ARTICLE 1

Just as natural selection has shaped the evolution of humans, plants, and
all living things on the planet, natural selection shapes viruses, too.
Though viruses arent technically living they need a host organism in
order to reproduce they are subject to evolutionary pressures.

The human immune system uses a number of tactics to ght pathogens.
The pathogens job is to evade the immune system, create more copies of
itself, and spread to other hosts. Characteristics that help a virus do its
job tend to be kept from one generation to another. Characteristics that
make it di"cult for the virus to spread to another host tend to be lost.

Take, for example, a virus that has a mutation that makes it particularly
deadly to its human host and kills the host within a few hours of infection.
The virus needs a new, healthy host for its descendents to survive. If it
kills its host before the host infects others, that mutation will disappear.

One way hosts protect themselves from a virus is to develop antibodies to
it. Antibodies lock onto the outer surface proteins of a virus and prevent it
from entering host cells. A virus that appears di#erent from other viruses
that have infected the host has an advantage: the host has no pre-
existing immunity, in the form of antibodies, to that virus. Many viral
adaptations involve changes to the viruss outer surface.

Below we look at two special cases in viral evolution: how evolution
occurs in inuenza viruses and in the human immunodeciency virus (HIV,
the virus that causes AIDS). Both of these viruses are RNA viruses,
meaning that their genetic material is encoded in RNA, not DNA. DNA is a
more stable molecule than RNA, and DNA viruses have a proofreading
check as part of their reproductive process. They manage to use the host
cell to verify viral DNA replication. If the virus makes a mistake in copying
the DNA, the host cell can often correct the mistake. DNA viruses,
therefore, do not change, or mutate, much. RNA, however, is an unstable
molecule, and RNA viruses dont have a built-in proofreading step in their
replication. Mistakes in copying RNA happen frequently, and the host cell
does not correct these mistakes. RNA virus mutations are frequent and
can have important consequences for their hosts.

Inuenza Viruses

Inuenza viruses are simple entities belonging to one of three types: A, B,
or C. They consist of no more than seven or eight RNA segments
enclosed within an envelope of proteins. Mutations in viral RNA and
recombinations of RNA from di#erent sources lead to viral evolution.

Antigenic Drift

Inuenza viruses can evolve in a gradual way through mutations in the
genes that relate to the viral surface proteins hemagglutinin and
neuraminidase (HA and NA in shorthand). These mutations may cause the
viruss outer surface to appear di#erent to a host previously infected with
the ancestor strain of the virus. In such a case, antibodies produced by
previous infection with the ancestor strain cannot e#ectively ght the
mutated virus, and disease results. (Hemagglutinin and neuraminidase
lend their rst initials to u subtypes. For example, the 2009 inuenza
pandemic was caused by an inuenza A H1N1 virus.) As mutations
accumulate in future generations of the virus, the virus drifts away from
its ancestor strain.

Antigenic drift is one reason that new u vaccines often need to be
created for each u season. Scientists try to predict which changes are
likely to occur to currently circulating u viruses. They create a vaccine
designed to ght the predicted virus. Sometimes the prediction is
accurate, and the u vaccine is e#ective. Other times the prediction
misses the mark, and the vaccine wont prevent disease.

Antigenic Shift

Antigenic shift is a process by which two or more di#erent types of
inuenza A combine to form a virus radically di#erent from the ancestor
strains. The virus that results has a new HA or NA subtype. Antigenic shift
may result in global disease spread, or pandemic, because humans will
have few or no antibodies to block infection. However, if the new inuenza
A subtype does not easily pass from person to person, the disease
outbreak will be limited.

Antigenic shift occurs in two ways. First, antigenic shift can occur through
genetic recombination, or reassortment, when two or more di#erent
inuenza A viruses infect the same host cell and combine their genetic
material. Inuenza A viruses can infect birds, pigs, and humans, and
major antigenic shifts can occur when these virus types combine. For
example, a pig u virus and a human u virus could combine in a bird,
resulting in a radically di#erent u type. If the virus infects humans and is
e"ciently transmitted among them, a pandemic may occur.

Second, an inuenza A virus can jump from one type of organism, usually
a bird, to another type of organism, such as a human, without undergoing
major genetic change. If the virus mutates in the human host so that it is
easily spread among people, a pandemic may result.

In all cases, antigenic shift produces a virus with a new HA or NA subtype
to which humans have no, or very few, preexisting antibodies. Once
scientists are able to identify the new subtype, a vaccine can generally be
created that will provide protection from the virus.

