Hare. A great overview of the some of the history, problems and questions associated with those ‘creeping’ viruses of humans. Whilst Peter’s lab do some cool work (this one is a recent favourite – Open Access), he doesn’t include virus latency in his list of big questions in herpesvirology! 😦 For the sake of my fragile little feelings, I’ll assume this is because we’re answering some of the questions, rather than it not being interesting…
This article has been pretty popular online this past week. As Ebola lingers on towards the West African rainy season starting in April, we’re running out of time to aggressively end the outbreak once and for all. This article covers some important points, most notably:
Aggressive contact tracing can now be pursued in areas with few cases. This tactic is very expensive in terms of money and people power, but is the best way to halt further disease spread. However…
…a large proportion of cases in Guinea and Sierra Leone occur in people with no known contact with the sick. In other words, our current surveillance is failing to catch all known cases.
Small individual outbreaks are becoming isolated in different geographical regions, requiring aid work to be mobile rather than relying on bringing the sick to centralised centres. However…
…it’s going to rain soon. A LOT. This is going to hinder all transport in the region.
The virus isn’t gone yet, and if we let it, it’ll probably come back with a vengeance. I’ve not exhausted the important stuff in this piece. Check it out.
The beginnings of an interesting epidemiological detective story here. Recent Measles outbreaks in Quebec can easily be linked to the Disneyland outbreak in the states, but a small cluster of cases in Ontario have come from somewhere else entirely. But where? Measles was eliminated from Canada in the 1990’s, so the virus was likely imported from abroad.
Just goes to show, virus diseases may be extremely rare in your neck of the woods, but in today’s global society, I’d recommend you carry on vaccinating yourself and your family.
Bacteriophage are extremely cool. Every living thing on the planet has its own viruses, and bacteria are no exception. Despite the advent of antibiotics, doctors in the Soviet Union experimented and developed virus preparations to kill common bacterial diseases. Now with the shadow of antibiotic resistance hanging over the globe, people in the West are turning to these plucky ‘bacteria-eaters’ as our future saviours.
It’s not quite as a simple as that though. Bacteriophage (or phage) therapy requires knowing exactly what bug you’re trying to kill. Why? Because bacterial species are incredibly diverse and bacteriophage are highly species-specific. Think about mice and men – both are mammals, but whilst you could send a cat in to remove your mouse problem, sending in a cat to solve your human problem is going to result in more humans and lots of pictures on the internet.
This article gives a great introduction into the successes and failures of individual Western forays into the exciting world of bacteria-exploding viruses.
Parasitoid wasps are nightmarish critters of death and manipulation. For all the times you’ve been stung by a wasp, just be glad it didn’t lay its carnivorous unborn into your still living flesh. Evolution has ‘gifted’ us a huge number of such insects, which happily prey on as large a number of different bugs to both incubate their eggs and eventually provide the newly hatched young with a live-in shelter to eat their way out of.
“Mike?!” you yell, “Why are you ruining our brains forever with this? Where are the viruses?!”
Worry not, viruses are at work here. In fact, this article deals with just one such virus story (I’ll save the other for a later write-up).
In brief, because you should dive into the linked article:
Wasp injects ladybird (ladybug) with an egg. Ladybird carries around egg, which later hatches and eats its way out of the ladybird. Wasp wraps itself in a cocoon to develop into an adult and the still living (but presumably now-porous) ladybird guards the cocoon from predators. Why? Because a virus, named D. coccinellae Paralysis Virus, or DcPV, that lives in the wasps and their eggs, infects the brain of ladybirds and turns them into zombie guards. Nature. You are scary.
OK, let’s get serious. A report into what we know about Ebola transmission has been published this week, and the media has leapt on to the authors’ opinion that the virus might spread by air as well as by contact. I don’t see a problem with the media’s interpretation of the report: the news seems to be carrying the salient points made by the piece. But the fact of the matter is that the evidence to back up aerosol transmission of Ebola just isn’t there. We know that people get infected when they come into close contact with the very sick and/or dying: people leaking virus-laden fluid into their immediate surrounding environment.
The possibility of transmission of virus cast into the air by the coughing sick – possible, but paling in comparison to the aforementioned infectious fluid – does not match up to the fear of a ‘Hollywood-style’ virus epidemic. The sick spread the virus to one or two people by close contact, they do not infect dozens by lacing the air with virus particles.
