Beneficial Mutation: HIV Resistance?

Editors note: This article was updated to reflect recent research.

I got a little bored the other night and decided to go looking for an example of a beneficial mutation that evolutionists rely on so much.  I’ve addressed some of these before in my Tetrachromatic Vision , Microbes and Antibiotics , and ApoA-1 Milano articles but I figured I should see if they have come up with any new ideas. I found several lists and did stumble on a few new ideas, though none actually presented mutations that were more than situationally beneficial.  The one I decided was the most dangerous is the one I will debunk for you today.

Before we go any further, I just want to take a moment and point out a few of the ridiculous claims evolutionists are passing off as beneficial mutations. They point out that wild almonds are poisonous but a mutation made them ok to eat and man cultivated them. Yes, that’s beneficial to man…not so much for the almond tree which suffers a net loss of function and defense.  Also, Murray Gray cattle were presented because they are more productive economically than traditional cattle.  While this benefits man, it does nothing for the cow so this is not a beneficial mutation.  Remember to carefully examine beneficial mutation claims for stuff like this.

HIV is a very real threat to a lot of people, and a painful daily nightmare to many others.  Thus the fact that a mutated gene provides partial, or in rare cases, complete immunity to the disease is fantastic news. Medical researchers are studying the mutated gene to try to understand how it works and how it can be used to combat HIV. However, evolutionists seized upon the discovery as evidence for their dogma.  Unfortunately for them, there are some issues with calling this a beneficial mutation.

HIV is an immunodeficiency virus. This means it works by essentially wiping out the immune system, leaving the victim vulnerable to other, usually less deadly diseases. However, to do this, it needs to take control of the white blood cells, called leukocytes. The leukocytes will serve as virus factories until they explode, spraying new viruses throughout the bloodstream. Getting inside is not easy. The leukocyte is surrounded by a membrane. Fortunately for the HIV virus, it is equipped to attach to a specialized receptor in the cell membrane called the Cytosine-Cystosine chemokine-5 receptor (CCR5). This receptor usually functions in keeping leukocytes at the site of a cut or infection, thus heavily boosting the immune system. The gene for this receptor is found on the third chromosome in humans.

Sometimes, because of man’s fallen condition, the CCR5 gene can become mutated into producing CCR5-delta 32. The mutation deletes thirty-two base pairs in the gene.  This mutation confers either partial or complete resistance to HIV. It does this by withdrawing the CCR5 receptor inside the cell. Without the CCR5 receptor to attach to, the HIV virus does not infect any leukocytes and the patient is thus either completely, or partially immune to HIV, depending on if the mutation is on both copies of chromosome three. This is undoubtedly beneficial to anyone infected with HIV. However, it is not a beneficial mutation.

In order for a mutation to be beneficial, it must confer a new, improved functionality upon an organism that provides no negative side effects.   The mutation of chromosome three that produces CCR5 delta 32 fails this test. The CCR5 receptor has a specific function. It is tasked with ensuring its leukocyte is able to stay at a wound or infection site in the body once it gets there. Pulling that receptor inside the cell causes a problem. Now the cell cannot undergo its normal processes to attach to integrin. Integrin is a specialized receptor that has numerous functions but in this case, is used to help bind leukocytes to a wound or infection site to heal it.  Since the leukocytes do not bind to the infection or wound, healing is slowed. Effectively this weakens the overall immune system.

Worse, recent research has demonstrated that the CCR5 delta 32 mutation is lethal.  A paper published in 2019 pointed out that this mutation caused a 21% increase in death rates in people with two copies of the mutated gene. This hardly is a beneficial mutation.

This is the key problem for the evolutionist attempting to cite CCR5 delta 32 as a beneficial mutation. It is only situationally beneficial. It works great if the carrier is exposed to HIV.  However, it weakens their immune system against literally every other kind of infection and decreases their lifespan.  Thus calling it beneficial is a significant stretch.  This is akin to the old evolutionary argument that sickle cell anemia was a beneficial mutation because it helped reduce malaria risk. That argument was spurious for the same reason this one is: both outcomes are negative.  A person with the CCR5-delta 32 mutation is less fit than the average population against other illnesses, while the person without the CCR5-delta 32 mutation is less fit against HIV. It’s purely dependent on which diseases they are exposed to, not some kind of evolutionary benefit.