Flu: A Social History of Influenza E-Book

Tom Quinn

• Herausgeber: IMM Lifestyle Books
• Kategorie: Geisteswissenschaft
• Sprache: Englisch

Seitenzahl: 408

Veröffentlichungsjahr: 2008

Beschreibung

It sounds innocuous compared to war, plague and famine, but flu is actually one of the world's biggest killers. Since the first documented pandemic of an influenza-like disease in 1580, 31 worldwide influenza outbreaks have been recorded, culminating in the pandemic of 1918 that killed an estimated 50 million.This fascinating book explores the havoc caused by the world's most deadly virus - and the destruction left behind in its wake. From its initial identification by the Greek physician Hippocrates in the 4th century BC to the Spanish flu pandemic of 1918, the author explores the social, medical and scientific ramifications of the major outbreaks that have occurred over the centuries - and the potential ramifications should such a pandemic occur in the modern world.The likelihood and consequences of a pandemic occurring in the event of the highly pathogenic H5N1 strain of avian flu jumping species is also explored, along with recent scientific attempts to alter the structure of the virus in order to destroy it or ameliorate its virulence.

Leseprobe

Tom Quinn is a journalist and social historian.The author of more than 30 books, includingBritain’s Best Historic Sites (New Holland, 2011), Tom is also the of Country Landowner magazine.

A Social History of Influenza

Tom Quinn

This edition published in 2011Printed edition first published in 2008 by New Holland Publishers (UK) LtdLondon • Cape Town • Sydney • Aucklandwww.newhollandpublishers.com

Garfield House86–88 Edgware RoadLondon W2 2EAUnited Kingdom

80 McKenzie Street, Cape Town 8001, South AfricaUnit 1, 66 Gibbes Street, Chatswood, NSW 2067, Australia218 Lake Road, Northcote, Auckland, New Zealand

Text copyright © 2011 Tom QuinnCopyright © 2011 New Holland Publishers (UK) LtdTom Quinn has asserted his moral rights to be identified as the author.

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 written permission of the publishers and copyright holders.

ISBN: 978 1 84537 941 4 [Print]ISBN: 978 1 78009 106 8 [ePub]ISBN: 978 1 78009 107 5 [Pdf]

Publisher: Aruna VasudevanSenior Editor: Kate ParkerDesign and cover design: Peter CrumpProduction: Melanie Dowland

Note: The author and publishers have made every effort to ensure that the information given in this book is safe and accurate, but they cannot accept liability for any resulting injury or loss or damage to either property or person, whether direct or consequential and howsoever arising.

To Wado

Contents

Acknowledgements

Introduction – The Barbarian at the Gate

Chapter 1   Viruses – What Are They and How Do They Work?

Chapter 2   The Age of Superstition – From Ancient Times to the 17th Century

Chapter 3   The Age of Reason – The 18th Century

Chapter 4   A Shrinking World – The 19th Century

Chapter 5   The World’s Worst Pandemic – The ‘Spanish’ Flu of 1918

Chapter 6   The Aftermath

Chapter 7   The Mutant Enemy – Asian Flu (1957) and Hong Kong Flu (1968)

Chapter 8   Jumping the Species Barrier – Avian Flu

Chapter 9   Finding a Cure

Glossary

Bibliography

Acknowledgements

‘The greatest part of a writer’s time is spent in reading, in order to write; a man will turn over half a library to make one book.’

When Samuel Johnson wrote that, 250 years ago, he was certainly thinking of libraries containing at most a few tens of thousands of volumes. Today, the author is faced with the prospect of turning over far more books – not to mention magazines and journals – than ever before, particularly if he is treading a well worn path.

Writing this book presented a curious mix of problems – specialist journals are a rich source of material about flu and viruses in general but they do not touch on the social aspects of disease or if they do it is only, as it were, incidentally. Similarly, books – with a few notable exceptions – tend to concentrate on the scientific aspects of influenza. The history of influenza as it affected individual lives is much harder to come by, especially when it comes to primary material – the nitty gritty of real lives reported in real time. Given that difficulty it has to be said that this book would hardly have got off the ground without the generous assistance of a large number of individuals and organizations, but particularly specialist libraries.

We tend to forget that libraries – specialist libraries – would not and could not function without the skills of the staff who run them. Books and journals may be available for all in these institutions but it is the librarians who provide the route map that makes any major collection of material genuinely accessible. Their efforts on behalf of specialist researchers usually go unnoted and unsung. My own experience in a number of libraries across the UK and elsewhere reminds me that few books – apart perhaps from works of fiction – would reach the booksellers’ shelves without the efforts of these individuals who work in obscure corners yet provide enormously helpful advice to anyone who needs their help. Authors draw hugely on the experience and knowledge of librarians to short circuit what might otherwise be a long and tedious journey towards the right journal, the appropriate reference work. At the same time librarians tend to be a rather selfeffacing lot, which may be why those who gave me the most help tended to be least keen on being publicly thanked. So without mentioning them by name I’d like to thank all those librarians who pointed me in the right direction or saved me from obvious blunders and fruitless searches.

