Genetic engineering in humans is the direct manipulation of the genome using molecular engineering techniques. Recently developed techniques for modifying genes are often referred to as “gene editing.” Genetic modification can be applied in two very different ways: “somatic genetic modification” and “germ genetic modification“.
The somatic genetic modification adds, cleaves or alters genes in some cells of existing humans and is commonly used to alleviate medical conditions. These gene therapy technologies are approaching clinical practice, but are limited to a few conditions and are very costly.
Germ genetic modification can alter genes in eggs, sperm or early embryos. Often referred to as “hereditary genetic modification” or “gene editing for reproduction.”.
These changes will occur in every cell of a human that develops from a gamete or embryo, and also in all subsequent generations. Germline modification has not been done in humans, but by far it will be the most important type of genetic modification.
If used for reinforcement purposes, it can open the door to new market-based eugenics. The laws of more than 40 countries prohibit human germline modification and pass the binding international treaty of the European Commission.
- 1 Genetic engineering in humans, but should we?
Watch How Genetic Engineering in Humans Change the World
Genetic engineering in humans, but should we?
This news has drawn great attention from the scientific community as it may change the human genome from today. Although the initial anger seems to have disappeared, a research professor at Dalhousie University is worried that the scientific community now seems to be asking how such things should be done, not should be done.
Professor Françoise Baylis, (CM, ONS, Ph.D.) wrote an opinion article on this topic, published in the scientific journal “Nature: Human Behavior” “titled, questioning the proposed translation path for germline genome editing”.
The creation of the CRISPR gene editor, people have the potential to produce so-called “designer babies”, or maybe ghosts. Then at the end of 2018, a Chinese researcher announced that he had successfully completed,…
what restrictions should we set for genetic engineering in humans?
Genes affect health and disease, as well as human characteristics and behaviour. Researchers have just begun to use genetic techniques to uncover the genomic contributions to these different phenotypes, and when they do, they have discovered various other potential applications for this technology.
For example, ongoing advances have enabled scientists to genetically engineer humans to achieve certain desired characteristics. Of course, the possibility of human genetic engineering raises many moral and legal issues.
Although there are few clear answers to these questions, the expertise and research of bioethicists, sociologists, anthropologists, and other social scientists can tell us how different individuals, cultures, and religions view the ethical boundaries of genomics use. In addition, these insights can help develop guidelines and policies.
Much of our current understanding of the effects of genetic self-cognition comes from disease detection. Once the disease genes are identified, molecular or cytogenetic diagnosis of many genetic conditions can be more easily performed.
Diagnostic tests provide the technical ability of individuals and/or carriers at risk before testing for symptoms to determine if they will develop a particular condition. This test is a particularly attractive option for individuals at risk of developing a disease that may be precautionary or treated, as well as those who may carry genes with a significant risk of reproductive recurrence.
In fact, due to advances in single-cell diagnosis and fertilization techniques, embryos can now be created in vitro; then, only those embryos that are not affected by a particular genetic disease can be selected and implanted in the female uterus. This process is called preimplantation genetic diagnosis.
For adult-onset conditions, ethical questions have been raised as to whether genetic testing should be performed without curing the disease. Many people want to know if a positive diagnosis of an imminent disease that is about to occur will harm at-risk individuals by creating excessive stress and anxiety.
Interestingly, social science research shows that the answer to this question is both here and there. It seems that if genetic testing reveals that the individual is a carrier of the recessive disease, such as Tay-Sachs disease or sickle cell anemia, this knowledge may have a negative impact on the health of the individual, at least in the short term (Marteau et al, 1992. Woolridge & Murray, 1988).
On the other hand, if predictive testing for adult-borne genetic diseases (such as Huntington’s disease) shows that at-risk individuals will develop the disease in later life, then most patients are concerned about the disease. It is lower and can alleviate the anxiety of the patient.
Unknown (Taylor & Myers, 1997). For many people who choose to make predictive tests, it is helpful to get control points by determining the answer. Some people appreciate the opportunity to change their lives, for example, to travel more, change jobs, or retire early, expecting to develop a debilitating condition in their lives.
