According to Moalem, there has been no explanation as to how the bubonic plague selected for people with the CCR5-Δ32 allele. Research the CCR5-Δ32 gene and explain how it affects our body to provide resistance to HIV. Also research the Yersinia pestis bacterium. Using this information, provide a possible explanation as to how the CCR5-Δ32 gene was selected for by the selective pressure of the Yersinia pestis bacterium. Or, if you want, explain how the CCR5-Δ32 gene may have been selected for by a different selective pressure. Finally, explain a single negative aspect to the CCR5-Δ32 gene because most genetic mutations that are selected for have a downside (e.g. hemochromatosis can starve out infecting agents of the bubonic plague but it causes iron buildups in our body which can lead to organ failure and Alzheimer's disease). References to cells, inheritance, and evolution are recommended.
(Name: Will Han email: wihan4@students.d125.org)
Homozygous carriers of the CCR5-Δ32 gene mutation have the ability to resist HIV-1 infections because what the CCR5-Δ32 gene mutation essentially does is it prevents functional expression of the CCR5 chemokine receptor normally used by HIV-1 to enter CD4+ T cells. Moalem also states on page 69 that one copy of this gene mutation “significantly hampers the virus’s ability to multiply, reducing the viral load in people who carry the gene and become infected.”
ReplyDeleteMany people speculate that this gene mutation provided earlier people resistance to the bubonic plague. The bacterium responsible for resistance to the bubonic plague is known as the Yersinia pestis bacterium. Yersinia pestis is primarily a rodent pathogen. Humans can become a host when bitten by a flea that was infected by a rat with this pathogen. When the bacterium enters the human body, most of the organisms are killed by leukocytes. However, some bacilli are taken up by tissue macrophages, which cannot kill the bacterium. The bacterium then are able to synthesize their virulence factors while protected by the macrophage. Eventually, the organisms kill the macrophage and are released into the extracellular environment, where they are able to resist phagocytosis and continue to spread.
Although many people think that the bubonic plague selected for individuals with this gene mutation, this gene mutation mainly provides protection from viruses. The fact that the bubonic plague was caused by a bacterium makes it unlikely that this disease was what selected for this gene mutation. Instead, it is more likely that a viral disease, like smallpox, selected for those with this gene mutation. Professor Christopher Duncan and D. Susan Scott support this claim when they published research in the March edition of Journal of Medical Genetics, which attributed the frequency of the CCR5-Δ32 gene mutation to its protection to another viral disease in history. Professor Duncan also said that “The fact that the CCR5-Δ32 gene mutation is restricted to Europe suggests that the plagues of the Middle Ages played a big part in raising the frequency of the mutation.” The idea that smallpox selected for this gene mutation is due to the fact that this gene mutation is more common in northern Europe, which was known to have more smallpox epidemics. Some scientists also believe it was a continuing series of viral, haemorrhagic fever that selected for the CCR5-Δ32 gene mutation, mainly because this virus uses CCR5 as an entry point to the immune system, and because there were various epidemics of this disease in European history.
A downside to the CCR5-Δ32 gene mutation is that chemokine receptors play an important role in the inflammatory response. Since the CCR5-Δ32 gene mutation creates nonfunctional chemokine receptors, the immune response of those with this mutation may be lower than those who do not have this mutation.
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0030339
http://www.sciencedaily.com/releases/2005/03/050325234239.htm
(Aaron Chai, achai4@students.d125.org)