Lauritsen book available on-line

John Lauritsen was a pioneer in Rethinking, for example warning in the very earliest days of the AIDS era about the toxicity of AZT and the damage caused by poppers and the psychological harm done to gay men. His books and other writings remain important reading — so much else has not yet caught up with his insights. He has just made available one of his out-of-print books:

I’ve made *Poison By Prescription: The AZT Story* (1990)
into a pdf book and put it in the “AIDS” section of my website.
Actually, most of the *Poison* articles were already included in
the AIDS Wiki and VirusMyth websites — but now the whole book is
there in facsimile, including front and back covers. There’s also
an Italian translation of the talk I gave in Vienna last summer,
done by Vicenzo Fraddosio. These two items are near the end of
the list on:

http://paganpressbooks.com/jpl/AIDS.HTM

John Lauritsen

Searching for truth at Harvard

Harvard Magazine published the standard sort of HIV/AIDS propaganda in its issue of September-October 2010, “The Social Epidemic — Battling HIV in sub-Saharan Africa”.  The piece is strong on local color and personal interest, a tribute to the “generous gift for international reporting” that enabled the author, associate editor Elizabeth Gudrais, to visit Tanzania, South Africa, and Uganda. But the article is woefully ignorant about HIV and AIDS, and this ignorance is reflected in such absurd repetitions of official nonsense as that 39% of KwaZulu-Natal residents “have HIV” and, in some places, “two-thirds of pregnant women have HIV”. First, of course, no test demonstrates the presence of “HIV infection”, only the presence of certain antibodies or bits of DNA or RNA. Second, the official early story of HIV/AIDS describes “HIV infection” as deadly, on average of about a decade after infection. As this article acknowledges, antiretroviral drugs treatment is still not available in most of sub-Saharan Africa. Those two mainstream assertions taken together would make it quite impossible that any country could have reached 39% infection, with a majority of pregnant women infected, without an earlier total collapse of the population — whereas the population of the whole region has continued to increase throughout the “AIDS” era  at a healthy (or unhealthy!) rate of several percent annually, without death rates rising noticeably [Rian Malan, “AIDS in Africa — In search of the truth”, Rolling Stone Magazine, 22 November 2001; “Africa isn’t dying of Aids”, The Spectator (London), 14 December 2003].
Gudrais’s “research” about HIV itself evidently consisted of being indoctrinated by the Harvard people who are, with the best but misguided intentions, bringing antiretroviral treatment to sub-Saharan Africa. Gudrais mention that many Africans stop coming for treatment, but fails to ask why this might be; yet anyone familiar with the literature would know that the dreadful “side” effects of antiretroviral drugs bring high drop-out rates also in the United States [“Avoiding life-saving treatment”, 2010/10/28].
I found it sad to read of the many well-meaning alumni, faculty, and students who are mentioned as having contributed time or funds to Harvard’s mission in Africa, which includes vaccine research. What reaction will there be from those who have been hoodwinked by officialdom for decades, once it becomes generally realized that HIV = AIDS is without a basis in fact? How will the Bill & Melinda Gates Foundation spin its long participation in this intellectual scam? How will the National Institutes of Health handle the fury of Congressional investigations after it is realized that NIH was actually a driving force in maintaining expensive programs that had long been discredited by the evidence, much of it published under NIH grants?

John Lauritsen wanted to give readers of Harvard Magazine the opportunity to think about these issues, but the concise, to-the-point letter he sent in August has not been published:

