It was once imagined that Europeans are protected from “HIV” by the CCR5Δ32 gene (CCR5 with deletion 32). However, comparison of the geographic distributions of CCR5Δ32 and of “HIV” disproves that suggestion [Mainstream duffers clutch at Duffy straws: African ancestry and HIV, 26 July 2008]. No sooner had we posted that information than HIV/AIDS “researchers” publish a brilliant scheme for mimicking the Δ32 deletion via genetic engineering, as “an attractive approach for the treatment of HIV-1 infection”:
“Homozygosity for the naturally occurring 32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted 50% of CCR5 alleles in a pool of primary human CD4+ T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo . . . . HIV-1-infected mice engrafted with ZFN-modified CD4+ T cells had lower viral loads and higher CD4+ T-cell counts than mice engrafted with wild-type CD4+ T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4+ T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN–modified autologous CD4+ T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection” (Perez et al. [23 authors, correspondence to C. H. June], “Establishment of HIV-1 resistance in CD4+ T cells by genome editing using zinc-finger nucleases”, Nature Biotechnology 26  808-16).
This brings out in force the Luddite that has been growing in me, fertilized by the copious manure that emanates non-stop from the drug industry and its academic henchpeople. (Luddites are named after the machine-destroying protesters in 19th-century Birmingham whose jobs were lost to mechanization during the Industrial Revolution. It’s come to be applied to antagonism against things that are widely applauded as scientific or technological “improvements” or “advances”.)
There are at least two immediately obvious things very wrong with this sort of anti-HIV approach, irrespective whether HIV has anything to do with AIDS. First, gene therapy remains an idea, not a reality—moreover, an idea whose time has passed because its basis has been found to be incorrect. Second, does not the CCR5 gene perform any functions apart from its possible connection to “HIV”? What are those functions? What happens to them if CCR5 is disrupted in a manner that natural selection (or the Creator, makes no difference) never invented or intended?
The idea of gene therapy stemmed from the initial interpretations of DNA as the carrier of hereditary information. It was thought at first that specific sequences of DNA form distinct and separate genes, individual units of hereditary information, each of them responsible only for the production of one particular protein. That has turned out to be not the case. Genomes are dynamic systems and not linear arrays of fixed genes. At various times, different sub-units of what are still called “genes” work together with sub-units of other “genes” to generate the proteins needed at any given time and place. The sophistication of these precisely scheduled interactions is such that genomes can produce many more proteins than they have “genes”: humans have fewer “genes” than corn and only 25% more than flatworms, even though humans are somewhat more complex creatures; see the fairly recent review by Ast, “The alternative genome”, Scientific American, April 2005, 58-65.
Given that current understanding, any notion of replacing a “defective gene” with a non-defective one presupposes that we know everything about which bits of which genes are needed for what, and at which times, in the development and life of the organism. Our knowledge is very far from that.
Official websites describe the problems quite well:
“Although gene therapy is a promising treatment option for a number of diseases (including inherited disorders, some types of cancer, and certain viral infections), the technique remains risky and is still under study to make sure that it will be safe and effective. Gene therapy is currently only being tested for the treatment of diseases that have no other cures” [published 18 July 2008]
“The Food and Drug Administration (FDA) has not yet approved any human gene therapy . . . . Current gene therapy is experimental and has not proven very successful in clinical trials. Little progress has been made since the first gene therapy clinical trial began in 1990. In 1999, gene therapy suffered a major setback with the death of 18-year-old Jesse Gelsinger. . . . [who] died from multiple organ failures 4 days after starting the treatment. . . . Another major blow came in January 2003, when the FDA placed a temporary halt on all gene therapy trials using retroviral vectors in blood stem cells. . . . after . . . a second child treated in a French gene therapy trial had developed a leukemia-like condition. . . . Before gene therapy can become a permanent cure for any condition, the therapeutic DNA introduced into target cells must remain functional and the cells containing the therapeutic DNA must be long-lived and stable. Problems with integrating therapeutic DNA into the genome and the rapidly dividing nature of many cells prevent gene therapy from achieving any long-term benefits. Patients will have to undergo multiple rounds of gene therapy. . . . Anytime a foreign object is introduced into human tissues, the immune system is designed to attack the invader. The risk of stimulating the immune system in a way that reduces gene therapy effectiveness is always a potential risk. Furthermore, the immune system’s enhanced response to invaders it has seen before makes it difficult for gene therapy to be repeated in patients. . . . Viruses, while the carrier of choice in most gene therapy studies, present a variety of potential problems to the patient—toxicity, immune and inflammatory responses, and gene control and targeting issues. In addition, there is always the fear that the viral vector, once inside the patient, may recover its ability to cause disease. . . . Conditions or disorders that arise from mutations in a single gene are the best candidates for gene therapy. Unfortunately, some the most commonly occurring disorders, such as heart disease, high blood pressure, Alzheimer’s disease, arthritis, and diabetes, are caused by the combined effects of variations in many genes. Multigene or multifactorial disorders such as these would be especially difficult to treat effectively using gene therapy. . . .” [last modified 13 May].
Perez et al. ingeniously avoided some of those problems, but the basic lack of knowledge remains. The disruption of CCR5 also disrupted the genome at other sites, chiefly at the neighboring CCR2: “Loss of CCR2 in CD4+ T cells is predicted to be well tolerated as CCR2-/- mice display phenotypes that are not disabling . . . . Mutant alleles of CCR2 have been correlated with delayed progression to AIDS in HIV-infected individuals, although no influence on the incidence of HIV-1 infection was observed . . . . Thus, parallel mutation of a small proportion of CCR2 in CD4+ T cells ex vivo is unlikely to be deleterious . . . . ”; and there was also disruption at “an intron of ABLIM2 on chromosome 4”. “Thus, except for CCR2 (5.39%), and rare (~1/20,000) events at ABLIM2, all the remaining sites showed no evidence of . . . [disruption], given a threshold level of detection of ~1 in 10,000 sequences”.
In other words, the engineering of the CCR5 gene is not 100% specific, other parts of the genome are affected. That no deleterious “side”-effects were observed in the experimental mice is hardly persuasive that the procedure could do in human beings only the one thing we want done and nothing else. Above all, Perez et al. say nothing about why CCR5 exists at all, what functions natural selection intended for it, and whether the CCR5Δ32 that supposedly protects against “HIV”—but doesn’t, according to epidemiological comparisons—is associated with any undesirable conditions.
So, I suggest, Perez et al. are tinkering with things they don’t understand and that are better left alone, hence my reference to Dr. Frankenstein. Incidentally: if you think “Frankenstein” was written by Mary Wollstonecraft Shelley, you should read John Lauritsen’s “The Man Who Wrote Frankenstein”, an illustration that it’s not only in medical science that the mainstream consensus can be wrong for long periods of time. The dogma that the Clovis people were the first Americans was maintained for more than half-a-century in the face of contradicting evidence as well as the implausibility of the idea that the earliest discovered habitation sites would correspond with the earliest actual sites. Back to literary scholarship: it is also not the case that William Shakspere of Stratford-on-Avon wrote Shakespeare’s works, see Diana Price, “Shakespeare’s Unorthodox Biography: New Evidence of an Authorship Problem” ).