One of the most extraordinary things about writing a book such as this is that the process of research brings one not into the dry history of kings and queens, of impersonal and imperial development, but rather gives one a rare glimpse into the personal everyday lives of long vanished individuals. These individuals left no great monuments but took part in, or were victims of, some of the most exceptional events of the past century and more.

Without the personal testimony of survivors of, for example, the great flu pandemic of 1918-19, a book such as this would not be possible. It must have been immensely painful for the survivors of families almost wiped out by Spanish flu to recall again for contemporaneous researchers the horror of those days, but their memories have helped scientists, medical researchers and historians immeasurably. I would like to thank those descendants of survivors who were unfailingly patient and polite in the face of what must have sometimes seemed an endless stream of enquiries from me. They were also diligent in answering my often lengthy letters.

In earlier centuries many doctors, struggling with the weight of history and their own inadequate equipment, were also prepared to spend a great deal of time writing in journals and in letters to colleagues. These accounts frequently contain remarkable detail on patients’ symptoms, the progress of the disease and their own attempts, however futile, to cure the sick.

Doctors were particularly good correspondents and much of what they wrote survives in record centres and libraries up and down the country – finding one’s way through these documents is a nightmare for the uninitiated and I would like to thank a number of individuals including Tom Pike, Tim Kehoe, Andrew Hall and Pietro Lampedusa for helping me through a mountain of documents.

I would also like to thank a number of living doctors who didn’t hesitate to share their expertise and knowledge of influenza – particularly avian influenza – with a layman.

Virologist Patricia Davis deserves a huge thank you for carefully reading the book and rescuing me from numerous foolish errors of both emphasis and fact. Errors and misjudgments that remain are, of course, all my own.

For help with practical, emotional, logistical and general historical matters I’d also like to thank Wado Wadham, Barbara O’Flaherty, Richard Jarman, Karen Warren, Faith Glasgow, Sarah Storey, Juliet Quick, Mr Scrivens, Deborah Fisher, Mary Corbett, Eric Gray, Mr Busby, Rachel Lennox, Richard Smith, The Latimer Road Fishing Club, Tom Marmoset, Lol Plummer, Louise Davies, Lord Sharpe of Bromley, The Hon Mel Capper, Nicola Bird, Emma Westall, Katy Quinn Guest, Alexander Quinn Guest, James Quinn Guest, the late Deborah Anne Quinn, Jessie Cooke, Nina Porter, Sara Doak, Corinna Marshall, Jane Smith, Robert Pike, Frances Jackman, Julian Bell, Jane Simms, Minky, Mona and Captain Swing.

If I have missed anyone in my relatively restrained list above, I’m sure they will understand but to what might best be termed the inner circle – that is, my children and partner Charlotte not to mention London’s most intelligent dog, Nutmeg – I’d like to say an extra thank you.

And last but by no means least I would like to thank the person with the most difficult job of all – Kate Parker at New Holland who has been unfailingly patient despite having to put up with shortfalls of text, late changes of heart, mis-spellings, obscure phrasing and occasional bouts of authorial lunacy!

A Social History of Influenza

Introduction – The Barbarian at the Gate

Biblical references to plagues and famines reveal one of our deepest and most entrenched fears. In the era before science it must have seemed that the gods had turned against human society when the crops failed or when, for no reason that could be discerned, people began to sicken and die. Across the Old World, abandoned villages and towns – many now buried beneath desert sands or on windswept promontories – bear witness to an ancient visitation by epidemic disease.

In England abandoned medieval villages are common – bubonic plague, the Black Death, was often responsible for mortality on such a scale in some communities that the survivors moved away for good, partly because the community was no longer capable of sustaining itself and partly, no doubt, because the villagers feared that the place itself had somehow been cursed by the gods or by evil spirits.

Punishment of the gods

For millennia the arrival of plague was among the most feared of all events and offerings to placate the gods were made when the first members of the community began to die – perhaps as in the case of smallpox – horribly disfigured and in great pain. When the sacrifices did not work the people would perhaps have believed that they had offended the gods so greatly that no amount of sacrifice could placate them. The curse of the gods that came in the form of disease would have reached a level of particular intensity some time between 10 and 20 thousand years ago when, according to the best archaeological evidence we have, settled communal life for human beings began in earnest.

