You are on page 1of 3

glossary | home | Custom Search

SUPPORT
THIS
PROJECT

print
Resource library : Evo in the news :

Evolution from a virus's view


December 2007 Get tips for using Evo
in the News articles,
The new disease making the rounds this winter sounds like a Steven like this one, with your
students.
Spielberg movie in the making: a common cold virus, which spreads via
casual contact, mutates into a virulent form that hospitalizes and
sometimes kills its victims. Touted last month as the "killer cold,"
Adenovirus-14 is far from fantasy, but neither is it scary enough to make a
blockbuster. In the past 18 months, the virus has caused just 10 deaths —
a minor toll when compared to the 36,000 caused by the flu in an average
year. Why hasn't Adenovirus-14 lived up to the threat advertised in
headlines? Evolution helps explain why some bugs are killers, why others
Adenovirus are not, and what chance a mutant cold virus has of reaching epidemic
proportions.

Where's the evolution?


To understand why some germs are virulent, we need to see the world from their point of view. To us,
disease-causing viruses and bacteria may be evildoers — invaders of our bodies — who, if they can be
said to have any aim at all, it is to do us harm. But shifting our perspective to their scale reveals these
pathogens to be evolving populations of organisms like any other, whose habitat just happens to be the
human body. Like other organisms, these germs are shaped by natural selection to live and
successfully reproduce. We view them as pathogens, however, because the resources they use to do
this (and which they destroy in the process) are the cells of our own bodies. Many of the traits that
make us feel sick during an infection are actually pathogenic adaptations — characteristics favored by
natural selection that help these germs reproduce and spread.

As an example, consider a unique ecological challenge faced by many pathogens: appropriate habitats
can be few and alarmingly far between. Put yourself in the position of a virus in its natural habitat — a
human host. You've infected some cells and managed to reproduce, but the host's immune system is
onto you now and is turning up the heat. This environment is no longer so hospitable. How can you get
your descendents to a friendlier habitat (i.e., a new, unexploited human body)? Without legs, wings,
fins, or any of the usual means of locomotion, your descendents' prospects for reaching a new host
under their own power are nil. However, natural selection has provided pathogens with a number of
sneaky strategies for making the leap to a new host, including:

Droplet transmission — for example, being passed along when one host accidentally sneezes on
another. The flu is transmitted this way.

Airborne transmission — for example, being exhaled by one host and inhaled by another.
Tuberculosis is transmitted this way.

Vector transmission — getting picked up by a carrier (the vector — e.g., a mosquito) and carried
to a new host. Malaria is transmitted this way.

Waterborne transmission — leaving one host (e.g., in feces), infecting the water supply, and
being taken up (e.g., in drinking water) by a new host. Cholera is transmitted this way.

Sit-and-wait transmission — being able to live outside a host for long periods of time until coming
into contact with a new host. Smallpox can survive for years outside of a host!

Pathogen lineages that fail to meet this challenge and never infect a new host are doomed. They will go
extinct when their human host dies or when the immune system destroys the infection.

Since transmission is a matter of life or death for pathogen lineages, some evolutionary biologists have
focused on this as the key to understanding why some have evolved into killers and others cause no
worse than the sniffles. The idea is that there may be an evolutionary trade-off between virulence and
transmission. Consider a virus that exploits its human host more than most and so produces more
offspring than most. This virus does a lot of damage to the host — in other words, is highly virulent.
From the virus's perspective, this would, at first, seem like a good thing; extra resources mean extra
offspring, which generally means high evolutionary fitness. However, if the viral reproduction
completely incapacitates the host, the whole strategy could backfire: the illness might prevent the host
from going out and coming into contact with new hosts that the virus could jump to. A victim of its own
success, the viral lineage could go extinct and become an evolutionary dead end. This level of virulence
is clearly not a good thing from the virus's perspective.
Download this graphic from the Image library.

Natural selection balances this trade-off, selecting for pathogens virulent enough to produce many
offspring (that are likely to be able to infect a new host if the opportunity arises) but not so virulent
that they prevent the current host from presenting them with opportunities for transmission. Where
this balance is struck depends, in part, on the virus's mode of transmission. Sexually-transmitted
pathogens, for example, will be selected against if they immobilize their host too soon, before the host
has the opportunity to find a new sexual partner and unwittingly pass on the pathogen. Some biologists
hypothesize that this trade-off helps explain why sexually-transmitted infections tend to be of the
lingering sort. Even if such infections eventually kill the host, they do so only after many years, during
which the pathogen might be able to infect a new host.

On the other hand, diseases like cholera (which causes extreme diarrhea) are, in many situations, free
to evolve to a high level of virulence. Cholera victims are soon immobilized by the disease, but they are
tended by others who carry away their waste, clean their soiled clothes, and, in the process, transmit
the bacterium to a water supply where it can be ingested by new hosts. In this way, even virulent
cholera strains that strike down a host immediately can easily be transmitted to a new host.
Accordingly, cholera has evolved a high level of virulence and may kill its host just a few hours after
symptoms begin.

