Walking around on our planet today, there are approximately 681,630,000 people of European descent who are either immune or have an abnormally high resistance to the Human Immunodeficiency Virus. What makes these people unable to be infected by one of the worst diseases currently known to mankind? Superpowers? Lots of orange juice? Maybe they pray a lot? Nope.

The one thing that these millions of people have in common is a genetic mutation on the CCR5 gene. The question of the origin of this genetic anomaly has spawned debate between scientists for the past two decades, and they now believe that the presence of this beneficial mutation owes its thanks to another scourge that has plagued mankind for thousands of years — smallpox.

Although smallpox is a uniquely human disease its causative agent, the variola virus, belongs to the genus of orthopox viruses (cowpox, monkeypox, etc.). The word pox refers to any rash consisting of pustules or skin lesions filled with pus. The variola virus appears to have evolved from one of these animal poxviruses in Central Africa thousands of years ago.

In his book “Viruses, Plagues and History,” Michael Oldstone said that scientists believe that the most likely guilty party was a species of wild rodent with a very large population. Humans are believed to have hunted these rats and become sick with the virus through ingestion. The rats, having co-evolved with this virus for millions of years, would be virtually symptomless. The species’ leap from wild animal to human produced a much more severe and deadly strain of the virus larger in scale but akin to last year’s outbreak of swine flu. Once infected with this “new” virus, the human host reacted in one of two ways: it either died or survived and had a new-found, lifelong immunity.

This resulted in the virus itself dying out in small populations rather quickly. However, the immunity provided to individuals from infection with the variola virus was not immediately passed to their offspring. Therefore, with every new population that arose, another resurgence of the disease came about.

Around 9000 B.C., as towns and cities began to form, human populations became dense enough, through new births and genetic drift, to allow smallpox to be transmitted continually without ever running out of hosts.

Oldstone tells us that “the demographic threshold at which a population could sustain the disease on an ongoing basis was around 200,000 people.”

Over thousands of years the variola virus emerged in new strains due to random mutation. These new and more virulent strains gradually started to overtake those strains leftover from the wild rodent and became uniquely specialized for infecting and replicating inside human cells.

There were two major factors that greatly influenced the toll that smallpox had on the human population. The first of these was epidemiological; the second was genetic.

The first factor is what is known as a “virgin soil” epidemic. Simply put, this is what would happen if smallpox was to be used as a bio-terrorist weapon today. According to the World Health Organization, “virgin soil” refers to a virus being introduced into an isolated community that has had no prior exposure to the disease. Just like when smallpox started thousands of years ago in its original form, some members of the population will survive and develop an immunity, and the rest will die off. It will take a re-accumulation of the population, through births and migration, for the virus to be able to trigger another epidemic. The WHO asserts that “somewhat paradoxically, the longer a society lived with smallpox, the less severe its demographic impact became. In densely populated urban areas, the disease smoldered continuously at a low level and the intervals between major outbreaks were fairly short. As a result, nearly everyone who survived to adulthood was immune and the victims were mainly small children. Since infants or toddlers were far more easily replaced than adolescents or adults, the economic and psychological burdens of smallpox on society were much less than they were when the young and old died indiscriminately.”

The genetic factor that played a role in who survived a smallpox outbreak was that of genetic resistance. As people with an inability to resist or survive the virus died off, the progeny from those left had a naturally higher immunity to the disease.

Right now you are probably asking yourself, “How did all of this develop into a genetic mutation that protects against HIV?” The answer lies in something called the CCR5 gene.

The CCR5 gene is one of the primary players in the way our bodies fight off every type of virus from the rhino and coronaviruses that cause the common cold to the Zaire virus that causes Ebola. We have learned through the research of Grant McFadden that the Human Immunodeficiency Virus is what is referred to as a supervirus. It works its way into the healthy CCR5 protein through the use of chemokine receptors, which are found on the surface of the cell. Subsequently, the supervirus also finds its way into CD4 T-cells and macrophages. CD4 T-cells initiate the body’s response to invading viruses and micro-organisms. Macrophages are a type of white blood cell that ingest foreign material. They play a primary role in the destruction of bacteria and tumor cells and also release substances that stimulate other cells of the immune system. In layman’s terms, if HIV is the key, then the CCR5 gene is the lock that is effectively disabled by the mutation.

In some populations, the CCR5 gene has experienced a mutation that has deleted 32 base pairs in the gene sequence. This deletion causes the CCR5 gene to be void of the chemokine receptors on the surface of the cell. Research has shown that persons with two inherited copies of the mutated gene have a near perfect immunity to HIV. The heterozygous population, with only one inherited copy of the mutated gene, has a 70 percent chance of immunity. Scientists have also learned that possessing any number of the mutated form of CCR5 has no other side effects.

Unfortunately, the CCR5 gene is completely absent in those of Asian and American Indian descent. It is mostly prevalent in those of European and Nordic descent and minimally in those of African ancestry.

Although this mutation has enabled millions of people to be resistant to one of the deadliest diseases to plague mankind today, those without it are still at risk. There has been some progress in the form of animal testing on a vaccination for those who have a clean bill of health. Scientists believe they are still decades away from finding a cure for those people currently living with HIV.

By: Dawn Koogle

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