Showing posts with label adaption. Show all posts
Showing posts with label adaption. Show all posts

Wednesday, April 22, 2009

Another Creationist?

Do we have another creationist on the blog? This one is a bit tougher to decifer. This person does pose an interesting question (see below).


Mynym wrote:
..and every fact that has something to do with evolution confirms its truth.
Interesting... so what type of biological observation would not confirm "evolution," whatever it may be?

Actually there is a few answers to this but I think I will take HIV for two-hundred Alex.

Berkley University has a website dedicated to understanding evolution. One of their web pages lists in detail how the HIV virus evolves. I will re-post their findings below. You can also see this example in the PBS Evolution series which can be found here. I warn you, it is long but well worth the time.

D

Re-posted from: http://evolution.berkeley.edu/evolibrary/article/_0_0/medicine_04

HIV: the ultimate evolver

Evolutionary biologists can help uncover clues to new ways to treat or vaccinate against HIV. These clues emerge from the evolutionary origins of the virus, how human populations have evolved under pressure from other deadly pathogens, and how the virus evolves resistance to the drugs we've designed. Controlling the disease may be a matter of controlling the evolution of this constantly adapting virus.

HIV micrographThe human immunodeficiency virus (HIV, shown here budding from a white blood cell) is one of the fastest evolving entities known. It reproduces sloppily, accumulating lots of mutations when it copies its genetic material. It also reproduces at a lightning-fast rate — a single virus can spawn billions of copies in just one day. To fight HIV, we must understand its evolution within the human body and then ultimately find a way to control its evolution.

Taking an evolutionary perspective on HIV has led scientists to look in three new directions in their search for treatments and vaccines:

  • What are the evolutionary origins of HIV?
  • Why are some people resistant to HIV?
  • How can we control HIV's evolution of resistance to our drugs?

Origins of HIV-1
1. What are the evolutionary origins of HIV?
HIV, like any evolving entity, has been deeply marked by its history. Scientists studying the evolutionary history of HIV found that it is closely related to other viruses. Those viruses include SIVs (simian immunodeficiency viruses), which infect primates, and the more distantly related FIVs (the feline strains), which infect cats.

However, studies of these related viral lineages showed something surprising: primates with SIV and wild cats with FIV don't seem to be harmed by the viruses they carry. If scientists can figure out how non-human primates and wild cats are able to live with these viruses, they may learn how to better treat HIV infections or prevent them altogether.

The diagram shows some of the evolutionary history of HIV as we know it today. An ancestral virus (bottom) evolved into strains that infected chimpanzees (SIV). Over time, new strains began to infect humans (HIV).

2. Why are some people resistant to HIV?
HIV is by no means the first plague that human populations have weathered. Many pathogens have deeply affected our evolutionary history. In fact, the human genome is littered with the remnants of our past battles with pathogens — and one of these remnants, a mutation to a gene called CCR5, may lead researchers to a new treatment for HIV.

The CCR5 mutation in EuropeThe mutant CCR5 allele probably began to spread in northern Europe during the past 700 years when the population was ravaged by a plague. (It may have been bubonic plague or some other pathogen; research on this topic continues.) The mutant CCR5 probably made its bearers resistant to the disease, and so its frequency increased.

In some parts of Europe today, up to 20% of the population carry at least one copy of the protective allele. However, the populations of Asia and Africa were not exposed to the same epidemics; very few Asians and Africans now carry the allele (see map above). Thus, CCR5 is fairly common in northern Europe but its frequency diminishes as one moves south, and the mutation is rare in the rest of the world.

We now know that the mutant CCR5 allele has an unexpected side effect: it confers resistance to HIV. Scientists hope that studying this by-product of past selection will help them develop new treatments for the HIV epidemic ravaging human populations today.

3. How can we control HIV's evolution of resistance to our drugs?
HIV evolves so quickly that it evolves right out from under our treatments. When a patient begins taking an HIV drug, the drug keeps many of the viruses from reproducing, but some survive because they happen to have a certain level of resistance. Because of HIV's speedy evolution, it responds to selection pressures quickly: viruses that happen to survive the drug are favored, and resistant virus strains evolve within the patient, sometimes in just a few weeks. However, basic evolutionary theory points out a way that this evolution of resistant viral strains can be delayed. Patients are prescribed "drug cocktails" — several different HIV drugs taken together.

When taking any single drug, it is fairly likely that some mutant virus in the patient might happen to be resistant, survive the onslaught, and spawn a resistant lineage.

a patient takes a single antibiotic, and all bacteria resistant to that drug survive

But the probability that the patient hosts a mutant virus that happens to be resistant to several different drugs at the same time is much lower. Although multiple-drug-resistant HIV strains do eventually evolve, drug cocktails delay their evolution.

a patient takes several antibiotics, and few bacteria survive because most are not resistant to all of the drugs

An evolutionary trade-off
If a patient is already infected with a drug-resistant HIV strain, basic evolutionary theory has also pointed out a way to make the drug useful again. Studies of the evolution of resistance often show that you don't get something for nothing. Specifically, it "costs" a pest or pathogen to be resistant to a pesticide or drug. If you place resistant and non-resistant organisms in head-to-head competition in the absence of the pesticide or drug, the non-resistant organisms generally win.