Though transmission mode is far from the only factor that affects how virulence evolves — the
immunity level of the host population, the distribution of the hosts, and whether the host has other
infections, for example, matter as well — this key piece of the pathogen's ecology does help illuminate
why some diseases are killers. More importantly, it suggests how we might sway pathogen evolution
towards less virulent strains. In situations where high virulence is tied to high transmission rates (e.g.,
cholera), reducing transmission rates (e.g., by providing better water sanitation) may favor less
virulent forms. The idea is to create a situation in which hyper-virulent strains that soon kill or
immobilize their hosts never get a chance to infect new hosts and are turned into evolutionary dead
ends. In fact, biologists have observed this phenomenon in South America: when cholera invaded
countries with poor water sanitation, the strains evolved to be more virulent, while lineages that
invaded areas with better sanitation evolved to be less harmful.

And that brings us back to Adenovirus-14. Adenoviruses are transmitted through the air or via contact.
We might expect this sort of transmission to require a fairly healthy host (one who gets out and comes
into contact with others) and, hence, to select against virulent strains. Indeed, adenoviruses are rarely
killers, but in close quarters — for example, in the military barracks where Adenovirus-14 has been a
particular problem — barriers to transmission may be lowered. This could open the door for the
evolution of more virulent strains. Military personnel, however, are in the process of pushing this door
shut again. At Lackland Air Force Base, which has seen the most serious outbreak of Adenovirus-14,
wider testing, more hand-washing stations, increased attention to sanitization, and isolation of patients
is helping to reduce the transmission of the disease and, in the process, may favor the evolution of less
virulent strains of the virus.

Read more about it


Primary literature:

Ewald, P. W. (1996). Guarding against the most dangerous emerging pathogens: Insights from
evolutionary biology. Emerging Infectious Diseases 2(4):245-257.

Galvani, A. P. (2003). Epidemiology meets evolutionary ecology. Trends in Ecology and Evolution
18:132-139.

News articles:

A news report on Adenovirus-14 from Reuters

An interview on managing the evolution of disease virulence from WGBH


Understanding Evolution resources:

A tutorial on natural selection and evolutionary fitness

An advanced reader on DNA and mutations

A news brief on the emergence of another new virus, avian flu

Discussion and extension questions


1. Review some background information on natural selection. Explain how a mutation allowing a
virus to make more copies of itself would spread through a population of viruses living within a
single person. Make sure to include the concepts of variation, selection, and inheritance in your
explanation.

2. Read more about the concept of evolutionary fitness. Describe what factors would increase the
evolutionary fitness of a virus like Adenovirus-14.

3. Explain what an evolutionary trade-off is. Be sure to include the concept of fitness in your
explanation.

4. Consider a disease transmitted from mother to child before or soon after the child is born. In this
situation, would a pathogen be likely to evolve high or low levels of virulence? Explain your
reasoning.

5. Consider the disease malaria, which is passed from person to person when one is bitten by a
mosquito that has previously bitten an infected individual. Would the pathogen that causes
malaria be likely to evolve high or low levels of virulence? Explain your reasoning.

6. This article describes how evolution might shape pathogen virulence. Do some research and
describe at least one other example of pathogen evolution observed by people.

Related lessons and teaching resources


Teach about the evolution of virulence: In this short video for grades 9-12, evolutionary biologist
Paul Ewald describes strategies for controlling viral evolution.

Teach about applications of evolutionary biology in medicine: This tutorial for grades 9-12
explores just a few of the many cases in which evolutionary theory helps us understand and treat
disease. Bacterial infections, HIV, and Huntington's disease are highlighted.

References
Cases of 'boot camp flu' dropping at Lackland AFB. (2007, December 3). AP Texas News.
Retrieved December 4, 2007, from Houston Chronicle

Centers for Disease Control and Prevention. (2007, November 16). Acute respiratory disease
associated with Adenovirus Serotype 14. Morbidity and Mortality Weekly Report.
Retrieved December 4, 2007, from CDC

DeNoon, D. J. (2007, November 20). Killer cold virus: Questions, answers. WebMD Medical News.
Retrieved December 4, 2007 from WebMD

Ewald, P. W. (1996). Guarding against the most dangerous emerging pathogens: Insights from
evolutionary biology. Emerging Infectious Diseases 2:245-257.

Galvani, A. P. (2003). Epidemiology meets evolutionary ecology. Trends in Ecology and Evolution
18:132-139.

Adenovirus micrograph provided by CDC/ Dr. G. William Gary, Jr.

Home | About | Copyright | Credits | Contact | Subscribe | Translations

Read how others have recognized the Understanding Evolution website.

You might also like