25 August 2010
Harvard Magazine
yourturn@harvard.edu
“The Social Epidemic: Battling HIV in sub-Saharan Africa” by Elizabeth  Gudrais (September-October 2010) echoes the prevailing myths about  “AIDS” in Africa, without ever coming to grips with the real issues. Although Africa has supposedly been devastated by “AIDS”, the population  in South Africa, Uganda and elsewhere on the continent has grown.  “AIDS” in Africa is not the same as “AIDS” in Europe and North America;  in both it is a new name for old diseases.  <http://www.altheal.org/statistics/fiala.htm>
The sad reality is that most people in Africa are poor — so poor they  can’t even get clean drinking water. The goal should be to eliminate  poverty and unsanitary living conditions, rather than providing  unvalidated “HIV” tests and harmful and worthless drugs.
The sub-article (“The Politics of Paying for HIV Care”) gets to the  point: “Harvard’s PEPFAR program has paid for antiretroviral therapy  (ART) for more than 130,000 people….” That is, profits for Big  Pharma. The drugs being marketed to Africa — AZT and Nevirapine — are  toxic and have no benefits demonstrated through honest, double-blind,  placebo-controlled studies.
To my knowledge there is no proof that “AIDS” is caused by HIV-1 (North  America and Europe), by HIV-2 (Africa), or by any other infectious  agent. If there is such proof, Harvard Magazine would do us all a  service by publishing an article stating the HIV-AIDS hypothesis in a  clear and falsifiable manner, marshalling evidence for that hypothesis,  and answering criticisms made by AIDS critics (dissidents/rethinkers)  like myself.

John Lauritsen
Harvard College Class of 1961 (AB 1963)
Author: _The AIDS War_ (1993)
http://paganpressbooks.com/jpl/AIDS.HTM

World AIDS Day: How about a look back?

The conference, Rethinking AIDS 2009, was a treat in many ways, some of which I described in “The Family of Rethinking AIDS”. A special pleasure for me was to meet in person people I had respected for quite some time, indeed admired for their work and their integrity. I learned something new from the substance of many of the presentations, and perhaps even more from conversations.

I continue often to be abashed at how little I know about the early days of AIDS, and especially that so many incisive insights and explanations were published long ago that have seemed to me like fresh revelations. The difficulty is that AIDS Rethinking doesn’t have the organized indexes and abstracts and review articles and textbooks that established disciplines do. Tony Lance illustrated that in his talk when he mentioned that after he had recognized intestinal dysbiosis as a central explanation for much in the early days of AIDS, he found that Koliadin had made similar suggestions on the old virusmyth website. Who could possibly have read, and even in that case who could possibly remember, all the material on that website, and in Continuum, and in the early newsletters, and in the dozens of Rethinking books, and in the hundreds of articles scattered over obscure periodicals and websites?

The difficulty is compounded by the lack of agreement among Rethinkers over all sorts of details. We are all of the opinion that HIV has never been shown to be the sole, necessary and sufficient cause of AIDS, but beyond that we differ widely; not only over substantive issues but also over how best to proceed in trying to bring regard for the facts into the public arena. In established disciplines, one can read authoritative overviews of manageable size; concerning HIV/AIDS Rethinking, without having read EVERYTHING one cannot be sure that something of importance has not been missed.

Amid these hindrances, it makes sense to look at where Rethinking has been, and we’re fortunate that John Lauritsen accepted the invitation to talk about that at RA2009. He has now posted his initial draft, which was far too long for the 25 minutes he was allotted at the conference, and he invites comments and suggestions for additions or corrections. I enjoyed his talk immensely, and gained even more from reading his longer discussion of  “The History of the Controversy”.

 

 

Believing and disbelieving

(This is a long post. HERE is a pdf for those who prefer to read it that way).

“How could anyone believe that?” is a natural question whenever someone believes what is contrary to the conventional wisdom, say, that HIV doesn’t cause AIDS, or that Loch Ness monsters are real animals.

Since the role of unorthodox views in and out of science has been the focus of my academic interests for several decades, I had to think about that question in a variety of contexts. My conclusion long ago was that this is the wrong question, the very opposite of the right question, which is,

“How does anyone ever come to believe differently than others do?” (1)

********************

It’s a widespread illusion that we believe things because they’re true. It’s an illusion that we all tend to harbor about ourselves. Of course I believe what’s true! My beliefs aren’t wrong! It’s the others who are wrong.

