Let’s step into the mindset of an Intelligent Design (ID) creationist for a moment, as we examine a recent scientific study investigating why a small minority of people are immune to the Human Immunodeficiency Virus (HIV), while the vast majority are not.
A research team from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR) at the University of Copenhagen, led by Professor Simon Rasmussen, has discovered that this immunity is conferred by a genetic mutation. This mutation originated in a single individual who lived near the Black Sea between 6,700 and 9,000 years ago.
According to Discovery Institute Fellow William A. Dembski, this mutation would represent what he calls “complex specified information”, a concept he attributes to an intelligent designer. Dembski argues that only such a designer could create the necessary genetic information, as mutation and natural selection alone are not goal-directed and therefore cannot produce the desired specificity. However, Dembski is notably vague about how we can objectively determine what genetic information is “specified” and what is not. He appears to rely on subjective judgement, essentially deeming any beneficial mutation as “specified”, while dismissing deleterious mutations as irrelevant.
Even granting Dembski his biased subjectivity, we are left with the implication that the mutation which conferred HIV immunity to this individual's descendants must have been “specified” by his proposed intelligent designer.
This raises an obvious question: if the intelligent designer of humans could have provided our species with immunity to HIV, why did it choose not to do so from the outset? Why rely on what appears to be a slow, natural evolutionary process to spread this mutation through the population—one that depends on people dying of HIV while those with the mutation survive and reproduce, creating the selection pressure for its spread? A process so gradual that, to this day, it remains a rare trait in the human gene pool, with only 18-25% of Danes carrying the mutated gene.
It also raised a couple of theological question for creationists: why would an omnibenevolent creator create HIV with its 'designed' ability to bypass our immune system the same designer allegedly designed to protect us and how is that an intelligent act by an omnibenevolent deity?
Background: Origins and Spread of HIV. What is HIV?The research has been published in the journal Cell and is also summarised in a news article by the University of Copenhagen Faculty of Medical Sciences.
The Human Immunodeficiency Virus (HIV) is a retrovirus that attacks the immune system, specifically targeting CD4+ T cells, which are crucial for fighting infections. If left untreated, HIV can lead to Acquired Immunodeficiency Syndrome (AIDS).
Origins of HIV
HIV is a zoonotic virus, meaning it crossed over to humans from another species. The predominant strain, HIV-1, originated from a simian immunodeficiency virus (SIV) found in chimpanzees (Pan troglodytes) in Central Africa. This cross-species transmission likely occurred through bushmeat hunting and handling, where humans were exposed to infected blood. Genetic studies trace the most recent common ancestor of HIV-1 groups M (the pandemic strain) to the early 20th century, around 1910-1930,in what is now the Democratic Republic of Congo (Kinshasa).
A less prevalent strain, HIV-2,arose independently from SIVsmm (from sooty mangabeys) and is largely confined to West Africa.
Spread of HIV
HIV Immunity and CCR5 Mutation
- Early Spread (20th Century):
Urbanisation, colonial infrastructure (such as railways), increased mobility, and medical practices involving unsterilised equipment are believed to have facilitated the early spread of HIV in Central Africa.- Global Pandemic:
HIV remained largely unnoticed until the early 1980s,when cases of severe immunodeficiency began appearing among young men in the United States, initially linked to the gay community but soon recognised as affecting heterosexuals, haemophiliacs, and intravenous drug users.- Worldwide Impact:
Today, HIV affects over 38 million people globally. Sub-Saharan Africa remains the most severely affected region, accounting for around two-thirds of global cases. Antiretroviral therapy (ART) has significantly improved life expectancy and quality of life for people living with HIV, though no vaccine or cure currently exists.
A small percentage of people, particularly of European ancestry,carry a genetic mutation known as CCR5-Δ32,which prevents HIV from entering immune cells. This mutation likely arose thousands of years ago and provides resistance to certain strains of HIV, illustrating how human populations can develop partial genetic defences over time through natural selection.
Researchers map 7,000-year-old genetic mutation that protects against HIV
Modern HIV medicine is based on a common genetic mutation. Now, researchers have traced where and when the mutation arose – and how it protected our ancestors from ancient diseases.
What do a millennia-old human from the Black Sea region and modern HIV medicine have in common?
Quite a lot, it turns out, according to new research from the University of Copenhagen.
18-25 percent of the Danish population carries a genetic mutation that can make them resistant or even immune to HIV. This knowledge is used to develop modern treatments for the virus.
Until now, it was unknown where, when, or why the mutation occurred. But by using advanced DNA technology, researchers have now solved this genetic mystery.
HIV and resistance
HIV (human immunodeficiency virus) destroys white blood cells that defend the body against infections. Untreated HIV leads to AIDS.