Settled community living had at least one massive drawback that could not have been recognized at the time – it ushered in the dawn of epidemic if not pandemic disease as virulent bacterial and viral infections began to exploit the large numbers of potential victims concentrated in particular areas. Before the era of settled villages and then towns of increasing size, human groups would have typically been small and either nomadic or semi-nomadic and probably based around extended families, much as chimps and bonobos – our nearest relatives – still live today. Isolated communities containing small numbers of related individuals were far less likely to suffer devastating epidemics.

The ability to domesticate animals and to grow crops was a key factor in the earliest development of settled communities and the life and prospects offered first by the farmstead and village and then by the walled town must have been compelling. We have never looked back and the number of people who live in cities and towns still grows year by year across both the developed and the developing worlds.

As the scale of early settled communities increased so too did the scale of viral and bacterial attack whose impact would previously have been minimal. The risk of attack by disease was analogous, if you like, to the risk of attack by those still unsettled tribes drawn to the concentrated and immovable mass of a settled town with its wealth of potential plunder. A walled town would have seemed an easy target for a marauding tribe tempted by the lure of money, slaves, women and food. Greek and later Roman society’s greatest strength and paradoxically its greatest weakness was the city. Living in a city brought the perennial, almost mythological fear of attack from outside whether by disease or by barbarian hordes. Germanic tribes – who typically moved about rather than choosing to live in cities as the Romans did – always posed a threat to those who lived a more settled existence.

The diseases that periodically struck at cities were at least as deadly as these human attackers, and it was impossible to stop them. The plagues came out of nowhere to lay waste to whole populations and, having done their evil work, they disappeared as mysteriously as they had come, leaving baffled and weakened survivors or a ghost town inhabited only by the dead.

We know from archaeological evidence that infections, including some that are still with us today, destroyed some of the ancient world’s most famous cities. Viral and bacterial disease took a firmer grip on people’s lives at this time because they were perfectly fitted to thrive where humans gathered and lived in large numbers. Man had no knowledge of the relationship between hygiene and infection; no awareness of bacteria, let alone viruses; ancient peoples could only wait and hope to placate their gods.

If placating the gods failed, they might try a host of different approaches: isolating the afflicted (not a bad idea even by modern standards, but difficult to do effectively) or wearing red, or sniffing vinegar-scented nosegays. Even if these things did no good in reality they must have been comforting – better than doing nothing at all.

Superstitious remedies

Other ideas had disastrous consequences. During the terrible outbreak of bubonic plague that afflicted England, particularly London, in 1663–4 it was assumed that dogs and cats were spreading the contagion so as many as could be found were killed. The result was actually to make the situation far worse since plague was spread by fleas carried by rats. With the cats and dogs almost eliminated there were no predators left to control the rat population and the plague spread more easily as rats (and their fleas) multiplied.

Practical but mistaken measures like this were matched by what we now see as equally mistaken ideas for looking after those who had already succumbed to a particular disease. Bizarre practices with no basis in science developed, and not just for viral and bacterial disease. As recently as 1700 it was still medically accepted practice following surgery for gallstones for the wound to be sewn up and then old milk poured over it. This must have increased the risk of infection at a time when the operation was highly dangerous anyway – one in two died. The fact that 50 per cent of those cut for the stone survived presumably made 17th-century surgeons believe that they had been saved by the application of milk. In fact far fewer would probably have died had the milk not been applied in the first place – the bacteria it contained would certainly have been more harmful than beneficial.

With epidemic disease, attempts at curative measures seem, from a modern perspective, to have been almost random – bleeding the patient was popular, mercury was sometimes given and there was a near obsession with the need to empty the bowels, the latter idea derived from the ancient Greek physician, Hippocrates.

Such ignorance lasted well into the 20th century, as we will see. By then of course we did not rely on guesswork for all our medical procedures but on science. Science was applied in many areas but it has only recently – much more recently – begun to catch up with what is arguably our greatest medical adversary, the virus. This is why, as recently as 1918, in addition to sensible scientific measures all sorts of crackpot cures were tried for flu that had no effect at all and may even have made things worse. Desperate situations call for desperate remedies and in this respect modern man – faced with a disease he cannot control – is not that different from his ancient ancestors.

But if city and town populations were woefully ignorant of the risk of infection through open wounds, lack of hygiene and overcrowding they were even more in the dark when it came to understanding how or why a third or even half their numbers might suddenly be struck down by something that severely incapacitated then killed quietly, quickly and inexplicably.

A combination of a superstitious suspicion that malign influences must be at work combined with a vague sense of being enveloped by a mysterious and invisible miasma gave us the name of what is probably the most infectious of all illnesses – influenza. Various dates are given in various sources for the origins of the word but late medieval Italy is probably the most likely. According to the Oxford English Dictionary the word influenza (Italian for ‘influence’) was first recorded around 1504. The Italians thought of flu as a malign influence somehow linked to the position of the planets – whenever influenza struck, astrologers explained that the planets were misaligned, which resulted in this strange malady that could not be seen or heard or smelled, yet had the power to kill.