However, we don’t acquire beliefs because they’re true, we acquire them through being taught that they’re true. For the first half-a-dozen or a dozen years of our lives, before we have begun to learn how to think truly for ourselves, as babies and children we almost always believe what parents and teachers tell us. Surely that has helped the species to survive. But no matter what the reason might be, there’s ample empirical evidence for it. For instance, many people during their whole lifetime stick to the religion that they imbibed almost with mother’s milk; those who reject that religion do so at earliest in adolescence.

That habit of believing parents and teachers tends to become ingrained. Society’s “experts”  — scientists and doctors, surrogate parents and teachers — tend to be believed as a matter of habit.

So how do some people ever come to believe other than what they’ve been taught and what the experts say?

**********************

I was prompted to this train of thought by receiving yet again some comments intended for this blog and which were directed at minor details, from people whom I had asked, long ago, to cut through this underbrush and address the chief point at issue: “What is the proof that HIV causes AIDS?”

Whenever I’ve asked this of commentators like Fulano-etc.-de-Tal, or Chris Noble, or Snout, or others who want to argue incessantly about ancillary details, the exchange has come to an end. They’ve simply never addressed that central issue.

And it’s not only these camp followers. The same holds for the actual HIV/AIDS gurus, the Montagniers and Gallos and Faucis. Fauci threatens journalists who don’t toe the orthodox line. Gallo hangs up on Gary Null when asked for citations to the work that made him famous.

Why can’t these people cite the work on which their belief is supposedly based?

Finally it hit me: Because their belief wasn’t formed that way. They didn’t come to believe because of the evidence.
The Faucis and Gallos came to believe because they wanted to, because a virus-caused AIDS would be in their professional bailiwick, and they were more than happy to take an imperfect correlation as proof of causation.
The camp followers came to believe simply because they were happy to believe what the experts say and what “everyone else” believes. Who are they to question the authority of scientific experts and scientific institutions?

***********************

To question “what everyone knows”, there has to be some decisive incentive or some serendipitous conjunction. I’ll illustrate that by describing how I came to believe some things that “everyone else” believes and some things that “everyone else” does not believe.

The first unorthodox opinion I acquired was that Loch Ness monsters are probably real living animals of some unidentified species. How did I come to that conclusion?
Serendipity set the stage. Reading has been my lifelong pleasure. I used to browse in the local library among books that had just been returned and not yet reshelved, assuming that these would be the most interesting ones. Around 1961, I picked from that pile a book titled Loch Ness Monster, by Tim Dinsdale. I recall my mental sneer, for I knew like everyone else that this was a mythical creature and a tangible tourist attraction invented by those canny Scots. But I thumbed the pages, and saw a set of glossy photos: claimed stills from a film! If these were genuine . . . . So I borrowed the book. Having read it, I couldn’t make up my mind. The author seemed genuine, but also very naïve. Yet his film had been developed by Kodak and pronounced genuine. Could it be that Nessies are real?
I was unable to find a satisfactory discussion in the scientific literature. So I read whatever other books and articles I could find about it. I also became a member of the Loch Ness Investigation, a group that was exploring at Loch Ness during the summers, and I followed their work via their newsletters — I couldn’t participate personally since I then lived in Australia.
A dozen years later, on sabbatical leave in England, I took a vacation trip to Loch Ness. More serendipity: there I encountered Dinsdale. Later I arranged lecture tours for him in the USA (where I had migrated in 1965). Coming to know Dinsdale, coming to trust his integrity, seeing a 35mm copy of his film umpteen times during his talks, brought conviction.
It had taken me 12-15 years of looking at all the available evidence before I felt convinced.