The genetic mutation that protects against HIV is found in the so-called CCR5 gene. Carriers of the mutation lack a receptor – a kind of “door” – on their cells that the virus uses to infect the body. This missing receptor can make a person resistant or even immune to HIV.
Today, HIV is treated with medication that makes it difficult for the virus to replicate. The medicine cannot completely eliminate HIV but can suppress it, so the disease is not felt.
Sources: Statens Serum Institut, AIDS-Fondet, and Professor Simon Rasmussen, CBMR
It turns out that the variant arose in one individual who lived in an area near the Black Sea between 6,700 and 9,000 years ago. HIV is a relatively new disease – less than 100 years old – so it’s almost coincidental and very fascinating that a genetic variation that arose thousands of years ago also protects against a modern virus like HIV.
Professor Simon Rasmussen, corresponding author
Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR)
University of Copenhagen, Copenhagen, Denmark.
Analyzed 900 skeletons
To determine where and when the mutation arose, researchers first mapped it by analyzing the genetic material of 2,000 living people worldwide. They then developed a new AI-based method to identify the mutation in ancient DNA from old bones.
The researchers examined data from over 900 skeletons dating from the early Stone Age to the Viking Age.
By looking at this large dataset, we can determine where and when the mutation arose. For a period, the mutation is completely absent, but then it suddenly appears and spreads incredibly quickly. When we combine this with our knowledge of human migration at the time, we can also pinpoint the region where the mutation originated.
Kirstine Ravn, first author.
Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR)
University of Copenhagen, Copenhagen, Denmark.
Thus, the researchers were able to locate the mutation in a person from the Black Sea region up to 9,000 years ago – an individual from whom all carriers of the mutation descend.
Was an advantage back then
But why do so many Danes carry a millennia-old genetic mutation that protects against a disease that didn’t exist back then?
The researchers believe the mutation arose and spread rapidly because it gave our ancestors an advantage:
People with this mutation were better at surviving.
People with this mutation were better at surviving, likely because it dampened the immune system during a time when humans were exposed to new pathogens.
Dr. Leonardo Cobuccio, co-first author
Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR)
University of Copenhagen, Copenhagen, Denmark.
What’s fascinating is that the variation disrupts an immune gene. It sounds negative, but it was likely beneficial. An overly aggressive immune system can be deadly – think of allergic reactions or severe cases of viral infections like COVID-19, where the immune system often causes the damage that kills patients. As humans transitioned from hunter-gatherers to living closely together in agricultural societies, the pressure from infectious diseases increased, and a more balanced immune system may have been advantageous.
Kirstine Ravn.
Publication:
HighlightsAn additional point that creationists are likely to overlook is that the research team clearly interpret their findings as the result of an evolutionary process involving random mutation and differential survival through natural selection with no hint that they are finding the Theory of Evolution inadequate to explain the observations and are about to turn to creationism as a better explanation.Summary
- The CCR5delta32 deletion arose on a pre-existing haplotype comprising 84 variants
- The CCR5delta32 haplotype originated in the Western Steppe at least 6,700 years ago
- Positive selection of CCR5delta32 occurred in the Late Neolithic and Bronze Age
- The haplotype places the CCR5delta32 allele in a new medical context
The chemokine receptor variant CCR5delta32 is linked to HIV-1 resistance and other conditions. Its evolutionary history and allele frequency (10%–16%) in European populations have been extensively debated. We provide a detailed perspective of the evolutionary history of the deletion through time and space. We discovered that the CCR5delta32 allele arose on a pre-existing haplotype consisting of 84 variants. Using this information, we developed a haplotype-aware probabilistic model to screen 934 low-coverage ancient genomes and traced the origin of the CCR5delta32 deletion to at least 6,700 years before the present (BP) in the Western Eurasian Steppe region. Furthermore, we present strong evidence for positive selection acting upon the CCR5delta32 haplotype between 8,000 and 2,000 years BP in Western Eurasia and show that the presence of the haplotype in Latin America can be explained by post-Columbian genetic exchanges. Finally, we point to complex CCR5delta32 genotype-haplotype-phenotype relationships, which demand consideration when targeting the CCR5 receptor for therapeutic strategies.Graphical abstract
Particularly inconvenient for proponents of Intelligent Design is the team's recognition that the human immune system is far from optimal. In fact, it is responsible for several life-threatening or life-limiting conditions, which would have become more apparent as humans domesticated animals and acquired their pathogens. A mutation that reduced this immune over-sensitivity would therefore be advantageous. The immunity to HIV is a fortuitous by-product of this reduced over-reactivity.
All of this directly contradicts the claims made by ID creationists of a perfect, omnibenevolent designer crafting a flawless human body. In reality, these findings are entirely consistent with the Theory of Evolution: the human body is the product of a utilitarian evolutionary process, shaped by compromise, chance, and opportunistic adaptations, rather than by the hand of an intelligent designer striving for perfection.
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