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There are many examples of an apparent resistance to HIV/AIDS, and they have been known for some years now. There are at least several hundred recorded cases of sex workers in central and southern Africa, arguably at the highest risk of infection anywhere in the world (as incidence of the virus are extremely high and condom use very unpopular) who are unaccountably not infected. This can only be explained by some kind of natural immunity. The problem with conducting organised research into this phenomenon is that the people in question are very reluctant to come forward, because of the stigma associated both with their profession and the disease itself. Lack of financial resources doesn't help, either.

Another piece of evidence that the HIV virus is not one size fits all is the distribution of HIV/AIDS infection across the continent of Africa. Central and southern Africa are notorious for being the areas with the highest incidence of the disease in the world - as high as %30 in some countries. Unaccountably, North Africa is one of the places with the lowest incidence, and the Middle East has the lowest infection rate of anywhere in the world, including the industrialised countries where condom use and sex education are of a much higher level.

Initially this striking difference in such relative physical proximity tended to be attributed to differences in social mores and behaviour induced by religion. However, it emerges that Black Africans are not so promiscuous, and Middle Eastern Muslims not so chaste, as was previously believed. Even in countries where the two populations come into contact, such as Sudan, Libya and Egypt, the demarcation line seems at least to run among racial grooves. Unfortunately, the aforementioned social taboos make research of individuals in these countries very difficult, as well as the fact that many of them live under totalitarian regimes which do not allow much interaction with Western scientists for their citizens.

This evidence, impressive as it is, is somewhat complicated by the fact that different parts of the world are afflicted with different strains of the virus. The disease is not exactly the same for someone who is infected in Europe as, say, Botswana. Southern Africa emerges to have been struck by the double whammy of the lowest natural immunity levels and the most virulent strain of the virus. Nevertheless, the evidence to suggest natural immunity is mounting and research is being done, however slowly.

It's possible that around 14% of the population of Europe and the United States have at least a resistance, if not total immunity to HIV.

Why?

Apparently, because their ancestors survived the Black Plague.

A mutation that affects the protein structure of the cell membrane of immune cells, referred to as Delta 32, has been found to be present in significant numbers among both direct descendents of bubonic plague survivors, and among some gay men who received heavy exposure to the virus in the 1970's through unprotected sex with infected men who later died of AIDS, and yet failed to become infected themselves.

Tests in which the blood of these individuals is exposed to levels of HIV thousands of times higher than a typically infective dose have revealed that no matter what dosage of HIV they are exposed to, their cells are not penetrated by the virus. Apparently, this is due to the absence of a surface protein that bonded to by the protein coat of the HIV virus.

An individual may have either one or two copies of this mutation. It is suspected that individuals with one copy are the source of stories dating to the time of the Black Death that recall an individual being exposed to infection, acquiring symptoms of the disease, and then recovering. Their recovery was often attributed to external factors (one woman is said to have recovered because she drank bacon grease), but some scientists now suspect that genetic defense was the real answer.

Others, who are presumed to have had two copies of the mutation, failed to develop symptoms, despite constant exposure to the disease. Two anecdotes from a small village in England where studies where first carried out refer to a widow whose husband and six children all succumbed, but who never developed symptoms herself, and to a village grave digger who handled virtually every infectious corpse in the village without ever falling ill.

Back in the 20th Century, individuals with a single copy of the mutation have been observed to experience a longer delay in the onset of infection than those without it. Individuals with two copies of the mutation are those who seem to be totally immune to the infection.

Before you go out and go crazy barebacking the night away, sharing needles, and transfusing mysterious blood you find on the street, recall that global studies show that in the areas where the Black Death raged (and among their descendents), around 14% of the population has at least one copy of the mutation. In Asia and Africa, and among native North Americans (American Indians, silly, not you), the percentage is effectively zero, as the ancestors of the inhabitants of these areas didn't pass through the Bubonic Plague bottleneck. The percentage of this mutation is calculated to have been at its highest around the time of the Black Plague, and since then has been diluted.

