Monday, April 28, 2014
Statistics and Reflection
Our BOINC grid completed 725.84 units of work over the semester installed on our computer. We feel that this project has contributed to our learning both of disease pathology and evolution of disease in a very real way. Our opportunity to speak with a professional in the field was an interesting way to see how concepts learned in the classroom can be applied in the real world, especially in the healthcare field. We felt that we made a difference through our small contribution to the grid; we learned a lot about grid computing in general and how we can help a lot just by donating a little of our computer space. This has been a very unique service learning project that we were happy to be a part of.
Saturday, April 5, 2014
“Evolutionary Ecology of Human Papillomavirus: Trade-Offs, Coexistence, and Origins of High-Risk and Low-Risk Types” Questions
Questions – Cervical Cancer
These questions address the Journal of Infectious Diseases article entitled “Evolutionary
Ecology of Human Papillomavirus: Trade-Offs, Coexistence, and Origins of
High-Risk and Low-Risk Types” by Orlando et al. (2011). Be sure to explain your answers.
1.
On
page 1, the authors describe two patterns of selection on the quantitative
trait virulence. Name these two patterns, described
below:
a. “Natural selection often favors
intermediate phenotypes”
In the above statement, the authors
are describing the pattern of selection known as stabilizing selection in which
individuals with intermediate values for the trait virulence have the highest
fitness. These individuals are favored by selection.
b. “…some ecological circumstances may promote
extremes of persistence or virulence”
In the above statement, the
authors are describing disruptive selection in which individuals with the
extreme values of virulence, low or high, have the highest fitness. In this
type of selection, the extremes are favored while the intermediate phenotypes
are selected against.
2.
Apply
Darwin’s postulates to HPV populations in human hosts (see page 2 for
guidance).
Postulate 1: There is
variation within a population. There are 9 different states, allowing for
variation, when dealing with this model of HPV. There are 3 celibate states of
people, being susceptible (S), infected (I), and resistant (R). There are 6
other states relating those 3 states; SS, SI, SR, II, IR, RR. This relates to
people in relationships. There is also variation in different HPV strands.
There are high risk (HR) and low risk (LR) types. HR types produce less virions
and have a longer duration of infection, immune response is slower. LR types
produce more virions and have a shorter duration of infection, so immune
response is quicker. HR types strive in long monogamous relationships while LR
types strive in many short relationships.
Postulate 2:
Variation is passed from parents to offspring. HPV replicates its DNA
within human host cells. LR types create more LR types and HR types create more
HR types.
Postulate 3: Some
individuals have greater fitness and results in over reproduction. There
are many copies of each type of virus in the human body.
Postulate 4:
Selection acts on the population. If the human host is in a long monogamous
relationship, HR types will thrive and continue to replicate because there will
be more sexual encounters allowing for a longer duration of infection. The LR
types will die in that particular human. If the human host is in many short
relationships, LR types will thrive and continue to replicate because there are
less sexual encounters and the virus needs to be transmitted quickly with each
encounter and be able to have a shorter duration of infection with more virions.
The HR types will die in that particular human. There is also selection acting
in resistant humans. They can no longer contract that particular type of virus,
so the virus will not be passed on even if they are in a relationship with an
infected person. That particular type of virus will eventually die off either
if it has nowhere to move on.
3.
What
is an adaptive landscape (sometimes called a Wrightian landscape)? Please include a 3D figure (with
citation).
An adaptive landscape
represents the mean fitness of a population. It looks like a mountain and
involves multiple dimensions in space. As populations evolve adaptively, they
move up the mountain towards the peaks. Multiple gene frequencies are
represented on the graph. The high peaks represent high fitness and the low
peaks represent low fitness, as illustrated in the figure below. Many loci are
represented on an adaptive landscape and contribute to the fitness of a
population.
Figure represents 2 loci: http://evolution.berkeley.edu/evosite/evo101/images/adaptivelandscape.gif
4. The authors define Evolutionarily
Stable Strategies on page 4. Can you please explain ESSs in understandable
terms?
Basically,
ESSs depend on the simple principle of consumer and resources. Since the amount
of susceptible individuals depends on the types of viruses present, different
strains have different viral fitness, or the “per-capita growth of infected
individuals”. A specific virus has to fight against the other phenotypes to
have the highest fitness. An ESS is a form of convergent evolution in which the
virus’s “strategy” converges upon several different factors to become most
advantageous. Once the ESS is fixed in a population, nothing can disrupt it.
Since natural selection acts so strongly on the ESS, no other mutations can be
large enough to tilt the strategy of the population to have the best fitness.
A
thought experiment given by Cornell University really helps to illustrate this
concept. Suppose that one group of people, or population, is using the same
strategy in a game, such as poker. The benefit is that everyone is using the
same strategy, so all are receiving the same benefits. Now let’s say that one
smaller group within the population begins using a different strategy. The
minority would win out over the majority if they receive more adaptive
benefits. So now, the minority strategy would beat out the majority strategy,
which is no longer evolutionarily stable. If the minority has less
fitness/survival than the majority, then the majority group has an ESS that is
fixed in the population.
Adapted from http://ess.nbb.cornell.edu/ess.html
5. Given the paper’s conclusion (see page
7), what would you predict about the efficacy of HPV vaccines? Why should an
OB/GYN know about evolution?
Since
HPV responds to natural selection and other evolutionary forces, getting rid of
one strain of the virus would act as an open niche for other strains to fill.
This would create even more of a problem due to a larger amount of mutated
viruses. HPV strains compete and will evolve at a fairly high rate, so this
mutation of virus will occur relatively fast. According to the authors, the
vaccine would act as a “strong selective force”. This means that the virus
wouldn’t necessarily completely wipe out a selected strain, but it would act as
a mechanism of evolution against it. Then, the potentially dangerous viral
interactions would be diminished.
OB/GYNs
should definitely have some sort of background in evolution because of the way
that the HPV virus can mutate and change with evolutionary forces. HPV is a
huge worldwide problem, and OB/GYNs see and treat it almost daily. They need to
be able to recognize the strains in order to complete the right testing and
treatment if necessary. Also, evolution plays a role in the formation of
cervical and breast cancers. People’s individual genetics interact with their
environments, and doctors need to be able to understand the risk factors to
educate their patients about.
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