Consider a patient who takes a particular drug and winds up with viruses resistant to the drug. If the patient stops taking the drug for a while, evolutionary theory predicts that her viral load will evolve back towards a non-resistant strain. If she then takes very strong doses of the drug, it may be able to halt the replication of those non-resistant viruses and reduce her viral load to very low levels.

Defeating resistant viral forms

This therapy has shown early, promising results — it may not eliminate HIV, but it could keep patients' virus loads low for a long time, slowing progression of the disease.

Ultimately, understanding the evolutionary history of HIV and its pattern of evolutionary change may help us control this disease.

Friday, January 23, 2009

15 Gems of Evolution (Part 11)

11) Evolutionary history matters

Evolution is often thought to be about finding optimal solutions to the problems that life throws up. But natural selection can only work with the materials at hand — materials that are themselves the results of many millions of years of evolutionary history. It never starts with a blank slate. If that were the case, then tetrapods faced with the task of moving on land would not have had their fins transform into legs; they might perhaps have evolved wheels.

A real-life case of the ingenuity of adaptation concerns a moray eel (Muraena retifera), a long, snake-like reef predator. Historically, bony fish use suction to catch their prey. A fish approaching food opens its mouth wide to create a large cavity into which prey and water flood. As the excess water leaves through the gills, the fish sucks the prey down into its throat and pharyngeal jaws, a second set of jaws and teeth derived from the skeleton that supports the gills. But morays have a problem because of their elongated, narrow shape. Even with their jaws agape, their mouth cavity is too small to generate enough suction to carry prey to their
pharyngeal jaws. The solution to this conundrum was documented in 2007.

Through careful observation and X-ray cinematography, Rita Mehta and Peter Wainwright from the University of California, Davis, discovered evolution’s breathtaking solution. Rather than prey coming to the pharyngeal jaws, the pharyngeal jaws move forwards into the mouth cavity, trapping the prey and dragging it backwards. This, the researchers say, is the first described case of a vertebrate using a second set of jaws to both restrain and transport prey, and is the only known alternative to the hydraulic prey transport reported in most bony fish — a major innovation that could have contributed to the success of moray eels as predators.

The mechanics of the moray’s pharyngeal jaws are reminiscent of the ratchet mechanisms used by snakes — also long, thin and highly predatory creatures. This is an instance of convergence, the evolutionary phenomenon in which distantly related creatures evolve similar solutions to common problems. This study demonstrates the contingent nature of evolution; as a process it does not have the luxury of ‘designing from scratch’.

Reference
Mehta, R. S. & Wainwright, P. C. Nature 449, 79–82 (2007).
Additional resource
Westneat, M. W. Nature 449, 33–34 (2007).
Author websites
Rita Mehta: http://www.eve.ucdavis.edu/~wainwrightlab/rsmehta/index.html
Peter Wainwright: http://www.eve.ucdavis.edu/~wainwrightlab

Tuesday, January 20, 2009

15 Gems of Evolution (Part 8)

8) A case of co-evolution

Species evolve together, and in competition. Predators evolve ever deadlier weapons and skills to catch prey, which, as a result of Darwin’s canonical ‘struggle for existence’, become better at escaping them, and so the arms race continues. In 1973, evolutionary biologist Leigh Van Valen likened this to the Red Queen’s comment to Alice in Lewis Carroll’s Through the Looking Glass, “it takes all the running you can do, to keep in the same place. If you want to get somewhere else, you must run at least twice as fast as that!” The ‘Red Queen’
hypothesis of co-evolution was born.

A problem with studying Red-Queen dynamics is that they can be seen only in the eternal present. Discovering their history is problematic, because evolution has generally obliterated all earlier stages.

Happily, Ellen Decaestecker from the Catholic University of Leuven in Belgium and her colleagues discovered a remarkable exception, in the co-evolutionary arms race between water fleas (Daphnia) and the microscopic parasites that infest them; their research was published in 2007. As the water fleas become better at evading parasitism, the parasites become better at infecting them. Both prey and predator in this system can persist in dormant stages for many years in the mud at the bottom of the lake they share. The sediments of the lake
can be dated to the year they were formed, and the buried predators and prey can be revived. Thus, their interactions can be tested, against one another, and against predators or prey from their relative pasts and futures.

Confirming theoretical expectations, the parasite adapted to its host over a period of only a few years. Its infectivity at any given time changed little, but its virulence and fitness rose steadily — matched at each stage by the ability of the water fleas to resist them.

This study provides an elegant example in which a high-resolution historical record of the co-evolutionary process has provided an affirmation of evolutionary theory, showing that the interaction of parasites and their hosts is not set in time but is instead the result of a dynamic arms race of adaptation and counter-adaptation, driven by natural selection, from generation to generation.

Reference
Decaestecker, E. et al. Nature 450, 870–873 (2007).
Additional resources
The Red Queen Hypothesis: http://en.wikipedia.org/wiki/Red_Queen
Van Valen, L. Evol. Theory 1, 1–30 (1973).
Author website
Ellen Decaestecker: http://bio.kuleuven.be/de/dea/people_detail.php?pass_id=u0003403