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Michael Brooks

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'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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Hollywood WantsTo Kill You

‘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

‘Great fun and makes you feel a hundred times cleverer.’

Charlie Higson, actor, comedian and bestselling author

‘A witty and informative look at how Hollywood kills us off. As a film buff and scientist I love this book.’

Maggie Aderin-Pocock, space scientist and presenter of The Sky at Night

‘Bracingly smart, deliciously nerdy and dead funny.’

Roger Highfield, Director of External Affairs at the Science Museum

About the Authors

Rick Edwards is a writer and television presenter. He is the host of BBC 1’s quiz !mpossible. Rick has a Natural Sciences degree from Cambridge, which he is finally getting some use out of.

Dr Michael Brooks is an author, journalist, and consultant for the New Scientist. His biggest accomplishment to date is not the PhD in Quantum Physics – it’s writing Rick’s favourite popular science book, 13 Things That Don’t Make Sense.

Together, they wrote the Sunday Times Science Book of the Year, Science(ish): The Peculiar Science Behind the Movies. They also present the award-winning podcast Science(ish) for Radio Wolfgang. Follow their every move on Twitter @science_ish and the website www.scienceish.org.

 

First published in hardback in Great Britain in 2019 by Atlantic Books, an imprint of Atlantic Books Ltd.

This edition published in 2020.

Copyright © Rick Edwards and Michael Brooks, 2019

The moral right of Rick Edwards and Michael Brooks to be identified as the authors of this work has been asserted by them in accordance with the Copyright, Designs and Patents Act of 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of both the copyright owner and the above publisher of this book.

10 9 8 7 6 5 4 3 2 1

A CIP catalogue record for this book is available from the British Library.

Internal illustrations © www.alternativeaesthetics.co.uk

Paperback ISBN: 978 1 78649 695 9

E-book ISBN: 978 1 78649 694 2

Printed in Great Britain

Atlantic Books

An imprint of Atlantic Books LtdOrmond House

26–27 Boswell Street

London

WC1N 3JZ

www.atlantic-books.co.uk

Contents

Introduction

1 Hollywood Wants to Kill You… WITH A VIRUS!

2 Hollywood Wants to Kill You… WITH ASTEROIDS!

3 Hollywood Wants to Kill You… WITH PREDATORS!

4 Hollywood Wants to Kill You… WITH ROBOTS!

5 Hollywood Wants to Kill You… WITH INFERTILITY!

6 Hollywood Wants to Kill You… WITH CLIMATE CHANGE!

7 Hollywood Wants to Kill You… WITH INSOMNIA!

8 Hollywood Wants to Kill You… WITH PLANTS!

9 Hollywood Wants to Kill You… WITH OLD AGE!

10 Hollywood Wants to Kill You… WITH NUCLEAR ARMAGEDDON!

11 Hollywood Wants to Kill You… WITH DEATH!

Acknowledgements

Index

Introduction

This book is for people who can tick the following boxes:

 I am going to die one day

 I enjoy watching movies

We should point out straight away that reading this book will probably not prevent your eventual death. There are limits to what you can achieve as an author, even when you’re as good at writing as wot we are.

Our goal is a little more modest. We think that, with Hollywood’s help, we can improve on who you are. So, if you can tick both boxes, read on.

It may not look like it, but this is a self-help book. We’re aware it doesn’t have an explicitly self-helpy kind of title. It’s not Six Ways You Can Improve Your Life by Obsessing Over Your Inevitable Demise While Stuffing Yourself with Overpriced Popcorn and Lukewarm Nachos or Harness Hollywood and Live Forever (In Your Loved Ones’ Hearts). But it will make you a better person through our three-step programme:

• Step one: watch some movies. Easy, huh?!

• Step two is almost as easy: read our descriptions of the various ways in which those movies usher in the Grim Reaper.

• Step three is a bit harder: it involves actually facing up to your own death.

The good news is, step three is optional. By the time you’ve completed step two, you’ll be a better person anyway. Why? Because, by completing steps one and two, you’ll be aware that death is everywhere in the movies. It’s not really that Hollywood wants to kill you. It’s more that it has no choice. Threatening to kill things is how you get a human being’s attention, and your attention is something Hollywood wants very badly.

Every good screenwriter and director knows that something in our programming desires, loves and craves a brush with death. We like to smell the ferrous tang of blood (metaphorically, at least). We thrive on the adrenaline that accompanies the threat. Perversely, it makes us feel alive, and that’s what encourages us to be better people and make the most of life.