The scientific method

By the standards of the time the attribution made sense. Western society was only beginning to understand some aspects of the study of science, or natural philosophy as it was then known. The Renaissance involved a return to the questioning that had typified the ancient Greek and Roman search for knowledge. The medieval church was beginning to lose its grip on a world it had insisted humankind should not question or try to understand. To do so was blasphemous. Still the old ideas lingered, however, and it was to take several centuries – until the invention of the electron microscope in the 1930s in fact – until the last barrier to understanding some of our most lethal diseases was removed.

For those at the dawn of the modern scientific age some headway could be made in treating some diseases, but flu and other virus-borne diseases were attributed to a malign influence because there was no alternative explanation. Diseases that weakened and often killed yet seemed to come from nowhere were made to fit into a world view that saw the influence and intervention of gods and demons as a daily reality.

It is highly unlikely that influenza made its first appearance at the time it was first recorded. It has, like so many viral and bacterial diseases, flourished since those first settled communities, and has probably been around in some form since homo sapiens first evolved. Without concentrations of people it would have been far less noticeable and perhaps even milder in its effects.

Bacteria and viruses reproduce incredibly quickly relative to human reproduction and the greater the number of generations of an organism the greater the chance of genetic mutation – genetic mutations are errors in the process of DNA (deoxyribonucleic acid), or in the case of flu, RNA (ribonucleic acid) copying. Most mutations do not give the organism a reproductive advantage. But every now and then a mutation does give an organism a reproductive advantage over individuals who do not share that mutation. Individuals with the mutation are more likely to reproduce so they come to dominate the population. Mutations often confer an advantage on viruses because they enable the virus to avoid the immune response of the human body, which would otherwise destroy it. As we will see viruses – and particularly the flu virus – mutate at an astonishing rate.

This book is about the flu virus and its effects on humanity over the past four centuries and more. I’ve looked briefly at reports of disease from much earlier – from ancient Greece for example – but it is very difficult to be sure we are talking about influenza in the sense that we now understand it when we read ancient accounts of disease and epidemics.

Epidemics and pandemics

A pandemic is defined as a disease that crosses between countries and whole continents. The word pandemic is derived from the Greek pan meaning all, and demos meaning people. An epidemic spreads across particular countries. Much has been written about the most infamous flu outbreak of all – the great pandemic of 1918 – but historians have tended to concentrate on the medical rather than social side of what happened, and they have largely ignored earlier epidemics and pandemics.

There were a number of significant flu epidemics and pandemics before 1918 and there have been several since. Most worryingly, however, is the fact that despite the best efforts of modern science we are permanently in danger of a new flu epidemic if not a pandemic.

The early part of this book looks at the evidence for flu infections since the time of Hippocrates, who is popularly supposed to have first mentioned what may have been flu or a flu-like disease. Without the benefit of science it was difficult during earlier epochs to define and clearly demarcate various illnesses – even today many of us find it difficult to distinguish between a cold and a mild bout of flu. In earlier times the difficulty was much greater as communities, though often substantial in size, were relatively isolated by the difficulties of travel and communication, and what afflicted one community might not seem quite the same as an illness that seemed to spread rapidly through another community.

In England the ‘sweating sickness’ mentioned in various documents during the 15th and 16th centuries may have been a virulent form of flu or it may have been a form of what we now call hanta virus. Again, at this distance it is difficult to know. In Edinburgh at the end of the 16th century an ailment called ‘the new acquaintance’ was almost certainly flu, but again it is difficult to be certain.

I hope that to a lesser or greater extent we can untangle the knot that surrounds early reports of flu and see how much those reports had in common across wide geographic areas. We can then see how society coped and developed in the face of repeated infection, sometimes mild, sometimes far more severe. And we will see how influenza and the possibility of prevention and cure was perceived by some early commentators and how it was seen in relation to other types of infection.

By the early 19th century or possibly earlier most people had a pretty shrewd idea that flu was a distinct illness, though of course they still had no idea what pathogen (disease-causing agent) caused it, nor how it was transmitted. The pandemics and epidemics of that century are reasonably well documented. Less well known and until now unexplored is the fascinating story of how society coped with the effects of flu, who died and who lived.

Chapter 5 covers the 1918–19 pandemic not just from a national perspective – that has already been done, particularly in regard to America – but from a global one. This section also examines the attempt not just to save lives but to stem the seemingly inexorable spread of the disease. The range of tactics adopted both socially and in the strictly medical sense was astonishing, and at times when we see what our great-grandparents did during this period we realize that in many ways their actions were not unlike those of 17th-century Londoners who killed cats and dogs to try to stop the spread of the plague.