Of course, as genetic research progresses, tests of features and behaviours unrelated to disease are constantly evolving. Most of these characteristics and behaviours are inherited as complex conditions, which means that multiple genes and environments, behavioural or nutritional factors may contribute to the phenotype.
Currently, available tests include eye colour, chirality, addictive behaviour, “nutrition” background and athletic ability. But does understanding the genetic background of a person with these non-disease characteristics negatively affect a person’s self-concept or health perception?
Research is now starting to solve this problem. For example, a group of scientists conducted genetic testing of muscle characteristics in a group of volunteers participating in a resistance training program (Gordon et al., 2005).
These tests look for single nucleotide polymorphisms that determine whether an individual has a genetic predisposition to muscle strength, size, and performance.
Investigators found that if these people did not receive positive genetic information about muscle characteristics, they believed that exercise programs had a positive impact on their own abilities. However, those who do receive positive test results are more likely to consider beneficial changes beyond their control and attribute any such changes to their genetic makeup.
Thus, the lack of genetic susceptibility to muscle characteristics actually gives the subject a feeling of empowerment.
The results of the above studies may surprise many people because the main problem associated with non-disease trait testing is that people without positive traits may develop a negative self-image and/or inferiority complex.
Another problem that bioethicists often consider is that people may find that the genes involved in the biological or behavioural characteristics they carry are often considered negative.
In addition, many critics worry that the prevalence of these characteristics in certain ethnic groups may lead to prejudice and other social problems.
Therefore, rigorous social science research by individuals from different cultural backgrounds is essential to understanding people’s perceptions and establishing appropriate boundaries.
Building Better Athletes with Genetic engineering
Over the years, the desire for better athletic performance has prompted many trainers and athletes to abuse scientific research and try to gain an unfair advantage over their competitors.
Historically, these efforts have involved the use of performance-enhancing drugs that were originally used to treat people with the disease. This practice is called stimulant and it is often involved in erythropoietin, steroids and growth hormone (Filipp, 2007).
In order to control this unfair competitive advantage, the International Olympic Committee established the World Anti-Doping Agency (WADA) in 1999, which prohibits athletes from using drugs that improve their performance.
The World Anti-Doping Agency also conducts various testing programs to try to capture athletes who violate anti-doping rules.
Today, the World Anti-Doping Agency faces new obstacles to overcoming the problem of genetic stimulants. This practice is defined as the non-therapeutic use of cellular, genetic or genetic components to improve athletic performance.
Gene agonists use genetic research to transfer genetic material to human cells to treat or prevent disease (Well, 2008). Because gene agonists increase the number of proteins and hormones normally produced by cells, testing for genetic performance enhancers will be very difficult, and a new race is being developed to develop methods for detecting this form of stimulant. (Baoutina et al., 2008).
In the late 1990s, the so-called “Schwarzenegger Mouse” invention immediately realized the potential to change genes to build better athletes.
These mice were given this nickname because they were genetically engineered to increase muscle growth and strength (McPherron et al, 1997; Barton-Davis et al, 1998).
The purpose of developing these mice was to study muscle disease and reverse the decline in muscle mass during ageing. Interestingly, Schwarzenegger mice are not the first animals in their class.
This title belongs to the Belgian Blue Bull (Figure 1), a special breed known for its enormous muscle mass. These animals produced by selective breeding have mutated and non-functional copies of the myostatin gene.
Which typically control muscle development. Without this control, the cow’s muscles never stop growing (Grobet et al., 1997). In fact, Belgian blue cattle have become so large that most of the females of this breed cannot give birth naturally, so their offspring must be delivered by cesarean section.
Schwarzenegger mice differ from these cows in that they highlight the ability of scientists to discover new muscle development through genetic engineering, which gives athletes a distinct advantage.
But does giving an ideal trait produce other, more harmful consequences? Is genetic stimulant and other forms of genetic engineering worth exploring, or as a society, should we decide that manipulating genes for non-disease purposes is immoral?
Genetic testing may also apply another scientific strategy to the field of eugenics, or to intervene to promote a social philosophy that improves the genetic characteristics of humans. In the past, eugenics was used to demonstrate practices including involuntary sterilization and euthanasia.