That’s why all human cultures tell stories that revolve around the danger of death. For as long as there has been recorded history and conversation, there have been stories about death. The first recorded story, written on clay tablets 4000 years ago, is a collection of poems known as The Epic of Gilgamesh. What’s it about? A king’s fear of death and his quest for immortality. Some of the most gripping stories written since involve a hero who does battle with a deadly monster: Beowulf vs Grendel, Theseus vs the Minotaur or Rocky vs Ivan Drago.

This human desire for tales that deal with mortality has shaped Hollywood. That’s why you’ll usually get a brush with death near the beginning of your movie. In Bambi, the mother dies (sorry). Beauty and the Beast’s Belle has also lost her mother. In fact, so many Disney heroes have lost a parent that it’s hard to understand how they ever get their child-friendly ratings. Disney practically has you tripping over wicked stepfathers and evil stepmothers, or caring but incompetent aunts and uncles. From Frozen to Star Wars, dead relatives launch a shocking number of its plots.

And death is never far away elsewhere in Hollywood, because keeping death close heightens your movie experience. That’s why every hero or heroine has to face their own mortality, or deal with an existential threat that looms over them, their family, their community, their planet… maybe even their whole galaxy. Whether they take the form of viruses, sharks, asteroids, homicidal aliens or plain old knife-wielding psychos, death-dealing monsters are always somewhere close by.

It may not sound great, but it is. Partly, because it’s an excuse to explore science. Much of scientific endeavour is really about finding ways to avoid death. That’s why the pages of this book are filled with the exploits and insights of scientists. They look into outer space to examine the threat from asteroids. They try to work out how to describe death itself – do we mark the cessation of life from when the heart stops beating or when the brain can no longer light up an MRI scanner? How predators evolved, how they kill and how to avoid them have been major scientific themes throughout much of human history. There are very modern questions, too: is our entire species at risk because of artificial hormones released into the environment in modern plastics, for example? Is climate change about to hit a tipping point where our planet is plunged into chaos? Is our current epidemic of sleeplessness going to destroy our minds? And, after COVID-19, one of the greatest pandemics of human history, what exactly can we do about the existential threat that viruses create? Are disease and death inevitable, or are we on the cusp of a cure for everything?

In fact, Hollywood’s obsession with death is doing us all a favour. For if there’s one thing scientists know, it’s that a reminder of death makes us get things done. It’s the root of most medical advances, for obvious reasons. But it’s also the root of agriculture, the construction industry, clothing and all the technologies that started as military innovations. Civilization is, in many ways, a by-product of our uneasy relationship with death.

But it actually goes deeper than that. Various scientific experiments have shown that unapologetic reminders about death make us behave better towards our fellow humans. One study interviewed people about their attitudes to charity and found that people who were standing next to a funeral home during the interview placed a higher value on charitable giving than those interviewed elsewhere. Reminders about death make people reject the pursuit of wealth and fame, and make them focus on the relationships in their lives and becoming a better person.

In fact, made aware of our inevitable death, we strive to form a lasting legacy by creating things like books, or films, or families that will cherish our memory. An experiment that reminded German subjects about their mortality made them more likely to express a desire to have children.

Which is what makes this a self-help book. Dissecting the various ways in which Hollywood wants to kill you – or at least make you contemplate death – will ultimately make you better in every way. Mahatma Gandhi once said, ‘Live as if you were to die tomorrow; learn as if you were to live forever.’ This book can help you do both.

You’re welcome.

Rick and Michael

1

Hollywood Wants to Kill You… WITH A VIRUS!

‘DON’T TALK TO ANYONE! DON’T TOUCH ANYONE!’

– 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 – 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. That’s because it is one of the most realistic – as, thanks to the coronavirus pandemic, you’ll no doubt be aware. Global health experts have hailed Contagion’s plot as a highly plausible scenario if we’re unlucky enough to come up against the wrong virus. Pay attention: this film could save your life.

How Do Viruses Work?

Contagion’s tagline is ‘nothing spreads like fear’, but that’s 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. That’s why they spread faster than fear.

