Monday, March 30, 2009
Even though Allison is his last name I keep thinking its a girl!
On Page 174 it talks about Allison's adventures in Africa experimenting with Sickle Cell Disease. So the question is... How does the shape of sickled cell affect its ability to resisit Malaria? So Basically how does the structure relate to its function? How does the passage of Malaria through the generations affect evolution? Are humans battling evolution for humans when they attempt to interfere with natural selection through pesticides and DDT, or are they catlayzing the evolution chain for mosquitos to become this super mosquito that is immune to everything but time? Is our interaction with the environment solely affecting mosquitos and humans or are they affecting other things too? What are the environmental casualties that were just caught in the cross fire between mosquitos and humans such as crops and plants? How are we affecting them and changing their evolutionary pace?
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The sickle cell trait is named for its sickle-like appearance of red blood cells (RBCs) in humans. It is genetically dominant in humans; those with only one copy of the mutation exhibited sickle cell under certain conditions while those with two copies had the full disease. The hemoglobin molecule, an oxygen carrying protein of RBCs, was found to have a mutation in sickle-cell infected patients, discovered by Linus Pauling in 1949. Allison demonstrated in 1953 that humans with sickle cell traits were fairly resistant to “induced malarial infections and that children with sickle cell harbored lower numbers of parasites than children with normal hemoglobin” (Carroll 176).
ReplyDeleteThe shape of a sickle-cell may affect its ability to resist malaria because “the distorted red blood cells caused by the gene are broken down quicker than normal by the body so malaria has no home in which to thrive” (source: http://news.bbc.co.uk/1/hi/health/4587311.stm). The scythe-shape of the sickle cell aids it in helping to preventing malaria; thus, most of the blood cells carrying malaria are destroyed although some blood cells do escape, but not enough to cause malaria. The sickle cell mutation, while harmful in two copies, can lend survival advantages in one copy. The G6PD deficiency showed that the risk of malaria was reduced approximately 46 to 58 percent; the G6PD deficiency also inhibited parasite growth. Another mutation prevents malaria from entering the cells. Malaria and humans’ resistance to malaria are, in a way, coevolving with each other, similar to how the rattlesnake and the newt coevolved (Carroll 166).
Allison discovered that tribes in Kenya that lived close to Lake Victoria or the Kenya coast were more likely to have a higher frequency of the sickle cell trait, about twenty percent; in contrast, tribes that lived in the highlands or arid regions, the percentage was less than one percent. Allison then hypothesized that the sickle cell frequency in different tribes was related to resistance to malaria; “he knew that malaria and the mosquitoes that carry it were much more prevalent in low-lying, moist area, and nearly or completely absent in higher elevations or where freshwater was lacking” (Carroll 175).
The correlation between malarial zones and sickle cell frequency “cuts across tribal and language boundaries”; this is seen on figure 7.3. The sickle cell mutation is caused “by a single change in the sixth triplet of the gene (from GAG to GTG) and arose . . . five times in human populations” (Carroll 177). In other words, evolution, like history, repeats itself. A form of malaria gains entrance to RBCs by latching onto the Duffy protein; African populations have a mutation that eliminates the Duffy protein on RBCs whereas Caucasians and Asians rarely have this mutation. Malaria’s passage throughout African generations has allowed African populations to keep a useful mutation in their genes that allowed them to resist malarial infection. Malaria, which is not as rampant in Asian or Caucasian populations, has not caused Asian or Caucasian populations to keep the mutation as a genetic advantage.
Malaria’s most virulent form arose in the last 3200 to 7700 years and corresponds with the spread of agriculture (which began about 10,000 years ago). Cleared forests led to increased amounts of sunlit pools of water where mosquitoes carrying the parasites breed. Humans changed the environment around them when they switched from a hunter and gatherer lifestyle to a more sedentary one; the plants and crops were thus affected when humans started farming and clearing forests. This subsequently facilitated the breeding of mosquitoes and spread of malaria. Humans are both “battling evolution for humans when they attempt to interfere with natural selection through pesticides and DDT” and “catalyzing the evolution chain for mosquitoes to become this super mosquito that is immune to everything but time” (Scotty); this is because every time humans try to artificially manipulate the course of evolution, they are also making parasite and bacteria more powerful, such as the case of 99.9% bacteria killing hand sanitizers or the DDT and drugs mentioned in the book (181); eventually the parasite became immune to such drugs such as Chloroquine. This is because drugs create a condition where only the “fittest” of the bacteria survive, the 0.1%, and then, their drug-resistant mutations survive as well.
Works Consulted: http://discovermagazine.com/1992/nov/canwewipeoutdise150/?searchterm=sickle%20cell
When one has full blown sickle cell disease (homozygous recessive), one will die due to the complications of the disease, however, when one has sickle cell trait (heterozygous), this person is better equipped to fight off malaria. This is primarily due to the fact that people with sickle cell trait have almost normal shaped blood cells under normal oxygen tensions. However when oxygen tensions fall, such as at high elevations and in areas of low atmospheric O2 concentrations, the red blood cells gain the sickle shape. The malaria parasite lowers the oxygen tension in red blood cells by affecting the hemoglobins affinity to O2. Therefore, in people who have sickle cell trait and malaria, the infected cells will gain the sickle shape. Such a change in shape affects the immune systems ability to recognize the blood cell as self, and therefore, and immune response is triggered and all of the sickle shaped (infected) blood cells are destroyed by phagocytes and Tc cells. This gets rid of many of the malaria pathogens.
ReplyDeleteSickle cell trait also causes resistance to malaria due to the fact that sickle trait red cells produce higher levels of the superoxide anion (O2-) and hydrogen peroxide (H2O2) than do normal red blood cells. Each compound is toxic to malarial parasites.
http://sickle.bwh.harvard.edu/malaria_sickle.html+sickle+cell+disease+and+resistance+to+malaria&cd=3&hl=en&ct=clnk&gl=us