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Los Angeles: The first babies in the world whose genes have been modified to help protect them from HIV infection are more likely to die sooner, according to a study.
According to an analysis by scientists from the University of California (Berkeley) in the United States, the controversial genetic mutation that a Chinese scientist attempted to create in twins born last year is associated with a 21% increase in mortality later in life.
Researchers analyzed more than 400,000 genomes and associated health records contained in a UK database, UK Biobank, and found that people with two mutated copies of the gene had a significantly higher mortality rate between 41 and 78. years than those with only one copy or none. .
Previous studies have linked two mutated copies of the gene, CCR5, to a fourfold increase in the mortality rate after influenza infection, and the higher overall mortality rate may reflect this greater susceptibility to death from influenza. However, the researchers said that there could be a number of explanations, since the protein for which CCR5 encodes, and which no longer works in those with the mutation in both copies of the gene, is involved in many bodily functions.
"Beyond the many ethical issues related to CRISPR babies, the fact is that now, with current knowledge, it is still very dangerous to try to introduce mutations without knowing the full effect of what these mutations are doing. Said Rasmus Nielsen, a professor at UC Berkeley. "In this case, it's probably not a mutation that most people would like to have. In fact, your situation is worse on average, "said Nielsen.
"Because a gene can affect multiple characters and that, depending on the environment, the effects of a mutation can be very different, I think that there can be many uncertainties and unknown effects in any germ line edition, "said Xinzhu Wei, postdoctoral fellow, first author of the research published in the journal Nature Medicine.
The CCR5 gene encodes a protein that, among other things, is on the surface of immune cells and helps some HIV strains, including the most common, to enter and infect them. Jiankui He, the Chinese scientist who, last November, announced that he had experimented with CCR5 on at least two babies, said he wanted to introduce a gene mutation that would prevent this. Natural mutations that deactivate protein are rare in Asians, but a mutation found in about 11% of Northern Europeans protects them from HIV infection.
The genetic mutation, Delta 32, refers to a segment lacking 32 base pairs in the CCR5 gene. This mutation interferes with the cell surface location of the protein for which CCR5 encodes, counteracting HIV binding and infection. It has not been able to duplicate the natural mutation, but appears to have generated a similar deletion that would also inactivate the protein, researchers said. One of the twin babies would have had a copy of CCR5 modified by the CRISPR-Cas9 gene modification, while the other baby would have had both copies published.
However, inactivating a protein present in all humans and in most animals is likely to have negative effects, said Nielsen, particularly when it is performed on both copies of the gene, a so-called mutation. homozygous.
After the publication of his experiment, Nielsen and Wei, who are studying the current genetic variation to understand the origin of human, animal and plant traits, decided to examine the effect of the CCR5-Delta 32 mutation from the British Biobank. Two independent measures indicated a higher mortality rate for those with two mutated genes. Fewer people than expected with two mutations listed in the database, indicating that they had died at a higher rate than the general population. Less than expected survived from 40 to 78 years.
"The proportions before registration and survival after registration tell the same story, namely that you have minimal survival or higher mortality if you have two copies of the mutation," Nielsen said. "There is simply a deficit of individuals with two copies," he said.
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