Viruses are extraordinary things. We say ‘things’ because we don’t know what they are, exactly. Biologists don’t agree on whether they are alive – 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 it’s 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 aren’t evil, as such. They don’t mean to do you harm. It’s just that executing the steps of this program inevitably causes you harm because the molecular machine they are looking for exists inside your cells. It’s the act of breaking into the cell, taking over the machine and getting out again that leaves a trail of devastation in its wake. We’re not saying they’re sorry about it, but it’s also nothing personal: viruses are actually indifferent to you. You’re not tasty (see Chapter 3) or a threat (see Chapter 4); you’re just useful and expendable.

It’s 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 it’s 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. That’s why, when you have a cold, your doctor tells you to just rest and please stop asking for antibiotics. It’s the best hope you have of deploying your body’s 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 ‘capsid’ shell that your immune system doesn’t 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 ‘H’ 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 ‘Spanish’ 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 flu’s Rowas somewhere between 1.4 and 2.8. The virus involved in the 2014 Ebola outbreak had a similar Ro. That’s not the only statistic you should worry about, though. The H5N1 bird flu virus has a Ro of less than 1 because it can’t be transmitted through the air, but it is also frighteningly lethal, killing 66 per cent of infected people, compared to the Spanish flu’s paltry 10–20 per cent.

The ‘N’ stands for neuraminidase. This molecule evolved to get the newly made virus particles out of the cell where they were assembled; it’s 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, there’s a good chance the immune system won’t spot it. This is one reason why we have to make a new flu vaccine every year. It’s 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 can’t learn what to look for.

So, perhaps we should see viruses as cool, deadly, dispassionate killers: the psychopaths of the microscopic world. It’s worth noting, too, that there are viruses that infect fungi, bacteria, insects and plants. They are part of the rich tapestry of life – and, astonishingly, you wouldn’t be alive without them.

Somewhere up to 8 per cent of your genome – the instructions to make a copy of you – 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 placenta’s 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 there’s one thing worse than a virus existing inside an animal, it’s 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 ‘reservoirs’: 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, it’s 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 Emile’s 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 don’t 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. That’s 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 ‘concentrated animal feeding operations’ (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 aren’t adhered to impeccably – which you have to concede is possible – 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 swapgenetic material, emerging as a different strain

It wouldn’t 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 – chickens, for example – and wild ones, such as ducks. There’s 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 pig’s 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 have the perfect opportunity to become infectious to humans. The emergence of a significant pathogen from such cavalier operations seems to be a matter of when, not if.

Not that CAFOs are the only potential source of a Contagion-like outbreak. Anywhere people are living in close proximity with animals is potentially a big risk. We’ve already met one ill-fated toddler. Lam Hoi-Ka, a three-year-old from Hong Kong, is another. He died in May 1997 of H5N1 bird flu. We don’t know how he caught it, but doctors quickly recognized the horrific symptoms (among other things, his blood curdled) and declared that anyone showing similar symptoms should be isolated immediately. Fortunately, H5N1 hasn’t evolved a mechanism that allows it to spread easily between humans (a few genetic mutations might do it, but it’s not straightforward even when scientists deliberately worked at making it happen). In the end, seventeen people were hospitalized, five of whom died from their H5N1 infection. The Hong Kong authorities killed every chicken on the island. But the disease still escaped – and it is deadly. Consider this: the Spanish flu killed just 2–3 per cent of those it infected. H5N1 appears to kill more than half the people it infects. And it is living in birds in at least sixteen countries.

That’s hardly surprising when you stop and think about it. In the twenty-first century, a virus can travel across the globe with unprecedented ease. Which is good news for the viruses, but very bad news for us.

Do Viruses Always Spread Like Wildfire?

Much of the suspense of Contagion’s story comes from the knowledge of a hidden threat just waiting to pounce. The lingering shots of the surfaces that infected people have just touched are surprisingly disturbing. And we should be disturbed. We should fear the fomites.

Every time you have a virus on your hand and it gets smeared on to an object – a doorknob or an elevator button – that object becomes a ‘fomite’. The word comes from the Latin word for ‘tinder’ because a sixteenth-century Italian doctor recognized that such contaminated surfaces could start the fire of contagion.

Fomites – objects or surfaces that host freestanding virus or bacterial particles – are everywhere in the modern world, especially where hordes of people are moving quickly through a space. In 2017, microbiologist Paul Matewele swabbed London’s public transport system in eighty different places. He found that seats, rails, walls and doors were awash with bacteria. The tube lines were host to ninety-five different types of bacteria. Taxis had somewhere around forty and buses had thirty-seven. Some of these varieties were among the type labelled ‘antibiotic-resistant’. There is, it seems, cause for concern. We can add to the advice in the film that Dr Erin Mears gives the hapless stooge on the bus. Yes, don’t talk to anyone. Don’t touch anyone. But also, don’t touch any thing. You’ll be creating deadly fomites.

