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Viruses: A Very Short Introduction
VERY SHORT INTRODUCTIONS are for anyone wanting a stimulating and
accessible way into a new subject. They are written by experts, and have
been translated into more than 45 different languages.
The series began in 1995, and now covers a wide variety of topics in every
discipline. The VSI library currently contains over 700 volumes—a Very Short
Introduction to everything from Psychology and Philosophy of Science to
American History and Relativity—and continues to grow in every subject
area.
Available soon:
HANNAH ARENDT Dana Villa
MICROBIOMES Angela E. Douglas
GÖDEL’S THEOREM A. W. Moore
ANSELM Thomas Williams
VIRUSES
A Very Short Introduction
THIRD EDITION
Great Clarendon Street, Oxford, OX2 6DP, United Kingdom
Oxford University Press is a department of the University of Oxford. It furthers the
University’s objective of excellence in research, scholarship, and education by publishing
worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and in
certain other countries
© Dorothy H. Crawford 2011, 2018, 2022
The moral rights of the author have been asserted
First edition published 2011
Second edition published 2018
Third edition published 2022
Impression: 1
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, without the prior permission in
writing of Oxford University Press, or as expressly permitted by law, by licence or under
terms agreed with the appropriate reprographics rights organization. Enquiries concerning
reproduction outside the scope of the above should be sent to the Rights Department,
Oxford University Press, at the address above
You must not circulate this work in any other form and you must impose this same
condition on any acquirer
Published in the United States of America by Oxford University Press
198 Madison Avenue, New York, NY 10016, United States of America
British Library Cataloguing in Publication Data
Data available
Library of Congress Control Number: 2022938071
ISBN 978–0–19–286506–9
ebook ISBN 978–0–19–268849–1
Printed in the UK by Ashford Colour Press Ltd, Gosport, Hampshire
Links to third party websites are provided by Oxford in good faith and for information only.
Oxford disclaims any responsibility for the materials contained in any third party website
referenced in this work.
Contents
Acknowledgments
List of illustrations
List of tables
2 Kill or be killed
7 Persistent viruses
8 Tumour viruses
Glossary
Further reading
Publisher’s acknowledgements
Index
Acknowledgements
8 Graphs showing Ebola cases in Guinea, Liberia, and Sierra Leone, 2014–16
Reprinted from Ebola: Mapping the outbreak—BBC News with permission, based on
data taken from WHO Ebola situation reports, data summary, all data and statistics
and Ebola maps Ebola virus disease (who.int)
9 The yellow fever transmission cycle
Source from Fig 15 from D. H. Crawford, The Invisible Enemy (OUP, 2021) © Oxford
University Press
13 CD4 count and viral load during the acute, asymptomatic, and symptomatic
phases of HIV infection
Reproduced from A. Mindel and M. Tenant-Flowers, ‘Natural History and Management
of early HIV infection’, ABC of Aids (2001), with permission from BMJ Publishing Group
Ltd
Viruses are not cells but particles. They consist of a protein coat, the
capsid, surrounding and protecting a piece of genetic material. The
whole structure is called a virion. Capsids come in various shapes
and sizes, each characteristic of the family to which a virus belongs.
They are built up of protein subunits called capsomeres and it is the
arrangement of these around the central genetic material that
determines the shape of the virion. For example, pox viruses are
brick-shaped, herpes viruses are icosahedral (20-sided polygons),
the rabies virus is bullet-shaped, and the tobacco mosaic virus is
long and thin like a rod (Figure 1).
1. The structure of viruses.
Once it was appreciated that viruses carried either DNA or RNA, but
never both, a system of classification was devised based on the
following criteria to assign viruses into families, genera, and species:
Since the early 1980s, when the first virus genome was fully
mapped, genome sequencing has become a routine technique that
provides valuable information for virus classification. Indeed, with
increasingly sophisticated methods for virus discovery, many viruses
are now identified long before their actual physical structure is
visualized. In these cases, the molecular structure of the DNA or
RNA is compared with that of other known viruses to assign the new
virus to a family.