Like those 17th-century Londoners our great-grandparents were working blind against a strain of flu which had never been encountered before. The 1918 pandemic shows that what people lacked in precise medical skills and knowledge they made up for in ingenuity. All kinds of treatments were tried in the hope that almost by chance something might be found that really would work.

The future threat

The final section of the book takes a look at the very real threat from flu that faces us in the future and the means we now have to guard against that threat.

Avian and pig flu viruses are seen as the main danger, but it is their complex relationship with human flu viruses that will almost certainly lie at the heart of future pandemics. Vast concentrations of potential human victims live in our great cities and they must be protected from new and emerging viruses to which, in the worst cases, they will not have immunity.

It is among immense concentrations of livestock, particularly birds and pigs living in close proximity to large numbers of humans that the real risk of a pandemic lies. The situation in this respect is particularly difficult in certain parts of the world, most notably Southern China where humans share living space with large numbers of birds, increasing the chance of avian flu viruses jumping species. Most, if not all, new and particularly deadly strains of flu virus probably originate there.

The history of influenza is to some extent the history of medicine and how it has developed over the past few centuries from a largely unscientific endeavour in which appeals to authority always mattered more than hands-on experience into the modern fact- and evidence-based science we know today. The story of medicine reflects also the growing sophistication of the communities that doctors have served.

In a sense the history of flu splits into two major phases. The first phase was complete ignorance, during which time doctors simply tried out a range of traditional remedies, some of which – particularly opium – may have alleviated symptoms but none of which could possibly have tackled the central cause of the disease, which was not to be discovered until the 1930s.

The second phase of the history of flu begins with the biggest and most appalling loss of life in human history – that devastating outbreak of influenza that came just a decade or so before the discovery of the virus that caused the disease. So the second phase of our history starts with devastation and moves quickly into the post-1930s period of enlightenment when doctors at least knew what they were dealing with. The second phase brings us to the present when there is at least a reasonable chance that a truly effective antiviral drug or vaccine may be created.

A third and final phase is beginning now and involves the future terrors of avian flu – a disease to which we have no historic immunity and one which, if it mutated into a form that could be passed from human to human (rather than only from bird to human) might make the 1918–19 pandemic seem relatively benign.

Before we look at how society was affected by influenza in the distant and not so distant past and may be affected in the future we need to start with some basic science, for only science will enable us to define and understand the enemy we face. The most important initial question is: what exactly is a virus?

CHAPTER 1

Viruses – What Are They and How Do They Work?

The human body is a rich breeding ground for microscopic and submicroscopic life. The mouth for example is a mass of alien life forms – mostly fungal and bacterial – in fact there are far more microbes here even than in the rectal area! We are quite literally covered with bacteria, fungi and other forms of life – like some bipedal planet, each individual human provides a home for more microscopic and submicroscopic forms of life than there are people in the world! Imagine – you are a source of life and nourishment, permanently and for the whole of your life, for more than six billion creatures. Some of these creatures are beneficial, even essential to our continued health, others highly dangerous.

Bacteria

Against the latter our bodies wage constant and unremitting war. The discovery of the immune system and the way it works by Paul Ehrlich (work for which he won the Nobel Prize in 1908) revealed that the healthy human is not in a state of perfect balance and quiet equilibrium. Rather, the healthy body is like a magnificently defended castle, under constant siege. Some battles against would-be invaders have been partially won – the discovery of antibiotics, for example, gave humans a massive advantage over bacteria. What was once thought to be an outright victory for humanity, however, has turned out to be a temporary respite from the battle as various strains of bacteria become resistant even to our most powerful antibiotics.

But if bacterial infections were once among humankind’s great killers, that is no longer the case. The discovery of penicillin in the mid-20th century and its antibiotic derivatives has saved tens of millions of lives that would undoubtedly otherwise have been lost to tuberculosis and a host of other now commonly treated infections. Although the war against bacteria may never be completely won – numerous drugresistant bacteria always threaten – we have, as it were, got the measure of our adversary. The situation with viruses is far more complex.

The problem with viruses is that we have as yet no cure for any viral infection and vaccination is usually, at best, only partially successful. Smallpox eradication is a happy exception to this and no cases have been reported since 1980 following a worldwide campaign of inoculation. Polio is well on the way to eradication, too, but with other viruses the situation is far less promising. Vaccination is still our main line of defence against an adversary whose existence has been firmly established for fewer than 100 years. Before the 1930s no microscope could even see a virus and their existence was a subject for doubt and speculation.

Three great world killers – Human Immunodeficiency Virus (HIV), malaria and flu – are still with us. HIV infection can now be controlled by a complex and expensive drug regime but in poorer countries, particularly in Africa, it is still a major killer because the drugs are too expensive for local populations. Malaria, caused by a protozoan parasite and so not a virus, is nevertheless a huge problem and kills more than a million people, mostly children, every year. But in world history the biggest killer among a host of unpleasant viral enemies is flu.

