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TheIn January, the Chinese scientist who created the first "CRISPR babies" – binoculars born of gene-modified embryos – sent an email to an American bioethic friend suggesting that he doubted that he did.
"I've thought about it," writes Dr. William Hurlbut, a bioethicist at Stanford University, writing to He Jiankui. "I recognize that I have embarked too quickly on a first clinical trial without the necessary open dialogue with regulators, the scientific community and the public." Hurlbut shared the email with STAT – the first communication to be made public in which is known to have expressed regret.
The premature birth of the girls last October, which he calls Nana and Lulu, sparked a public outcry because he hastened to modify the DNA of human embryos in a way the consequences of which are largely unknown. – changes that would be inherited from the offspring of girls. A new article provides the latest evidence of why critics around the world have attacked it, formerly of the Southern University of Science and Technology of Shenzhen, for a deplorable ethical misconduct.
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People with rare genetic variants that he has tried to integrate into embryos using CRISPR's genome modification technology have a 21% higher mortality rate than those with the most common form of the gene, scientists reported on Monday.
"We continue to learn things we did not know [about the CCR5 gene that He tried to alter]and that should make us think, "said science historian J. Benjamin Hurlbut of Arizona State University, son of William Hurlbut. "Hereditary genetic modifications will be inherently an experience – an experiment conducted on children. We'd better know what we're doing before we go down that road. "
The CCR5 variant, called Δ32, is best known for its protection against HIV infection, the virus that causes AIDS. The gene encodes a receptor on the surface of immune cells. The Δ32 variant, which has 32 fewer DNA bases, produces a receptor too short to penetrate the surface of the cell, so that HIV can not use it as it normally does to penetrate in the cells. The Δ32 is the most widespread in northern Europe (it is thought that this is the case of the Vikings), but it remains rare; it is found in 16% of cases, against 6% of Italians, 4% of Greeks and even lower percentages of other ethnic groups.
In explaining his choice of the CCR5, he said he wanted to protect children from HIV infection, extremely stigmatized in China, while recognizing that Δ32 had been associated with a higher risk of serious complications and death from HIV. 39, influenza, as well as an infection by West. Nile virus.
To better understand the effects of Δ32 on health, Xinzhu Wei and Rasmus Nielsen of the University of California at Berkeley analyzed data from 409,693 people of British descent in the UK. Biobank, an ambitious effort to study the effects of genes on health and other characteristics. They examined three possibilities of Δ32: two copies (one of mum and one of dad, which 4,349 people possessed), one copy (83,038 people) or zero copy (both CCR5 genes of one person are complete, not missing 32 missing letters in Δ32, as was the case with 308,317 people).
People wearing two copies of Δ32 are about 20% less likely to reach age 76 than those with only one copy, according to Berkeley researchers in Nature Medicine. And given the frequency of the Δ32 mutation among the British (11.59%), fewer people with two copies volunteered for the British Biobank than they expected. This suggests that they might have become too sick to participate; these studies, in general, have more participants in good health than the very sick.
"The Δ32 / 32 individuals have a significantly higher mortality rate than the other two genotypes," the researchers wrote.
Nielsen, a professor of integrative biology at Berkeley, called "32" "probably not a mutation that most people would like to have. In fact, you are on average less well off, "especially because of the consequences of influenza and West Nile virus. The higher risk of premature death, he told STAT, "is probably linked to reduced efficacy of the immune response to specific diseases. The effects depend on the environmental context, in particular the pathogenic environment. "
The death rate of people with only one copy of Δ32, however, is no higher than that of people with none, probably because "immune function is largely preserved as long as you have a functional copy of the gene, "said Nielsen.
On the other hand, the persistence of centuries of Δ32 suggests that this confers benefits that go beyond the protection against HIV (HIV has appeared too recently to explain why a mutation of the Viking era it's hung). The best hypothesis comes from small studies suggesting that 32 protects against flaviviruses (like yellow fever) and smallpox, and could help people recover from a stroke.
The largest legitimate study to try to transform CCR5 genes into a protective form against HIV has been led by Sangamo Therapeutics. He reported no excess mortality among his adult participants – all adults – but it is probably because they were relatively young (30 to 55 years old) and that they were followed since then. barely 10 years, said Fyodor Urnov of the Innovative Genetics Institute of Berkeley, who helped lead the project. Sangamo study.
"The subjects have not been followed long enough," he said.
"If there ever was a poster child [for using]Currently, genome editing is only for the treatment of existing disease in consenting adults and pediatric subjects where parents can give their consent, that's it, "Urnov said about the paper. Nature Medicine.
It turns out that the chaotic experience he experienced missed his stated goal. Although he intended to modify the CCR5 gene of the embryos to produce the Δ32 variant, he instead created chaotic changes. Lulu has a normal CCR5 gene (i.e. CRISPR omitted) and another with a 15 base pair deletion, not a 32 base pair deletion. Nana has a CCR5 gene missing four base pairs and one with an extra base pair.
None of these CCR5 mutations exist in nature and their health consequences are unknown.
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