Today, many people are concerned that preimplantation genetic diagnosis may be well established and can be applied technically to select specific non-disease features (rather than eliminating the serious diseases currently used) implanted embryos, thus equivalent to a eugenics Form of study.
In the media, this possibility has been sensational and often referred to as the so-called “designer baby” creation, which is even included in the Oxford English Dictionary. Although possible, this genetic technology has not yet been implemented; nevertheless, it still brings many intense moral issues.
The selection and enhancement of embryo characteristics can lead to ethical issues involving individuals and society. First, does the choice of specific characteristics poses a health risk, otherwise, these risks do not exist?
The safety of procedures for preimplantation genetic diagnosis is currently under investigation and, as this is a relatively new form of reproductive technology, lacks long-term data and a sufficient number of subjects.
However, a security question often asked about the fact that most genes have multiple effects. For example, in the late 1990s, scientists discovered a gene associated with memory (Tang et al., 1999).
Modification of this gene in mice greatly improved learning and memory, but it also caused an increased sensitivity to pain (Wei et al., 2001), which is clearly not an ideal feature.
In addition to security issues, personal freedom issues arise. For example, when a child cannot express consent by himself, should parents be allowed to manipulate the child’s genes to select certain characteristics?
Suppose a mother and father choose an embryo based on their so-called musical sexual predisposition, but the child does not like music when he grows up. Does this change the child’s feelings about his or her parents, and vice versa?
Finally, as far as society is concerned, everyone cannot get this expensive technology. Therefore, perhaps only the most privileged members of society can have “designer children” with more intelligence or physical appeal. This can cause genetic aristocracy and lead to new forms of inequality.
At present, these questions and conjectures are purely hypothetical because the techniques required for feature selection are not yet available. In fact, this technique may not be possible considering that most features are complex and involve many genes. Nevertheless, if you can create genetically enhanced humans, then thinking about these and other issues related to genetic engineering is also important.
SCIENTISTS TAKE ON GENETIC ENGINEERING IN HUMANS
After all, the vision of a designer baby may not be that far away. Last year was full of news about genetic engineering most of which was driven by cutting and pasting technique called Crispr. At the top of the list. Crisp can modify human embryos to correct relatively common, often fatal, mutations.
A controversial cell biologist named Shoukhrat Mitalipov, who pioneered work in the US, said his team not only used CRISPR to correct mutations in newly fertilized embryos, but they did it through a mechanism.
If not novel, at least it is unusual. The response of the scientific community is direct and negative. They just didn’t buy a bit. So, Wednesday, in Nature Mitafilov published the initial working journal two groups of researchers published a criticism of the Mitalipov 2017 paper and Mitalipov’s sharp, acronym and infographic filled with criticism trying to respond. Because morality doesn’t matter – well, not yet – if science doesn’t actually work.
You know how the baby is made, right? Ok, Mitalipov’s team didn’t do that. Scientific research using existing human embryos is contraindicated in most cases in the United States, so scientists fertilize them with normal human eggs and fertilize them with sperm containing the mutant MYBPC3 gene.
This version is a disease called hypertrophic cardiomyopathy, which is the most common cause of sudden death in young athletes. People with two mutants MYBPC3 one from mom, another from dad, or homologous alleles, in genetic language rarely survived childhood. Only one person who replicates heterozygotes often develops heart problems as they age.
To try to correct the mutation, Mitalipov’s team used CRISPR to cut the mutant gene from the paternal chromosome and then insert the synthetic corrected version.
But the second step did not happen. In contrast, according to the analysis of Mitalipov, the cells replicated the wild-type gene from the maternal chromosome and inserted it. Results: The embryo has two wild-type alleles. It is called “homology-dependent repair” or “homologous homeopathic repair”.
“Some of these authors have been studying DNA repair, and somehow they missed the elephant in the room,” said Mitalipov, director of the Embryonic Cell and Gene Therapy Center at Oregon Health and Science University. We point out that there is a huge gap in how genes are repaired. We are not sure if it occurs in the somatic lineage, but in the embryonic lineage we have now demonstrated this.”
