HIV (human immunodeficiency virus) is a virus that attacks cells that help the body fight infection, making a person more vulnerable to other infections and diseases. It is spread by contact with certain bodily fluids of a person with HIV, most commonly during unprotected sex (sex without a condom or HIV medicine to prevent or treat HIV), or through sharing injection drug equipment.
If left untreated, HIV can lead to the disease AIDS (acquired immunodeficiency syndrome).
Without HIV medicine, people with AIDS typically survive about 3 years. Once someone has a dangerous opportunistic illness, life expectancy without treatment falls to about 1 year.
After a person is infected with HIV, the virus seeks out the body's immune cells and attaches itself to them in the hopes of producing more virus particles. HIV's "main target" are CD4 immune cells. In the acute stages of infection the virus destroys a lot of CD4 cells and produces many virus particles. In turn the immune system goes into overdrive to try and ward off infection. After the acute stage the virus enters into a period of clinical
latency that can last many years. During
this time the virus is active but reproduces minimally. In the last stage of infection, AIDS, the number of CD4 cells drops well below the normal level (below 200 cells per cubic millimeter of blood - 200 cells/mm3). The body's immune system is left critically damaged, leaving the person susceptible to illness.
A genetic mutation known as CCR5-delta 32 is responsible for the two types of HIV resistance that exist. CCR5-delta 32 hampers HIV's ability to infiltrate immune cells.
CCR5 co-receptor acts like a door that allows HIV to enter the cell. The CCR5-delta 32 mutation changes its conformation, making it smaller and less prominent, thus locking that door and preventing the entrance of the virus.
This mutation is present in approximately 1% of people descended from Northern Europeans, particularly Swedes. These lucky people are homozygous carriers of the mutated gene - meaning that they inherited a copy from both of their parents. Another 10 -15% of people with European heritage inherited one copy of the gene. While having one copy of the mutation does not fully prevent infection, It does however reduce the carrier's chances of infection and delays the progress of AIDS. Since the CCR5-delta 32 is tied primarily to the Eurasia region, the mutation has not been found in Africans, East Asians, or Amerindians.
Why does the CCR5-delta 32 mutation appear in people of European descent only?
There is no solid answer to this question yet but many theories have been suggested. What researchers know for sure is that the mutation has been in the population longer than HIV has been infecting people. HIV resistance is just a consequence of the mutation, not a motive for its existence. How long the mutation has been in humans varies depending on which scientist you ask. The answers range from 700 to 2900 years.
One hypothesis suggests that the mutation originated in the Vikings. It is estimated that the allele was present in Scandinavia 1,000 to 1,2000 years ago. Through their many invasions, the Vikings spread the allele from Scandinavia to Iceland, Russia, and central and southern Europe. Which would provide an explanation of why the gene appears more frequently in Northern Europeans than it does in Southern Europeans.
Another line of reasoning is that past epidemics were the driving force behind the prevalence of this mutation in Europeans. Scientists hypothesize that the mutation gave some sort of advantage to people against the epidemic. If we take that the mutation had formed 700 years ago it coincides perfectly with the Black Death. According to this idea, the Black Death drove natural selection in the human population. Those with the mutation were more likely to survive the plague and pass on their genes than those without it, which caused an increase in the percentage of people with the mutation. Smallpox is another epidemic that has been suggested. Those in favor of smallpox have continuity on their side. Unlike the Black Death, smallpox has not been eradicated, but on the opposite has been continuous this entire time. Alison Galvani, a Yale University professor of epidemiology, notes that smallpox's longevity provided a reason for the mutation to continue throughout the generations. It's also interesting to note that HIV and smallpox both utilize the CCR5 receptor to infiltrate other cells.
Could it just be a coincidence? Or is that proof of their correlation?
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