Fomites play a significant part in the spread of certain contagions. The Ebola virus, for instance, isn’t spread through sneezing or coughing. It’s spread through touching contaminated bodies, faeces, vomit, corpses, floors, walls, buckets, clothing – anything where the liquefaction of the victim’s body has caused the virus to ooze on to it.

Plenty of other viruses create fomites, too. When researchers examine the places humans hang out, they find influenza on the towels of day-care centres and family homes; coronavirus on phones, doorknobs, toilet handles and computer mice; norovirus on drinking cups, lampshades and bed covers of hospitals and cruise ships; rotavirus on the refrigerator handles in paediatric wards; hepatitis on the glazed tile surfaces of bars; and adenovirus on the drinking glasses of coffee shops.

Keep the toilet lid closed, people

It’s a known problem on aeroplanes: those violent flushes create perfect conditions for throwing a spray of aerosolized waste into the tiny air volume of the aircraft toilet cubicles. But it’s not just a problem with airborne toilets. The medical literature tells of one person infecting 329 others with SARS via some dodgy facilities. In March 2003, a fault with the plumbing in the Amoy Gardens residential complex in Hong Kong caused a backflow from the drainage system when the toilets were flushed. This turned some of the toilet water into an aerosol spray that contaminated the air. The problem was made worse by powerful fans that effectively sucked the aerosolized water – and the viruses it carried – out into the bathroom.

A hundred years ago, all this was only a problem if you were in the locale of an outbreak. But these days, thanks to our global transport network and highly mobile urban populations, the outbreak can come to you. And it will.

‘We’ve created, in terms of spread, the most dangerous environment we’ve ever had in the history of mankind.’ That’s what Bill Gates told a reporter from Vox magazine in 2015. He wasn’t guessing about that; he had been looking at computer models of how past diseases would spread now. A new disease with the virulence of the Spanish flu, for instance, would thrive today. Thanks to the extraordinary interconnectedness of the modern world, with its cheap, ubiquitous flights, dense urban populations, crowded commuter trains and office blocks boasting mile upon mile of interconnected air conditioning flues, these days the Spanish flu strain would kill millions of people in a matter of months. To be precise, thirty-three million people in 250 days, if Gates’s computer model is to be believed.

The scenario is remarkably plausible, when you think it through from first infection – patient zero – to pandemic. Imagine patient zero gets put in contact with the virus by, say, shaking hands with a chef who’s just been handling infected meat and didn’t thoroughly wash his hands. Her hands are now coated with virus particles.

A study of people in public places found that they touched objects in their environment an average of 3.3 times an hour. They touched their own faces 3.6 times an hour. In private, the rate of touching the face is likely a lot higher. In Contagion it’s suggested as 2000 or 3000 times a day, which feels like an exaggeration. Whatever: now you’ve read this, and you’ve lived through a global pandemic, you’ll be aware that you do it a lot.

Every touch to the face is an opportunity for the virus particles on patient zero’s hands to get into her mouth. Being on the skin isn’t enough; it’s vital for most viruses to be ingested into the stomach or lodged in the mucous membrane of the airways. That’s when the lollipop appendage can grab on to a cell and crowbar its way inside.

Although the virus is hard at work inside her body now, patient zero isn’t showing any symptoms… yet. But she – like most healthy adults – will be able to infect people a full day before any symptoms develop. So she is already dangerous. She could still be infectious for a week after she starts feeling ill. What’s worse, if she is asymptomatic – harbouring the virus but never actually getting ill – she won’t adjust any of her behaviours, maximizing the chance of passing it on.

For now, then, she just continues with her day. And if that day involves international travel, a lot of people are in trouble.

She might kiss her lover goodbye, unwittingly making them the recipient of virus particles that are placed directly on the lips and into the mouth. Then she might ride the bus, slathering virus particles all over the handgrip and the seat back that she uses to steady herself as the bus lurches through the morning traffic. At the airport she’ll leave viruses here and there, but it’s on the plane that the devastation of twenty-first-century life really happens.