Embryologists and cell biologists don’t think they missed the elephant. They don’t think so. “We think there is another explanation,” said Paul Thomas, the editor of the SA genome at the South Australian Institute of Health and Medical Research, a lead author of a review article.
Thomas’s research shows that in mice, Crispy tends to cut large pieces of DNA from the genome, the so-called large deletions. He suspects that this is also what happened in the Mitalipov embryos – they missed a lot of deletion failures. “If you create a lot of deletes on a chromosome, you need to specialize in that event,” Thomas said. “If you use the test method they use, this is a very standard test and cannot be detected.”
It’s like trying to figure out how many bagels a bakery makes by calculating what’s on the shelf at the end of the day. Your statistics will say that the bakery mainly produces blueberries, but that’s because the good taste of poppy seeds, garlic, salt and plains is invisible until you arrive. Your number will overestimate the proportion of blueberry production to the overall bagel.
Is this just a problem for mice and men? of course. “Of course, more and more people are seeing a large number of mouse embryos missing. It is unclear whether a large number of deletions have occurred in human embryos because in fact we only have this research and a few other studies,” Thomas said.
So Mitalipov’s team returned to the lab. They took their old samples and re-analyzed them. This technique, called polymerase chain reaction, allows sequencing and analysis of a large enough amount of DNA. This time, they watched a longer chromosome.
“We used large-scale PCR for analysis, up to 10,000 base pairs, and we still don’t see any missing,” Mitalipov said. He did not expect to find anything. The first paper of his group reported a success rate – that is, a modified mutation rate – about 70%. Mitalipov said it is hard to believe that 70% of his embryos will have a large number of defects caused by Crispr. He said that this made the technology unusable.
However, the case has not yet been closed. “We were very surprised that they did not see any evidence of deletion in any of their responses,” Thomas said. “We don’t think they completely rule out this possibility.” One of Thomas’s co-authors, Fatwa Adikusuma, proposed a more accurate method of detection, such as qPCR (quantitative detection of DNA amount – hence Q value). Mitalipov has not tried it.
Other teams have other questions. For example, a team led by Dieter Egli of Columbia University and Maria Jasin of the Memorial Sloan Kettering Cancer Center (including the outspoken Georges Biotech expert George Church) wondered how the CRISPR complex could support the maternal wild-type gene because, In the early part of cell division, mother contribution and father contribution are separate.
According to Mitalipov, the parental DNA cluster contained in an envelope called a pronucleus is exposed enough time for the repair process to work. Paul Knoepfler, a cell biologist at the University of California, Davis, said: “If this is correct, what puzzles them is that they don’t report more mosaics in these embryos.
” Refers to a single organism with different genomes in different cells. “The fragility is so late, for example in the two-cell embryo stage, which can lead to different genetic results,” Knoepfler said – and this could lead to later unhealthy embryos.
So is it possible for Mitalipov to do the right thing? “As mentioned above, the new data is consistent with the genetic correction,” Jasin wrote in an email. However, she said that Mitalipov’s own response shows how difficult this research is.
When his team could not detect the parent’s allele, one of his embryos showed “allele dropout.” “Not sure if there is no genetic correction for gene homologous recombination in all embryos, some embryos, or in the most extreme cases,” adds Jasin.
Everyone, including Mitalipov, said that more research is needed to determine. It doesn’t matter to him; he knows that people have a lot of concerns about what he said. If his method does work, then it only applies to embryos with a wild-type copy of the gene, on the one hand, there must be a wild-type gene version to replicate the cells.
But more importantly, new ideas require time and work to penetrate into one area. “There is dogma, especially in biology,” Mitalipov said. “We just accepted our findings, calling it an unknown but powerful repair pathway in human embryos.”
This “dogma” definitely takes time to make way for this approach. “Mitalipov’s team has strengthened their case to some extent,” Knoepfler said. “Maybe this points to the direction we fundamentally understand the new mechanism in early human embryos, but it is also possible that we will treat this completely differently a year later.” Either way, for something going to the clinic, it’s my performance must exceed 70%. This means it’s time to do more work in the lab.