This may come as a surprise, but the history of flu is the history of a virus so successful that it can and has killed on a scale that dwarfs deaths from war, smallpox and HIV. The reason flu is such a powerful adversary is that even among viruses it is singularly difficult to deal with.

One of the most fascinating things about the flu virus and indeed all other viruses is that scientists are not even agreed about whether they count as living things. Bacteria are certainly living – they are the smallest of all life forms in the sense that they can survive independently of other creatures. They are single celled and contain DNA like every other living thing. DNA (deoxyribonucleic acid), is the double-stranded, helical molecular chain found within the nucleus of every living cell. It carries the genetic information that encodes proteins and enables cells to reproduce and perform their functions.

A bacterium is roughly 500 times bigger than a virus. A bacterium can read DNA messages, convert them into ribonucleic acid (RNA) and then make proteins from that RNA. RNA is a chemical found in the nucleus and cytoplasm of cells that plays an important role in protein synthesis and other chemical activities of the cell.

What viruses do inside our bodies

Bacteria can take in and use oxygen to fuel the work of making proteins and release, as a by-product, carbon dioxide. Scientists believe that bacteria are the blueprint cells for all life and, as we have seen, modern bacteria are, in a sense, direct descendants of the earliest life that appeared on earth.

A virus, on the other hand, is just a scrap of genetic material surrounded by a protein. It cannot reproduce on its own, yet the sole reason for its existence is reproduction. Although it does contain genetic information – viruses have up to 400 genes (although exceptions with over 900 genes have been found) compared to a human with 30,000 – it cannot make proteins itself and must enter a living cell to coerce that cell into doing its reproduction for it.

Once a virus gets inside another living creature’s cells it stops those cells performing the function for which they were designed. Instead the cells are forced to start churning out copies of the viruses that have infected them. Viruses don’t take over our cells deliberately in order to make us ill, but the flood of chemicals we release to combat them combined with the damage they do as they infect cells – an infected cell almost always dies – leads to the various and sometimes fatal diseases we experience. For example, if all or most of the cells that make up your liver are taken over by a virus and your immune system cannot destroy them quickly enough you will die for the simple reason that you cannot function without a liver.

Viruses may also weaken the immune system as it battles to get the upper hand to such an extent that the body becomes prey to secondary bacterial infection – in the case of influenza, pneumonia is the most serious secondary infection. And when pneumonia takes over the lungs the patient can quite literally suffocate, in the worst cases turning blue from lack of oxygen in the process – a condition known as cyanosis.

Different viruses cause different diseases because their proteins are designed to lock on to and infect different cells. In simple terms the virus tricks the cell into allowing it in. The viral protein of a particular virus will match the protein the human cell expects to recognize on the chemicals that it must admit in order for it to function. Once the cell allows the virus to enter it is doomed.

When we are infected with a cold or flu we cough because the cells in the respiratory tract are damaged by the viral attack and the antibodies we produce to fight them produce the cough reflex – coughing may help remove the disease from our bodies, but it also helps spread many kinds of virus to others. Where cold and flu viruses centre on the cells in the respiratory tract, haemorrhagic viruses – such as the infamous Ebola virus – damage the cells that make up the blood vessels in the lungs causing bleeding. In many cases the bleeding is catastrophic and the victim dies.

Developing immunity

It is very difficult to generalize about the effects of viruses – different viruses are spread in different ways and they affect and damage different parts of the human body. Most viruses have a host animal (although the natural host for Ebola has not been found) and in that animal the virus may cause little or no harm, or perhaps cause only mild illness, but when a virus jumps the species barrier – and the flu virus is particularly good at this – the species in which it now appears for the first time will usually have no immunity and the effects are likely to be catastrophic until, in time, the virus mutates into a milder form, or the newly infected species begins to develop immunity.

The classic case is myxomatosis in rabbits. Myxomatosis is endemic in Brazilian rabbits. They suffer little or no harm by carrying the virus because over thousands of rabbit generations they have developed immunity and have learned to tolerate the presence of a virus that no longer kills them. When the myxomatosis virus was released in Britain, probably in the 1950s and almost certainly deliberately as an attempt to eliminate rabbits, which were a serious agricultural pest, the result was that more than 98 per cent of the rabbit population was wiped out.

However, a very few rabbits (that surviving two per cent) had a slight genetic variation in their make-up which meant they were not killed by the virus. Since they and only they survived to breed, all their offspring shared the same resistance to myxomatosis – a classic example of Darwinism in action. The rabbits had a genetic advantage over other rabbits, so they succeeded in breeding where the other rabbits failed because they did not have that advantage and died out. Within a few years rabbit populations – all descended from the few that survived the first release of myxomatosis – were back at the number that had existed before myxomatosis was ever released. Though they suffer periodic outbreaks of myxomatosis still, the British rabbit population will never again be controllable using this virus. The same is true in Australia, where myxomatosis was used in the same way and with precisely the same short- and long-term effects.