The unorthodox view that underwrites this blog is that HIV doesn’t cause AIDS. How did I come by that belief in something that “everyone else” does not believe?
More serendipity. Having concluded in the early 1970s that Nessies were probably real, I became curious why there hadn’t been proper scientific investigations despite the huge amount of publicity over several decades. That led eventually to my change of academic field from chemistry to science studies, with special interest in heterodoxies. So I was always on the lookout for scientific anomalies and heresies to study. In the mid-1990s, I came across the book by Ellison and Duesberg, Why We Will Never Win the War on AIDS (interesting info about this here ; other Ellison-Duesberg articles here).
Just as with Dinsdale’s book, I couldn’t make up my mind. The arguments seemed sound, but I didn’t feel competent to judge the technicalities. So, again, I looked for other HIV/AIDS-dissenting books, and wrote reviews of a number of them. Around 2005, that led me to read Harvey Bialy’s scientific autobiography of Duesberg. For months thereafter, I periodically reminded myself that I wanted to check a citation Bialy had given, for an assertion that obviously couldn’t be true, namely, that positive HIV-tests in the mid-1980s among teenage potential military recruits from all across the United States had come equally among the girls as among the boys. The consequences of checking that reference are described in The Origin, Persistence and Failings of HIV/AIDS Theory.
As with Nessie, it had taken me more than ten years of looking into the available evidence to become convinced of the correctness of something that “everyone else” does not believe.

So am I saying that I always sift evidence for a decade before making up my mind?
Of course not. I did that only on matters that were outside my professional expertise.

Studying chemistry, I didn’t question what the instructors and the textbooks had to say. I surely asked for explanations on some points, and might well have raised quibbles on details, but I didn’t question the periodic table or the theory of chemical bonding or the laws of thermodynamics or any other basic tenet.

That, I suggest, is quite typical. Those of us who go into research in a science don’t begin by questioning our field’s basic tenets. Furthermore, most of us never have occasion to question those tenets later on. Most scientific research is, in Kuhn’s words (2), puzzle-solving. In every field there are all sorts of little problems to be solved; not little in the sense of easy, but in the sense of not impinging on any basic theoretical issues. One can spend many lifetimes in chemical research without ever questioning the Second Law of thermodynamics, say, or quantum-mechanical calculations of electron energies, and so on and so forth.

So: Immunologists and virologists and pharmacologists and others who came to do research on HIV/AIDS from the mid-1980s onwards have been engaged in trying to solve all sorts of puzzles. They’ve had no reason to question the accepted view that HIV causes AIDS, because their work doesn’t raise that question in any obvious way; they’re working on very specialized, very detailed matters — designing new antiretroviral drugs, say; or trying to make sense of the infinite variety of “HIV” strains and permutations and recombinations; or looking for new strategies that might lead to a useful vaccine; and so on and so forth. Many tens of thousands of published articles illustrate that there are no end of mysterious puzzles about “HIV/AIDS” waiting to be solved.

The various people who became activist camp followers, like the non-scientist vigilantes among the AIDStruth gang, didn’t begin by trying to convince themselves, by looking into the primary evidence, that the mainstream view is correct: they simply believed it, jumped on the very visible bandwagon, took for granted that the conventional view promulgated by official scientific institutions is true.

It is perfectly natural, in other words, for scientists and non-scientists to believe without question that HIV causes AIDS even though they have never seen or looked for the proof.

