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Hollywood Wants to Kill You
The Peculiar Science of Death in the Movies
Michael Brooks, Rick Edwards
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eBook - ePub
Hollywood Wants to Kill You
The Peculiar Science of Death in the Movies
Michael Brooks, Rick Edwards
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About This Book
'A wonderful book... Delightfully varied... As with all the best science writing, this book doesn't just give answers, it also asks interesting questions.' Daily Mail 'Captivating and intelligent! Who knew death could be this much fun?' Richard Osman Asteroids, killer sharks, nuclear bombs, viruses, deadly robots, climate change, the apocalypse - why is Hollywood so obsessed with death and the end of the world? And how seriously should we take the dystopian visions of our favourite films? With wit, intelligence and irreverence, Rick Edwards and Dr Michael Brooks explore the science of death and mass destruction through some of our best-loved Hollywood blockbusters. From Armageddon and Dr Strangelove to The Terminator and Contagion, they investigate everything from astrophysics to AI, with hilarious and captivating consequences. Packed with illustrations, fascinating facts and numerous spoilers, Hollywood Wants to Kill You is the perfect way into the science of our inevitable demise.
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Cosmologie1
Hollywood Wants to Kill Youā¦ WITH A VIRUS!
āDONāT TALK TO ANYONE! DONāT TOUCH ANYONE!ā
ā Contagion (2011)
In Contagion, a flu-like virus arises in Hong Kong. A visiting American businesswoman becomes infected just before she heads home, and brings the virus with her ā to devastating effect. Before long, she and her son are dead, and the authorities responsible for disease control soon realize they are facing a lethal pandemic.
Of the myriad ways in which Hollywood has imagined us dying en masse, the idea of a global pandemic is perhaps the most terrifying. Thatās because it is one of the most realistic ā as, thanks to the coronavirus pandemic, youāll no doubt be aware. Global health experts have hailed Contagionās plot as a highly plausible scenario if weāre unlucky enough to come up against the wrong virus. Pay attention: this film could save your life.
How Do Viruses Work?
Contagionās tagline is ānothing spreads like fearā, but thatās not really true. Viruses, arguably, spread faster. In the face of a pandemic, making people afraid enough to avoid all risk of catching the disease is half the battle. Unfortunately, viruses have evolved to win the battle. Thatās why they spread faster than fear.
Viruses are extraordinary things. We say āthingsā because we donāt know what they are, exactly. Biologists donāt agree on whether they are alive ā viruses sit right on the line between chemistry and biology, and they sit in a very menacing pose.
Perhaps the best way to think about viruses is as computer programs written in DNA, the molecule used to replicate biological machines (sometimes itās a related chemical, RNA). The program goes something like this:
1 Roam around until you find a molecular machine capable of replicating your DNA/RNA strand.
2 Take over that machine.
3 Replicate your DNA/RNA and create protein shields to protect it.
4 Assemble everything into a new virus particle.
5 Get out of there.
6 Go to point 1.
Viruses arenāt evil, as such. They donāt mean to do you harm. Itās just that executing the steps of this program inevitably causes you harm because the molecular machine they are looking for exists inside your cells. Itās the act of breaking into the cell, taking over the machine and getting out again that leaves a trail of devastation in its wake. Weāre not saying theyāre sorry about it, but itās also nothing personal: viruses are actually indifferent to you. Youāre not tasty (see Chapter 3) or a threat (see Chapter 4); youāre just useful and expendable.
Itās probably worth noting early on that we could also be talking about bacteria when we talk about Contagion. After all, they are deadly too. The Black Death that swept through Europe in the Middle Ages was the work of bacteria, not viruses, and it was more devastating than any viral outbreak has ever been. But at least we have some defences against bacterial infection these days.
Those defences are known as antibiotics. While itās true that some of our antibiotics are useless against some of these organisms (and some of these organisms are resistant to all of our antibiotics, which is dreadful in its own special way), we have NO technological weapons that kill viruses. None. We have some antivirals which can inhibit their spread, and our immune system can fight them to an extent, but there is no silver bullet against a viral infection. Thatās why, when you have a cold, your doctor tells you to just rest and please stop asking for antibiotics. Itās the best hope you have of deploying your bodyās natural defences to maximum effect.
Ironically, viruses do have defence mechanisms that work against us. The main one is stealth. That DNA they are ruthlessly working to replicate is contained within a protein ācapsidā shell that your immune system doesnāt actually recognize as a foreign body. The first your body knows about its presence is when a lollipop-shaped crowbar on the capsid shell pries open a cell membrane.
Take the influenza virus. You might have heard scientists talking about H1N1 or H5N2: the āHā is the lollipop-shaped crowbar. The molecule is called haemo-agglutinin, and it can take lots of different forms, each of which is designated with a number. The 1918 āSpanishā flu, for instance, was H1. In 1968, we saw H3 create a flu epidemic in Hong Kong. Every flu pandemic of the twentieth century brought a new H into the world.
How bad can it be?
Near the beginning of Contagion, disease control leaders gather to discuss what might happen. A central concern for them is Ro. This is the measure of how many new people will become infected by one carrier of the infection. The calculation is based on observing what has happened already in the outbreak, and the result will be affected by factors such as the percentage of people who have been vaccinated or local living conditions. If Ro is 10, each case will produce 10 more. The ideal would be a Ro of less than 1, which means the disease will die out fairly quickly. The 1918 Spanish fluās Rowas somewhere between 1.4 and 2.8. The virus involved in the 2014 Ebola outbreak had a similar Ro. Thatās not the only statistic you should worry about, though. The H5N1 bird flu virus has a Ro of less than 1 because it canāt be transmitted through the air, but it is also frighteningly lethal, killing 66 per cent of infected people, compared to the Spanish fluās paltry 10ā20 per cent.