Ultimately, it may be possible that this mutation may be exploited to 'inoculate' the uninfected, or even to treat the infected, through some form of gene therapy. Unfortunately, the therapeutic use of genetics remains in its infancy, and the mutation needs to be studied in greater depth. Strangely, while attention to AIDS in the media and the medical community has been intense (though arguably, particularly in the case of the crisis in Africa not as intense as you'd hope), there were almost no studies of why certain at-risk individuals weren't becoming infected- most clinical trials and studies right up until today have been on infected individuals.

The first studies of an apparently immune individual- a gay man named Steve Crohn- were carried out in the late 90's/early 00's by doctors in New York City. Crohn had been active in the gay scene in San Francisco right before HIV and AIDS were recognized. His lover was among the first individuals in the U.S to be recognized as having died of AIDS. In the decade following the discovery of AIDS, Crohn claims to have lost between 70 and 90 close friends and former lovers- all of whom engaged in the same practices as Crohn himself. Crohn was not infected, and volunteered for testing that showed that his blood seemed to be basically impervious to HIV. Testing has indicated that Crohn has two copies of the relevant mutation.

So some of us are immune to HIV. And the Bubonic Plague. And hopefully, we'll eventually know more. And in the meantime, don't take any stupid chances.


References:
PBS. Yes, PBS.

Genetic Resistance to the Human Immunodeficiency Virus

The mutation that apparently confers significantly increased resistance to HIV occurs in the gene that codes for CCR5, a chemokine receptor found in the plasma membrane of certain cell types.

In order to infect a cell, HIV uses its envelope glycoprotein to bind the CD4 receptor found on several cell lineages of the immune system. This then changes the conformation of the envelope, allowing the virus to bind a coreceptor -- the main ones being CCR5 or CXCR4. Coreceptor binding induces the process of fusion, allowing viral RNA to enter and infect a cell. This mutation in the CCR5-coding gene alters the conformation of the final protein product, affecting its ability to bind chemokines.The import of the CCR5 mutation is that initial stages of infection with HIV, including infection via mother to child transmission, have been observed to involve cells that express CCR5. (With HIV-1 subtype B, which is common in the United States and Europe, for example, coreceptor switching to CXCR4 occurs later in the course of disease progression.) Apparently, the HIV virion is also unable to recognize this mutated CCR5, thus preventing the first stage of infection.

The association with the Black Death and bubonic plague is not yet solid. There are, however, reasons why it was singled out:

1. The extraordinarily high frequency of the mutation in European populations and those of European descent in the United States is quite striking. CCR5 normally functions by acting as a receptor for chemokines, signalling intracellularly to modulate the state and activity of the cell. With such a crucial role in the maintainence of normal immune function, it would require a very strong selective pressure to make the mutation provide enhanced fitness, thereby ensuring the continued presence of the mutation in a given population.

2. Population-level genetic analyses indicated that this mutation and its spread may be relatively recent. Certainly, it occurred after the separation of Asiatic, African and European races, as this mutation is not generally found in non-Europeans (this does not mean to say that the mutation may not have arisen spontaneously on various occasions, only to die out due to the decreased fitness that it confers).

3. Aside from the high selective pressure, the frequency indicates that there may have been a bottle-neck in the recent past. Genetic analyses suggested that the most recent impact of this pressure occurred around 700 years ago. This estimate coincides with the Black Death which rampaged through Europe in the mid 14th century. This disease, which resulted in the death of about a third of Europe's population, is hypothesized to have exerted powerful selective pressure on the relatively rare number of people carrying the mutation, subsequently allowing for the increased transmission of this mutated gene to the next generation.

HIV-1 Versus HIV-2

There are two types of HIV, denoted as 1 and 2. HIV-1 is the most widespread and most extensively studied. HIV-2 is more closely related to the simian immunodeficiency virus, or SIV, and is quite rare, being more or less confined to West Africa. Studies done on a cohort of female sex workers have suggested significantly slower progression to AIDS. It is also possible that prior infection with the less pathogenic HIV-2 maybe prevent superinfection with a HIV-1 strain.

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