Between man and other animals and the viruses that infect them there is and has always been a kind of arms race. As viruses mutate – and they mutate at a relatively rapid rate (compared to humans) because they reproduce so quickly – they are able to infect those who do not have immunity to the new, mutated form of the virus. Being immune to the older form of the virus may impart partial immunity, but if the virus is very different that older immunity will be useless. But assuming a death rate below 100 per cent the human body slowly catches up and becomes immune or at least partly immune, which means the virus is in danger of being wiped out.

By this time, however, new victims without any immunity will often have been infected or the virus will change again to keep ahead of the body’s defences, and the body’s immune system is once again left behind. Extremely virulent viruses such as Ebola, though terrifying, are so deadly that any outbreak is likely to remain local because it kills or incapacitates so quickly that it soon exhausts the available supply of victims. In other words, these first victims die before they have had the chance to spread the disease further afield.

As we can see, one of the main problems with viruses is that there may be many different yet closely related viruses. Being immune to one of these will not protect you from all the others. One of the most interesting of all viruses from this point of view is the common cold.

The common cold

It took until the 1950s to grow the virus that causes the common cold. Scientists had long tried to infect study groups with the agent that causes the cold, but had failed. It took the work of David Tyreell in the late 1950s to come up with an answer. He changed the temperature of the culture in which scientists were trying to grow the cold virus so that it matched not the temperature of the body but the temperature of the nasal passages where the cold virus has, as it were, its home. Instantly he was able to culture the virus but he discovered that the newly isolated virus – which was named rhinovirus (rhino is Greek for nose) – was only one of many. We have since discovered that there are as many as 150 cold viruses, and immunity from one gives little or no immunity to the others. This explains why, typically, the average human is infected once or twice a year by one or other of the rhinoviruses and experiences the typical cold symptoms. The curious and as yet unexplained part of this is that humans should so regularly be infected with these and other respiratory infections – dogs, cats and monkeys, for example, do not suffer in the same way.

The situation is made even more difficult because there is an additional group of viruses that cause cold-like symptoms. There is no cure for the common cold nor is there likely to be; there is currently no chance of developing a vaccine that would be effective against that vast array of different viruses. We must be grateful that none of the cold viruses causes anything more than discomfort. If they were more serious – even life threatening – there would be little we could do to protect ourselves.

Ebola

Far more serious than the common cold is the Ebola virus, which first came to the attention of the public in the developed world after an outbreak in the African state of Zaire in the mid-1970s. Within a short time of the first case being identified more than 300 people had contracted the virus and some 280 died. Ebola virus is a haemorrhagic fever. That is, it attacks the cells that line the blood vessels and capilliaries, particularly those that affect the respiratory system. As the cells are destroyed blood begins to leak into the lungs and other organs until the victim drowns in his or her own blood. Ebola did not spread beyond Zaire partly through luck and partly through the fact that it is too efficient at killing for its own good – those who catch the disease usually die so quickly (it is roughly 90 per cent fatal) that they do not have time to infect large numbers of other people before they succumb.

Like other viruses such as hanta and HIV, Ebola seems to have come from nowhere to wreak havoc among human populations, but it is almost certainly the case that this and other newly arrived viruses have reached us via animal hosts; it is generally agreed that HIV came to us from one of our closest primate relatives, though how it made the jump from species to species and then mutated sufficiently so that it could be passed from human to human (rather than in each case from animal to human) is not fully understood.

The arrival of HIV and Ebola (not to mention avian flu) in human populations is something of a new development and it may be that we are simply encroaching too much and too often into parts of the world and among populations of animals with which previously we have had little contact. When we catch a virus to which we have no historical immunity – the classic example is HIV – the effects are likely to be deadly. Yellow fever is another example; it exists in monkeys and does them no harm, but when it infects man the mortality rate is very high. Like malaria, yellow fever – which causes bleeding, nausea, vomiting and finally jaundice – is carried by a species of mosquito.

A breakthrough – the electron microscope

By the early 20th century scientists still did not know that influenza and the common cold were caused by viruses, but they did know that certain illnesses were caused by an agent that could not be filtered – it was too small to be trapped as bacteria were trapped using dense porous devices made from, say, porcelain.

It was also clear that the agent that caused influenza and other diseases could not be grown or cultured. However, a number of scientists correctly guessed, despite the lack of clear evidence, that they were dealing with a bacteria-like agent that was simply too small to be detected under a conventional light microscope or trapped in the filters then in use. The invention of the electron microscope in 1938 changed all that – for the first time viruses could be seen. At last their precise nature could at least begin to be analyzed and recorded.