Plant viruses either enter cells through a break in the cell wall or are
injected by sap-sucking insect vectors like aphids. They then spread
very efficiently from cell to cell via plasmodesmata, pores that
transport molecules between cells. In contrast, animal viruses infect
cells by binding to specific cell surface receptor molecules. The cell
receptor is like a lock, and only viruses that carry the right receptor-
binding key can open it and enter that particular cell. Receptor
molecules differ from one type of virus to another, and while some
are found on many cell types, others have a much more restricted
distribution. This is exemplified by the two pandemic viruses: human
immunodeficiency virus (HIV), the cause of acquired
immunodeficiency syndrome (AIDS), and severe acute respiratory
syndrome-coronavirus-2 (SARS-CoV-2), the cause of COVID-19. The
cell receptor for HIV is the CD4 molecule, which is mainly expressed
on immune cells called helper T cells. This specific interaction
defines the outcome of HIV infection, since it leads to destruction of
CD4-positive ‘T’ cells that are critical to the immune response.
Without antiviral treatment the immune system eventually fails, and
lethal opportunistic infections ensue. In contrast, the cell receptor for
SARS-CoV-2, ACE-2 (angiotensin-converting enzyme-2), is widely
expressed in the body, particularly on cells in the respiratory tract,
blood vessels, heart, and kidneys, and this distribution determines
the manifestations of severe COVID-19 (see Chapter 5).
Once a virus has bound to its cellular receptor, the capsid penetrates
the cell and its genome (DNA or RNA) is released into the cell
cytoplasm. The main ‘aim’ of a virus is to reproduce successfully, and
to do this its genetic material must download the information it
carries. Mostly, this will take place in the cell’s nucleus, where the
virus can access the molecules it requires to begin manufacturing its
own proteins. Some large viruses, like pox viruses, carry genes for
the enzymes they need to make their proteins and so are more self-
sufficient and can complete the whole life cycle in the cytoplasm.
RNA viruses are one step ahead of DNA viruses in already having
their genetic code as RNA. As they carry enzymes that enable their
RNA to be copied and translated into proteins, they are not so
dependent on cellular enzymes and can often complete their life
cycle in the cytoplasm without causing major disruption to the cell.
Virus genomes mutate far more rapidly than the human genome,
partly because viruses reproduce in a day or two with many
thousands of offspring. Also, RNA viruses generally have no proof-
reading system so they have a higher mutation rate than DNA
viruses.
Thus, every time a virus infects a cell, its DNA or RNA may be copied
thousands of times, and as each new strand is incorporated into a
new virus particle, every round of infection throws up several mutant
viruses. This high mutation rate in viruses is their lifeline; in some, it
is essential for their survival. Each round of infection produces some
viruses that are non-viable due to mutations that interrupt the
function of essential genes, and others with mutations that cause no
change in function. But a few of the offspring will have beneficial
mutations, giving them a selective advantage over their siblings. The
benefit may be due to any number of changes, including a
heightened ability to hide from immune attack; to infect more easily;
to resist antiviral drugs; or to reproduce at a faster rate. Whatever
the advantage, it will lead to that particular mutant virus outstripping
its siblings and eventually taking over in the population. Measles
virus, for example, has been infecting the human population for at
least 2,000 years, but scientists calculate that the present-day
measles strain arose much more recently (see Chapter 7).
Presumably, this virus strain was ‘fitter’ than its predecessor in some
way and so eventually replaced the former strain worldwide. And as
I write we are regularly experiencing the emergence of new strains
of SARS-CoV-2 during the COVID-19 pandemic, with strains better at
transmission between hosts replacing their predecessors globally
(see Chapter 5).