What is not natural is to question that, and the relatively small number of individuals who became HIV/AIDS dissidents, AIDS Rethinkers, HIV Skeptics, did so because of idiosyncratic and specific reasons. Women like Christine Maggiore, Noreen Martin, Maria Papagiannidou, Karri Stokely, and others had the strongest personal reasons to wonder about what they were being told: since they had not put themselves at risk in the way “HIV” is supposedly acquired, and since they were finding the “side” effects of antiretroviral drugs intolerable, the incentive was strong to think for themselves and look at the evidence for themselves.
Many gay men have had similar reason to question the mainstream view, and some unknown but undoubtedly large number of gay men are living in a perpetual mental and emotional turmoil: on one hand much empirical evidence of what the antiretroviral drugs have done to their friends, on the other hand their own doctors expressing with apparent confidence the mainstream view. So only a visible minority of gay men have yet recognized the failings of HIV/AIDS theory.
One of the first to do so, John Lauritsen, was brought to question the mainstream view for the idiosyncratic personal reason that, as a survey research analyst, he could see that the CDC’s classification scheme was invalid.
Among scientists, Peter Duesberg recognized some of the errors of HIV/AIDS theory because he understood so much about retroviruses and because he had not himself been caught up in the feverish chase for an infectious cause of AIDS. Robert Root-Bernstein, too, with expertise in immunology , could recognize clearly from outside the HIV/AIDS-research establishment the fallacy of taking immunedeficiency as some new phenomenon. Other biologists, too, who were not involved in HIV/AIDS work, could see things wrong with HIV/AIDS theory: Charles A. Thomas, Jr., Harvey Bialy, Walter Gilbert, Kary Mullis, Harry Rubin, Gordon Stewart, Richard Strohman, and many others who have put their names to the letter asking for a reconsideration.

********************

To summarize:

Mainstream researchers rarely if ever question the basis for the contemporary beliefs in their field. It’s not unique to HIV/AIDS. HIV/AIDS researchers and camp followers never cite the publications that are supposed to prove that HIV causes AIDS for the reason that they never looked for such proof, they simply took it for granted on the say-so of the press-conference announcement and subsequent “mainstream consensus”.

The people who did look for such proof, and realized that it doesn’t exist, were:
—  journalists covering “HIV/AIDS” stories (among those who wrote books about it are Jad Adams, Elinor Burkett, John Crewdson, Celia Farber, Neville Hodgkinson, Evan Lambrou, Michael Leitner, Joan Shenton);
—  directly affected, said-to-be-HIV-positive people, largely gay men and also women like those mentioned above;
—  individuals for a variety of individual reasons, as illustrated above for John Lauritsen and myself;
—  scientists in closely related fields who were not working directly on HIV/AIDS.

That last point is pertinent to the refrain from defenders of HIV/AIDS orthodoxy that highly qualified scientists like Duesberg or Mullis are not equipped to comment because they have never themselves done any research on HIV or AIDS. But that’s precisely why they were able to see that this HIV/AIDS Emperor has no clothes — scientists working directly on the many puzzles generated by this wrong theory have no incentive, no inclination, no reason to question the hypothesis; indeed, the psychological mechanism of cognitive dissonance makes it highly unlikely that scientists with careers vested in HIV/AIDS orthodoxy will be able to recognize the evidence against their belief.
More generally, this is the reason why the history of science contains so many cases of breakthroughs being made by outsiders to a particular specialty: coming to it afresh, they are not blinded by the insider dogmas.

So there is nothing unique about the fact that the failings of HIV/AIDS theory have been discerned by outsiders and not by insiders, and that the insiders are not even familiar with the supposed proofs underlying their belief. Nor is it unique that the dogma has many camp followers who never bothered to look for the supposed proofs of the mainstream belief. What is unique to HIV/AIDS theory is the enormous damage it has caused, by making ill or actually killing hundreds of thousands (at least). The annals of modern medicine have no precedent for this, which is another reason why thoughtless supporters of HIV/AIDS orthodoxy may feel comfortable with it despite never having sought evidence for it.

So here’s the question to put to everyone who insists that HIV causes AIDS:

HOW  DID  YOU  COME  TO  BELIEVE  THAT?
WHAT  CONVINCED  YOU?

————————–
Cited:
(1) Henry H. Bauer, Beyond Velikovsky: The History of a Public Controversy, University of Illinois Press, 1984; chapter 11, “Motives for believing”.
(2) Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press, 1970 (2nd ed., enlarged; 1st ed. 1962)

Dr. Frankenstein turns to CCR5

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 [2008] 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” ).