Writing Assignment

HIV (human immunodeficiency virus) is a fairly new virus compared to some others, i.e. measles, small pox, polio, etc. HIV became popular during the 80’s. In modern times scientists have manufactured drugs to treat HIV patients, but we have yet to hear of the cure. In even more recent years to present, more in-depth research is being performed in an effort to find a way to combat it. This research involves delving into such areas as cultural statistics of vulnerability, the cellular make up of HIV, and the makeup of susceptible cells in humans. There is much more research to be performed, but these are a few of the areas that will be discussed in detail here. I am an advocate for the studies mentioned here; and a believer that the body is designed to evolve with its environment to protect and heal itself.

One well studied and known detail about HIV is that a particular group of people are immune to the virus. “HIV can only enter certain cells…By special proteins called receptors. Receptors sit on the outside of cells to receive messages and transmit them into the cell. HIV grabs onto cells that have a receptor called CD4… CD4 isn't enough. Another protein called CCR5 is needed as well…because it works with CD4, is the door that opens to allow HIV to enter the cell…Many people who are resistant to HIV have a mutation in the CCR5 gene called CCR5-Δ32. The CCR5-Δ32 mutation results in a smaller protein that isn't on the outside of the cell anymore. Most forms of HIV cannot infect cells if there is no CCR5 on the surface. People with two copies of the CCR5-Δ32 gene (inherited from both parents) are virtually immune to HIV infection. This occurs in about 1% of Caucasian people.” (The Tech Museum of Innovation) This is an eye opening discovery for scientists. This means that there is indeed a ‘repellant’, of sorts, to the HIV virus. But also interesting to discover, is the answer to why and how this mutation came about.

The how and why are yet to be absolutely determined, but there are some interesting ideas. All of which make, at least, some sense. This mutation evolution has a few theories worth noting: Vikings, The Bubonic Plague, and Smallpox. A significant detail that would increase or decrease the probability of each of these theories occurring is the age of the mutation. There are estimates that “range from 700 to 2900 years” ago. (Paoli) Something else to note is the geographic isolation of these mutation cases. The CCR5-Δ32 mutation is said to be exhibited more frequently in humans living in Northern Europe than in Southern Europe. So with the theory of Vikings is that they could have been carriers of the mutant allele in their home land, Scandinavia. Then they dispersed, visiting Iceland, France, the Mediterranean coasts and Russia. (Galvani, Novembre) This seems possible but inconclusive; why are Viking carriers either?

The Bubonic Plague has been accused as a catalyst in the rapid spread of the CCR5-Δ32. An article from the University of Liverpool highlights the series of plagues and epidemics that continued in the area where the immunity to HIV is mostly isolated. This article states: “…the plagues of Europe (1347-1660) were in fact a continuing series of epidemics of a lethal, viral, haemorrhagic fever that used the CCR5 as an entry port into the immune system. Using computer modeling, they demonstrated how this disease provided the selection pressure that forced up the frequency of the mutation from 1 in 20,000 at the time of the Black Death to values today of 1 in 10.” Additionally, it states: “Professor Duncan added: "Haemorrhagic plague did not disappear after the Great Plague of London in 1665-66 but continued in Sweden, Copenhagen, Russia, Poland and Hungary until 1800. This maintenance of haemorrhagic plague provided continuing selection pressure on the CCR5-Ä32 mutation and explains why it occurs today at its highest frequency in Scandinavia and Russia."” (University of Liverpool) This is certainly interesting because with this prevalence of epidemics that were accessing the human body through the same allele that HIV does, those who survived somehow had built up an immunity to those epidemics through a mutation of that allele. And this leads to the connection with an immunity to the modern day virus, HIV. Another article did all sorts of mathematical research and surveys of different ethnicities, and here are their comments: “Genomic DNA samples obtained from 4,166 individuals, as identified in 38 ethnic groups…The results suggest a north-to-south gene-frequency gradient (or cline), with the highest allele frequencies in northern Europe (14%) to a low of 4.4% in Greece. The CCR5-Δ32 allele was not found among Lebanese, Georgian, Saudi, Korean, Chinese, or American Indian (Cheyenne, Pueblo, and Pima) populations in samples of 40–100 individuals.” (American Journal of Human Genetics)

The final theory, I will discuss here, is small pox and its possible influence on the mutation of CCR5. As referenced in the article by Amber Angelle, researchers are leaning toward small pox as the culprit for the mutation rather than the black plague, because “…the scientists explained that smallpox was around far longer than the plague and killed far more people…” This would mean that the mutation was more probable for a larger population and further justify the present-day existence of the mutation. “Even when we assumed that the resistance allele was dominant, we found that bubonic plague could not generate sufficient selective pressure to account for current CCR5-Δ32 frequencies...Our results suggest that plague could not even have driven the resistance allele to 1% during the period that it existed in Europe. However, we found that the more continuous smallpox mortality that afflicted European children since the origin of the allele could have provided the necessary selective pressure to generate the rise of CCR5-Δ32 deletion to current frequencies of 10%.” (Galvani, Slatkin) This encourages my opinion that smallpox was the ‘designer’ of the mutated allele.

Science is continuing to look for new ways to combat HIV by digging deeper and deeper. Scientists have experimented with stem cells containing the CCR5 mutation and injected HIV infected mice in which the virus was destroyed. A bone marrow transplant was successful for curing an HIV-positive patient. When scientists “studied Kenyan women who were still HIV-free after working as prostitutes for at least three years”, they found increased levels of cystatin. These and other theories and untested ideas are a remarkable representation of how humans have educated ourselves to recognize the natural tendencies of human biology as a way to evolve for maximum survival. Our bodies are certainly designed for life into infinity. So, why don’t we live forever? That is an excellent topic for a later time.