We do not yet know the answer to this question, but there are three
theories—the virus-first, the progressive, and the regressive
theories, none of which explains the various features of all the
viruses we observe today. It is now generally accepted that viruses
are truly ancient. The fact that viruses sharing common features
infect organisms in all three domains of life—Archaea, Bacteria, and
Eukarya—suggests that they evolved before these domains
separated from their common ancestor, called the ‘last universal
cellular ancestor’ (LUCA). It is also generally accepted that the first
replicating molecule to evolve was RNA rather than DNA. So the
virus-first theory suggests that RNA viruses evolved before more
complex cells although they now depend on them for their survival.
Then DNA viruses may have evolved from their more ancient RNA
counterparts. This suggestion is supported by the existence of
retroviruses, with their ability to transcribe RNA into DNA. In so
doing, they reverse the more usual flow of genetic information from
DNA to RNA to protein.
The regressive theory proposes that large DNA viruses, for example
pox and mimiviruses, may represent previously free-living life forms
that have now lost their ability to reproduce independently. In
contrast the progressive theory suggests that viruses derived from
escaped fragments of genetic material that acquired a protein coat
and became infectious.
Whatever the truth of it, none of these theories can explain the
evolution of both RNA and DNA viruses, which may therefore have
evolved separately.
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of men. It was as though they were back in the days of the old
Hebrew prophets when the hand of the Lord stretched out and laid
itself upon wicked men for their punishment when the measure of
their time was full.
“He tried to stand above the law in this valley,” Hollister told her. “He
wanted to stop progress—said there shouldn’t be any dam to reclaim
the Flat Tops for settlers. Merrick will rebuild it. The land will be
watered. Your ranch will be good as ever in three months. And he’ll
be buried and forgotten.”
“And poor Don Black?” she whispered. “Poor Don, who never had a
chance in this world, or, if he had one, muddled it so badly?”
He could only hope that Don had gone to a better-ordered world
where circumstances did not dominate good intentions.
Betty’s sense of tragedy lingered just now no longer than a cinema
picture. The life urge in her clamored for expression. No world could
be a sad one with her and Tug in it.
“Shall I go in and tell your father now?” the young man asked.
“Soon.” She made a rustling little motion toward him and found
herself in his arms. “Isn’t it splendid, boy? To-day’s the best ever, and
to-morrow will be better than to-day—oh, heaps better—and after
that all the years forever and ever.”
He looked into the deep lustrous eyes of his straight slim girl. What a
wife she would be! How eager and provocative, this white flame of
youth so simple and so complex! Her happiness now would be in his
hands. The responsibility awed him, filled him with a sense of
solemnity.
“Forever is a long time,” he said, smiling, and quoted a stanza of
magazine verse they had lately read together.
It began, “How far will you go with me, my love?” Close-held in his
arms, Betty answered without a moment of hesitation.
“She smiled at the stile with a sweet disdain;
She scoffed at the bridge and the great oak tree;
And looked me full in the eyes and said:
‘I will go to the end of the lane with thee.’”
The door of the inner room opened and Clint stood on the threshold.
“Hello!” he said, surprised.
Betty disengaged herself, blushing. “He’s decided to take me after
all, Dad,” she said demurely.
“Hmp! Has he? Kinda looks that way.” Clint gripped Hollister’s hand
till it hurt. It was the best he could do just now to show the gratitude
he felt for what this man had done.
“That’s not quite the way I put it, sir,” Tug said.
“Doesn’t matter how you put it, boy. It’ll be her say-so from now on.
Don’t I know her? Hasn’t she bossed me scandalous since she was
knee-high to a gosling?”
“Now, Dad, you’re giving me a bad name,” Betty protested, hugging
her father.
“If he ain’t man enough to stand some bossing, he’d better quit right
now before he says, ‘I do.’”
“He likes being bossed, Dad,” Betty announced, and the imps of
deviltry were kicking up their heels in her eyes. “Don’t you, Tug?”
Hollister looked at the girl and smiled. “I’ll say I do,” he admitted.
THE END
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