Could the virus evolve to use a different route of transmission though? Suddenly infecting through the air rather than by contact? No. A scene in the movie Outbreak, in which scientists crowd around an electron microscope image of an Ebola-like virus, before and after the “evolution of hair-like molecules” which “enable the virus to spread through the air” is firmly lodged in fiction (for the record, despite being objectively terrible, that movie is ace).
This topic is deserving of full articles to explain this reasoning and the outbreak as it stands, and so I defer to two:
Finally, because choice of language is more important than we think, a small piece on ditching the term ‘pathogen’. This article isn’t virus-centric, but that’s really the point. We focus on the bugs – the “pathogens” – when we research disease, because we hold them up as the reason for the illness. But in reality, disease isn’t a one-way street. Our immune systems are often responsible for most of the damage done to us during infection, and some people can be asymptomatically infected with viruses, bacteria or fungi, when others become desperately ill.
The term pathogen isn’t going anywhere, but if we think about the pathology of infection a little more holistically, perhaps we’ll make better progress eliminating it.
The tempo of publishing to the site is a little lower than I want at the moment. While I’ll always publish the weekly links, I’ll return to longer writing when stuff ‘behind the scenes’ has calmed down a bit. Now is one of those times, but a more normal service should resume shortly. For this week, I’ve a report, a video and a podcast to feed your audio-visual thirst for virology:
News of Ebola’s ‘death’ may have been greatly exaggerated – including by yours truly. For the second consecutive week in a row the number of new cases has risen in all three afflicted countries. We’ll have to pay careful attention to disease trends from here on. Extinguishing the last embers of this outbreak may require even more water than anticipated.
Ever looked at a 3D reconstruction of a virus particle and found the whole thing boringly static? No me neither, BUT this video demonstrates just how fluid a poliovirus particle in motion may be. The second half of the video looks behind the curtain of such simulations. No wizards here (well, not magic ones anyway…), just massive supercomputer CPU arrays. It’s all really cool (literally and figuratively).
I’ll admit, I generally think of (and refer to) virus capsids as protein shells – but rigid and brittle these particles are not. Perhaps coats is a better metaphor, something protective but allowing for motion.
Speaking of language and its careful use, I only just got around to listening to the linked episode of This Week in Virology, featuring guest Paul Duprex of the National Emerging Infectious Diseases Institute in Boston. The episode focuses upon the debate surrounding so-called “gain of function” experiments. A previous example of such an experiment would be the adaption of influenza to transmit between ferrets, in order to understand the mechanics of virus evolution and transmission in new hosts.
Proponents of such work say it’s necessary to understand and combat the results of phenomena occuring in wild flu infections. Opponents suggest that such work may create new pandemic viruses that would endanger global human health if they were accidentally released. Given the nature of the debate, the rhetoric is being horribly ratcheted up by those against this work.
Whilst sometimes wishing it had a bit more teeth, I appreciate both Paul Duprex’s defence of the work and his calls for the return to reasoned debate, because there’s one to be had. To quote: “if it’s a fight, no one’s gonna win”. I think he’s probably right.
Measles virus is in the news recently for all the wrong reasons, but how can the virus make such a roaring comeback in developed countries if vaccination campaigns slip? The answer: it is insanely contagious. And it needs to be – once you’ve had the virus you are immune for life – so if susceptible humans are around to be infected, the virus needs to get at them to survive and continue spreading. The article also touches on a cool thought that seems paradoxical to how well the virus can spread: because it can only infect people and not animals, it’s a great candidate for eradication from the planet.
When it comes to transmission between hosts, measles is at the ‘hit-and-run’ end of the spectrum: infect human and get out before the immune system kills every last one of you. On the complete opposite end of the spectrum we have endogenous retroviruses.
Retroviruses, like HIV, bury themselves in your DNA. Every time an infected cell divides into two, you get twice as many copies of virus. But when such viruses get into sperm or egg cells, things get weird. If the infected sperm or egg goes on the make a new lifeform, every cell in the new life’s body will contain of copy of the virus! Surely this must be rarity, right? Nope. In human beings, this has probably occurred more than 30 times. But as the article concludes, apes (including humans), may have finally had enough of picking up these stowaways.
For a third story, this week saw a ‘great’ example of the science media hype machine in action, not helped by the study authors’ press release one bit. Here are 5 tweets from Stephen Curry regarding both the study and one example of an accompanying news report that deftly summarised the article I had planned to write this week. Curses.