Saturday, April 11, 2009
Detrimental Diseases helping Life pg. 174
According to the book we are currently reading, the sickle cell trait was first discovered in 1910. Later on, an expedition was put under way along the Kenyan cost to try and understand why tribes along the cost had a "20 percent" higher rate of sickle cell anemia then tribes more towards the interior of the land. What Anthony Allison, the scientist working in this expedition, found was that sickle cell anemia actually helps to combat malaria, which was also prevalent at the time. Please provide one example of how such a detrimental disease to humans can actually have some preventative properties. Also, tie into your response the evolutionary outlook that the disease creates for humans.
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One disease that also has positive effects, similar to sickle-cell anemia and its prevention of malaria, is Cystic Fibrosis. According to Carroll, the mutation that causes Cystic Fibrosis helps prevent typhoid fever by making the body more resistant to the bacterium that causes the disease (180). In terms of evolution, the Cystic Fibrosis mutation survived natural selection because at the time of first occurrence, it was more beneficial to suffer with Cystic Fibrosis than it was to suffer with typhoid fever. However, today doctors can provide antibiotics and other treatments to treat typhoid fever, so the Cystic Fibrosis mutation has become detrimental to the body. Thus, over time natural selection should remove the Cystic Fibrosis mutation from the rest of the human population because the gene is no longer beneficial, but rather detrimental. There is no longer the evolutionary pressure to keep the Cystic Fibrosis mutation.
ReplyDeleteOn pg. 178, Carroll talks about the G6PD enzyme. Deficiency of the glucose-6-phosphate dehydrogenase (G6PD) can cause hemolytic anemia because the enzyme, when functioning normally, helps erythrocytes function normally. G6PD is an enzyme that aids the body in processing carbohydrates and performing cellular respiration in order to produce ATP from glucose. G6PD deficiency is an X-linked recessive hereditary disease (meaning that the disease is more common in males). G6PD deficiency is the most common human enzyme deficiency. African, Middle Eastern, and South Asian people are usually the ones affected and some researchers believe that the mutation may have developed to prevent malaria, especially the type caused by Plasmodium falciparum (italicized). P. falciparum is the parasite that causes the most deadly form of malaria and the parasite uses erythrocytes as hosts. Therefore, if the erythrocytes are destroyed or damaged due to G6PD deficiency, the parasite has no host cell to occupy and the parasite won't survive. This was proved in a study reported by medical news today. (http://www.medicalnewstoday.com/articles/65129.php)
ReplyDeleteThere are now preventative treatments for G6PD deficiency as well as malaria. If people were to take these treatments, then the mosquitoes carrying the malaria would eventually die off from lack of resources. Therefore, it would follow suit that the G6PD deficiency may eventually die off because there would be no cause to prevent malaria if there was no malaria.
Thalassemia is another example related to preventing malaria, but since the opening paragraph discusses malaria I'm going to bring up another point. A useful thing to have happen is to aquire a disease such as German measles and mumps, in a sense being vaccinated from it so your body can become immune to it and have an have an arsenal of antibodies ready next time the disease shows up so it doesn't kill you. Now this isn't an inherited disease, but it is benefecial to undergo such a process so you can survive and reproduce. As David and Erin noted, since the diseases such as cystic fibrosis, sickle cell amenia and Thalassemia have now become determinal, it is only a matter of time before they are worked out of the evolutionary cirle. Or maybe they'll be cured with advanced technology, but that would too in essence remove it from the gene pool.
ReplyDeleteAs David Bruk has mentioned, genetic mutations can cause diseases.While a mutation of the CXCR4 coreceptor does not cause a specific disease, the mutation contributes to a myriad of health problems. We have learned that the CXCR4 coreceptor, which is also called fusin, acts as a receptor for chemokines. Studies have shown that genetic mutations that cause deletions of the genetic text that codes for CXCR4 cause defects in the heart, brain, and blood vessels. Like the G6PD deficiency mentioned by Erin Cohen, the mutation of the CXCR4 can be inherited from parents.
ReplyDeleteAlthough the genetic mutations have a negative effect on the body, the defective receptors also protect against HIV. In the immunity unit, we have learned that “the entry of the virus requires not only CD4 on the surface of the susceptible cell but also a second protein molecule, a coreceptor” (Campbell 919). The coreceptor CXCR4 is found on helper T cells, the cells that HIV targets. When a person has a deletion in the text that codes for CXCR4, the CXCR4 receptor becomes defective. The CXCR4 can no longer bind to chemokines, which may be the cause of the negative effects on the development of the heart, brain, and blood vessels. In order for the HIV to infect T cells, the virus also needs to bind to the CXCR4 receptor independently of binding to the CD4 molecules. Because the CXCR4 receptors of the individuals with the mutation are non-functional, the virus cannot bind to the CXCR4 receptors, and thus cannot infect the Helper T cell. The people who have the genetic mutation that deleted part of the CXCR4 text are innately resistant to HIV-1 entry.
Now, scientists are trying to genetically modify the CXCR4 receptors to minimize negative effects on the body and still prevent the HIV virus from binding to the receptor. If the scientists an figure out a way to permanently alter the CXCR4 receptor so the HIV virus cannot bind to the receptor, people will become resistant to HIV. The idea of the CXCR4 receptor becoming non-functional relates to the theme of structure/function, which deals with how the form of something affects its operation. In the case of the CXCR4 receptor, the deletion of part of the text results in a change in the form of the receptor, as amino acids that should be coded for are not being coded for. The change in the receptor causes the inability of both the virus and chemokines to bind to the receptor, changing the function of the receptor.
http://www.thebody.com/content/art4978.html
http://www.springerlink.com/content/j272502234470v13/