Why does antigenic shift occur only with inuenza A, and not inuenza B
and C? Inuenza A is the only inuenza type that can infect a wide variety
of animals: humans, waterfowl, other birds, pigs, dogs, and horses.
Recombination possibilities, therefore, are very low or nonexistent with
inuenza B and C.

A pandemic had the potential to occur in the bird u outbreaks in 2003 in
Asia. An H5N1 inuenza A virus spread from infected birds to humans,
resulting in serious human disease. But the virus has not evolved to be
easily spread among humans, and an H5N1 pandemic has not occurred.

HIV

The virus that causes Acquired Immune Deciency Syndrome (AIDS) is a
highly genetically variable virus, for several reasons. First, it reproduces
much more rapidly than most other entities. It can produce billions of
copies of itself each day. As it makes rapid-re copies of itself, it
commonly makes errors, which translate into mutations in its genetic
code. The more benecial the mutations are to the viruss survival, the
more likely that mutated virus will be to reproduce itself.

Another cause of the variability in HIV results from the viruss ability to
recombine and form new variants within an individual. This happens when
a host cell is infected with two di#erent variations of HIV. Elements of the
two viruses may combine to result in a new virus that is a unique
combination of the two parents.

The rapid rate of HIV evolution has important consequences. HIV can
quickly develop resistance to anti-HIV drugs. Additionally, targeting a
vaccine to a rapidly changing virus is challenging. To date, researchers
have developed several candidate HIV vaccines, but none has performed
well enough in clinical trials to warrant licensure.



http://www.historyofvaccines.org/content/articles/viruses-and-evolution




ARTICLE 2

These examples demonstrate pervasive and rapid evolution as a result of
human activity. In most cases, the causes of this evolutionary pattern are
clear: if a species is variable for a trait, and that trait confers a di#erence
in survival or production of o#spring, and the trait di#erence is heritable
by o#spring, then all three requirements of evolution by natural selection
are present. In such cases, the evolutionary engine can turn, although
evolutionary directions and speed can be inuenced by factors such as
drift, conicting selection pressure, and correlated characters (31).
The overwhelming impact of humans on evolution stems from the
ecological role we now play in the world, and the industrialization of our
agriculture, medicine, and landscape. Successful pesticides or antibi-
otics are often produced in massive quantities. DDT, for example, was
rst used by the Allied Army in Naples in 1943, but by the end of World
War II, DDT production was proceeding on an industrial scale. Currently,
we use about 700 million pounds of pesticide a year in the United States
(7). Antibiotic production is also high, with 25 to 50% going into
prophylactic use in live- stock feed (13).
Ine"cient use of antibiotics has been cited as a major cause of antibiotic
resistance. Partial treatment of infections with suboptimal doses leads to
partial control of the infecting cell population and creates a superb
environment for the evolution of resistant bacteria. Up to one-third of U.S.
pediatricians report overprescribing antibiotics to assuage patient
concerns, particularly in cases of viral childhood congestions that cannot
respond to the drug (32). Failing to complete a course of antibiotics is
associated with increased emergence of resistant tuberculosis and HIV in-
fections (33, 34 ), and di#erences in antibiotic use may partly explain
di#erences among nations in antibiotic resistance rates (2).
Spread of antibiotic resistance has been accelerated by transmission of
genes be- tween bacterial species (13). Recently, bio- technology has
applied this acceleration to other species as well, and a new human-
mediated mechanism for generating evolutionary novelty has emerged
insertion of exogenous genes into domesticated plants and animals.
Taken from bacteria, plants, animals, or fungi, these genes convey valu-
able commercial traits, and they are placed
into new host genomes along with genes that control expression and in
some cases allow cell lineage selection (35, 36). Examples include the
insertion of genes for insecticidal proteins (37 ), herbicide tolerance (38,
39) or novel vitamins (40) into crop plants; growth hormone genes into
farmed salmon (41); and hormone production genes into livestock
bioreactors (42). These e#orts e#ectively increase the rate of generation
of new traits-akin to increasing the rate of macromutation. When these
traits cross from domesticated into wild species, they can add to the fuel
of evolution and allow rapid spread of the traits in natural populations
(43). Genetic exchange from crops has already enhanced the weediness
of wild relatives of 7 of the worlds 13 most important crop plants (44 ),
although no widespread escape of an engineered gene into the wild has
been reported yet.

http://palumbi.stanford.edu/manuscripts/evolution.pdf


ARTICLE 3

Today, because of Darwins work, we have at least some understanding of
our ancestors and fellow members of the Homo genus (such as
Neanderthals, right), as well as some knowledge of where they originated.
But there remains much to be understood about our evolutionary history,
especially in terms of our physiology. We have opposable thumbs, yet it
seems that evolution has more work to do on the human body. We remain
disconcertingly susceptible to disease. Why is this?