The āNā stands for neuraminidase. This molecule evolved to get the newly made virus particles out of the cell where they were assembled; itās a kind of glass cutter that slices through a cell membrane. This, too, comes in many variants. In all, we know of eighteen Hs and eleven Ns.
This variation is part of the problem with viruses. There are so many different Hs because the RNA in influenza is a very poor copier of itself. The result of this is tiny changes in its make-up. This unceasing evolution makes it difficult for our immune systems to recognize it as a threat. The H is the only trigger our immune systems recognize, but if it changes shape just enough, thereās a good chance the immune system wonāt spot it. This is one reason why we have to make a new flu vaccine every year. Itās also why the HIV virus has been so devastating. It copies its own RNA so roughly that it evolved ridiculously fast, and our immune systems simply canāt learn what to look for.
So, perhaps we should see viruses as cool, deadly, dispassionate killers: the psychopaths of the microscopic world. Itās worth noting, too, that there are viruses that infect fungi, bacteria, insects and plants. They are part of the rich tapestry of life ā and, astonishingly, you wouldnāt be alive without them.
Somewhere up to 8 per cent of your genome ā the instructions to make a copy of you ā is composed of viral DNA. Roughly 100,000 pieces of your genetic make-up come from a particular kind of virus called a retrovirus, which inserts bits of its own genome into the DNA of cells it has infected. If it happened to infect sperm and egg cells, that viral DNA got passed on to the next generation.
In the past, our biology has occasionally put this DNA to work. Researchers now think that mechanisms as diverse as the immune system response and a placentaās protection of a growing foetus involve recruiting the facilities encoded in retroviral DNA that entered our ancestral genome more than 100 million years ago. So, although the virus feels like the bad guy in Contagion, know that viruses have already saved your life.
How Do Epidemics Begin?
In Contagion, we learn (spoiler alert) that the devastating, world-changing, havoc-wreaking virus was brought into the world after a bat dropped a piece of banana into a pig pen. If thereās one thing worse than a virus existing inside an animal, itās a virus that starts in one species and ends up in another.
Many viruses exist inside certain species without causing any harm. The bats that sparked the 2014 Ebola epidemic in West Africa, for instance, were āreservoirsā: they had the virus in their system but for reasons that are still debated, it triggered no symptoms. The problem arose when humans came into contact with the bats, giving the virus a new world of cellular machineries to explore.
As far as scientists can guess from tracing the roots of the 2014 Ebola epidemic, the whole thing may well have started with a toddler called Emile Ouamouno. In December 2013, Emile was playing in the roots of a bat-infested tree in Meliandou, a village in the south-east of Guinea. According to the villagers, he was grabbing and poking the bats. Toddlers being toddlers, itās very likely he came into contact with bat droppings, with some ending up on his fingers, under his fingernails and, eventually, in his mouth. Whatever the exact route, the virus got into Emileās body and he died a short while later. Within weeks, Ebola was rampaging across West Africa.
We first learned such cross-species transmission was possible back in 1933. A British researcher was working with ferrets that had been deliberately infected with influenza. One sneezed in his face, and he became ill. The scientists then worked out that they could transmit their own virus back to the ferrets. Presumably with some retaliatory sneezing.
This animal to human story is now familiar to virus researchers, and it seems to be the root of the 2019 coronavirus outbreak. In fact, in this century, three-quarters of new infectious diseases affecting humans have come from animals. Take HIV, for example. From genetic analysis, it seems that HIV arose from simian immunodeficiency virus (SIV) found in West African chimpanzees. Widely hunted for meat in the region, someone came into contact with infected blood and provided an environment in which the virus could mutate into the human form.
Mutation is key to the virulence of a virus. Essentially, different strains of the same virus can swap genetic material in a weird kind of viral sex. Often the new acquisitions donāt make much difference, but occasionally they are game-changers. In influenza, for instance, the result can be a new H or a new N. And that can mean a flu virus that has never infected humans suddenly possesses exactly the H it needs to bind to the receptors on human cells.
If the environmental conditions provide lots of opportunities for viral sex with multiple partners, the chances of something new and dangerous arising are heightened. Thatās why many experts on viruses warn that modern ways of life are facilitating viral orgies. Take factory farming, for example. In China, California and the American Midwest, agricultural operations known as āconcentrated animal feeding operationsā (CAFOs) bring together cows, pigs, geese, turkeys, chickens and anything else that can turn feedstock into a fat profit for the owners. These vast sites are awash with waste products and if the strictest food and hygiene regulations arenāt adhered to impeccably ā which you have to concede is possible ā the virus-laden faeces of one species will get into the food or drinking water of another. Inside the stomach of the second species, the virus will find a host of cousins with whom it can swap genetic material.
In a suitable environment, a virus will gather and swap
genetic material, emerging as a different strain
genetic material, emerging as a different strain
It wouldnāt be the first time such a thing happened. The Spanish flu killed somewhere between fifty and 100 million people in the early part of the twentieth century. Scientists who have attempted to trace its origins report that the virus contains genes from domestic birds ā chickens, for example ā and wild ones, such as ducks. Thereās also a genetic component from horses, donkeys and mules, which might have aided the jump to humans that were, at that time in history, constantly close to these animals.
Once we realized that the cells in the lining of a pigās respiratory tract, for instance, are coated with receptors that allow both bird and human flu to bind to them, we knew we might have a problem with insufficiently regulated CAFOs. Put pigs in the same space as birds and humans, and bird flu viruses h...