Surrounding the genetic material in each virus is a capsid – that is, a protein shell. Within this the tiny particle of DNA contains a code for the virus to reproduce itself. Viruses reproduce at an astonishing rate, but, as we have seen, they cannot do it on their own since they do not have the necessary molecular equipment. What they do have is the ability to make other living cells do the work of reproduction for them. Within hours of finding a new victim a virus, having entered a cell, will have (usually) destroyed that cell and turned it into a factory producing thousands of new viruses.

Doctors had long known that there were diseases such as tuberculosis that were caused by an agent they could see and grow; then there were others, such as yellow fever, measles, smallpox and influenza that seemed similar to diseases caused by bacteria, but no bacteria could ever be found or grown from those infected by the diseases. These pathogens became known as ‘invisible microbes’. Even when the electron microscope became available and viruses could at last be seen, it still took until the early 1950s for the deep structure of viruses to be understood, because the structure of DNA itself (the famous double helix) was not understood until Watson and Crick’s pioneering work in the 1950s.

How viruses spread

As we have seen viruses – like bacteria – have been with us as long as any life form and the most likely explanation for their origin (though scientists are by no means fully agreed on this) is that they somehow managed to break away from chromosomes to become independent and able to reproduce independently as parasites.

Like all living things they are programmed to survive and to do so by reproducing. Once inside a host cell the virus begins this process and new viruses from that first cell factory will quickly infect other cells. But if the virus kills its host too quickly it will not have time to allow the host to spread it to other suitable hosts and it will die in the original host; this is why victims of influenza are contagious before they show any signs of illness themselves. The influenza virus can survive outside a host for a couple of days at most, but it is supremely successful at survival where large numbers of people are gathered together. Influenza is spread by droplet infection (when we sneeze, for example, tens of thousands of microscopic droplets are propelled into the air), but if you touch a doorknob or any other surface that has fresh virus on it and then touch your mouth or nose you are likely to become infected. In isolated and small groups of humans the flu virus would quickly run out of new victims, which would endanger its own survival unless, like some other viruses, it was able to lie dormant for many years (like HIV) without killing or seriously harming its host.

Yellow fever works in a different way – because it is carried between victims by mosquito it doesn’t matter if it incapacitates each victim. In fact, in evolutionary terms incapacitating the host is a good idea for yellow fever because it means that the victim is in bed and therefore more likely to be bitten by the mosquito that carries the disease far and wide. Cleverly, yellow fever does not harm the mosquito at all; again, in evolutionary terms, this is a smart move. Killing the creature that carries a disease to a new host would make no sense.

The virus replicates itself in vast quantities; these copies pour out of each infected cell and infect other cells around the body. Within hours the body is mobilizing its counter attack with a formidable array of weapons. Assuming the victim of infection isn’t quickly killed, he or she will gradually begin to fight back as the immune system mobilizes and destroys the virus – that is why it is essential for the virus’s long-term survival that it should reproduce and then move on before it is overwhelmed by the body’s defences. It doesn’t matter if the viruses in a particular victim are eventually all killed, either by the immune system or the death of the victim, as long as some of the virus is passed on to a new host in whom the cycle continues and the virus’s long-term survival is guaranteed.

Viruses cannot swim or fly to another victim, so they are carried by droplet, insect, water or faeces. In faeces and water some viruses can survive for extended periods before a new host presents itself.

Infecting the host

The biggest problem for the virus is gaining entry to the host in the first place. The human body is covered with skin cells, the outer layer of which is dead and inert and therefore perfect for keeping out viruses, which cannot penetrate unaided. The genito-urinary tract and respiratory tract are potential weakspots, however. Here the mucous membrane may be only one cell layer deep, and though the mucous itself makes life difficult for the invading virus – because it is highly acid, as are the vaginal and oral secretions – weaker individuals or those whose immune system is less well developed or compromised in some way may give the virus a chance. The respiratory tract has a remarkable layer of cells covered in miniscule hairs, which move in a synchronized fashion to push any invading foreign items up and out of the body – they are extremely effective (along with the secretions that line the tract) at keeping invaders out. As a result of this extraordinary feat of bio-engineering, the lungs in a normal healthy person are usually sterile. But, despite the best efforts of our defences, viruses and bugs still get through. How do they do it?

The easiest way into the body is, of course, through damage to the otherwise impregnable layer of dead skin – a simple cut is all it takes. The cut may be all but invisible to the person who gets infected, but viruses seek and exploit every opportunity. If there is no cut already a virus may employ an insect to make the cut and deliver the virus – an example is the mosquito that delivers the yellow-fever parasite.