The scientists determined to answer this question, and numerous related
questions, could be considered pioneers of the eld of Darwinian, or
evolutionary, medicine. They are taking on not only the challenge of
investigating the relationship between health and evolution but also the
criticism that comes with the application of evolutionary study to the
practice of medicine. But their common sense approach to understanding
why we are susceptible to disease has the potential to improve diagnosis
and treatment and to change the way we think about our bodies.

The human body is equipped for survival on both an anatomical and a
molecular level. The human brain, which is highly sophisticated and
advanced in its capabilities relative to the brains of other animals, is a
primary example of an anatomical feature that has facilitated the survival
of our species. But the intricate molecular mechanisms involved in
transmitting signals about pain, for example, are equally important to our
survival. Without the sensation of pain, we unknowingly expose ourselves
to life-threatening situations. In fact, people who cannot feel pain have
short life spans.

The impact of evolution on the molecular and biochemical facets of
human health are often quite complex; one example being the evolution
of genetic protection against malaria. Malaria has existed in Africa for
millennia and is believed to have drastically impacted the establishment
and advancement of African civilizations. Over time, the persistence of
malaria across the central belt of the continent acted as a form of
selective pressure, inuencing the genetic development of resistance to
the disease and thereby enabling the survival of human populations.

Malaria protection is generally viewed as a genetic trade o#it evolved
only in people who carried genes for sickle-cell anemia, an inherited
disease in which blood cells are misshapen (shaped like sickles).
Throughout history Africans without the sickle-cell genes died from
malaria, usually before reproductive age. As a result, many people ended
up as carriers for the sickle-cell trait, producing a genetic advantage, as
carriers are typically asymptomatic for sickle-cell anemia and are
conferred a high level of protection against malaria.

The sickle-cell trait serves as a good example of how knowledge about
our evolution can inuence the practice of medicine, since physicians
have realized that carriers of the sickle-cell trait often require unique
treatment and genetic counseling. It has also inspired scientists to
investigate the evolution of other genetic disease-protection mechanisms,
including the suspected genetic trade o# between susceptibility to
tuberculosis and inheritance of the gene for cystic brosis.

Arguments that human conditions such as depression serve evolutionary
purposes have been made as well, and some of these have been quite
convincing. Evolutionary theory has, of course, already impacted our lives
in profound ways. Darwinian medicine is poised to do the same.


http://www.britannica.com/blogs/2009/02/darwinian-medicine-
understanding-disease-in-terms-of-evolution/













ACTUAL ESSAY!!! By: Alyssa Karr

How do diseases change the evolution of humans? The answer to that
is that it's the diseases job to invade the host and spread to others which
also goes down there family trees. Also the diseases stays for a certain
amount of time(certain amount of generations) and than it starts to die
and drift away. "First, antigenic shift can occur through genetic
recombination, or reassortment, when two or more di#erent inuenza A
viruses infect the same host cell and combine their genetic material."

The diseases job is to invade the host. When it has invaded the host it
makes copies and spreads and than eventually jumps to another host. If a
characteristic makes it hard for the disease to spread, the diseases will
just be lost. When we have the disease it changes the way we act/
sometimes appearances. Also it's hereditary and will be passed on
sometimes to the next generation.

Some diseases will stay for along time and be passed on to the next
generation. But eventually it will start to drift away. If the host has a
disease that was passed down and than gets a new infection, the old
disease has no chance of ghting the new infection. It will most likely kill
you because you won't have enough energy and healthy cells to ght o#
all the diseases you have.

First, antigenic shift can occur through genetic recombination, or
reassortment, when two or more di#erent inuenza A viruses infect the
same host cell and combine their genetic material. The two viruses would
mix together and make another new disease and could possibly be more
powerful than both of the two diseases.

That is how a disease could change the evolution of humans.










http://phys.org/news/2013-12-discovery-
million-year-old-fossil-human-bone.html.








http://www.csc.mrc.ac.uk/
Research/Groups/EPI/EGR/