Every year, three billion of us travel on the world’s airliners. A 747 might be carrying 500 people. Old planes have air quality systems that aren’t up to much. If it’s a new plane it’ll have the latest HEPA (high-efficiency particulate air) filters that’ll catch 98 per cent of viruses, but frankly if a passenger is infected with a virus and starts to cough or sneeze into the air around them, that’s immaterial. Passengers seated within a metre or so have a significant chance of becoming infected. If the infected person is cabin crew, people all over the plane are at risk.

The truth is, we don’t know much about the exact numbers involved. There have been relatively few studies, and they all encountered idiosyncrasies in the way different airlines and different planes process passengers, airflow and cabin cleaning routines. What we do know is that delayed flights where the air conditioning is turned off while the plane sits on the runway could be especially deadly.

In 1979, an airliner carrying fifty-four people was kept on the ground after an engine failure. The ventilation system was switched off during the three-hour delay. One of the passengers had flu; within three days, 72 per cent of the passengers were ill with the same strain of the virus.

Are you a super-spreader?

Ever heard of Typhoid Mary? Her proper name was Mary Mallon, and she was an Irish-American cook working in the New York City area at the beginning of the twentieth century. At some point she became infected with typhoid, but she showed no symptoms of the disease. That didn’t stop her passing it on to the people she cooked for. Researchers believe she infected fifty-one people. Even though only three of those died, she was forced into quarantine. Mary was kept in isolation for three years, after which she was released and told to find work outside the kitchen, which had provided optimum conditions for her infection to be transmitted. Unable to earn a decent income, Mary changed her name and went back to professional cooking. She infected dozens more people with typhoid before she was arrested and confined to quarantine again for the rest of her life.

Mary would now be called a ‘super-spreader’ of disease. Disease researchers see many infectious outbreaks where a small group of people is responsible for a large portion of the spread. There are plenty of examples of super-spreaders. A 1989 outbreak of measles in Finland saw one person infect twenty-two others. During the 2002 outbreak of SARS in China, one man infected thirty-three others, and another man infected 138 people during a Hong Kong outbreak of the disease. Over fifty people contracted Ebola from just two individuals in the 1995 outbreak in the Democratic Republic of the Congo.

Super-spreaders are hard to spot, but they tend to have lots of close contact with people, and avoid seeking medical help until they are experiencing debilitating symptoms (if they’re not just carriers and don’t ever display symptoms). If you know someone like that, and there’s an outbreak occurring in your community, keep your distance!

It’s not just planes, of course. Buses, trains, departure lounges, subway systems and shopping malls all provide conditions conducive to the spread of infectious disease. Whether it is an airborne variant or transmitted through touch, the sheer volume of people travelling around the world every day makes this the perfect time to be a human-infecting virus.

More than four million people go through the barriers of the New York subway every day, for instance. Around five million use the London Underground. Over the forty-day period of Chinese New Year, people make more than 400 million train and plane journeys in China. Any one of these, especially if they’ve recently been in contact with the wrong animal, has the potential to be patient zero in a global pandemic.

What Do Viruses Do To Us?

One of the most chilling lines in Contagion lies within a researcher’s appraisal of what happened to Gwyneth Paltrow’s character. Once infected with the virus, ‘her body had no idea what to do with it’. Unfortunately, that’s not Hollywood exaggeration. It’s exactly what we see when new viruses arise. And bodies that don’t know what to do throw everything they can at the novel threat, possibly destroying themselves in the process.

There’s no easy way to tell you this. Sometimes, viruses actually make you kill yourself. Not deliberately. The problem is, they trigger the body’s defence system so strongly that it goes on a rampage. Ultimately, it destroys everything in its path – including your healthy cells. That’s why the Spanish flu was, paradoxically, so deadly to the young and fit. These people’s immune systems were so robust that, when they went out to fight the flu virus, the immune response didn’t stop until the people themselves were dead.

The first thing an infected cell does when faced with a foreign invader is secrete interferon. This is a substance that prevents new proteins from forming. In theory, it means the virus can’t create copies of itself, even if it has control of the cellular machinery. In practice, a lot of viruses have evolved to fight back, cloaking the fact that they’ve taken over. With the 1918 flu virus, for instance, interferon was hardly deployed at all.

OK, so the virus has started to replicate itself. Now the body is aware it has a problem, and the immune system deploys its second line of defence: immune cells. These release a molecule called cytokine, which sounds the alarm and summons more blood, and thus more immune cells, to the site of infection. When they come across a damaged, infected cell, the immune cells kill and destroy it.