Simulation of mutations that support HIV treatment

A team of scientists at the University of California successfully modified the genome on stem cells to simulate a rare natural mutation that activates the body's defense against HIV.

In a promising new study, a team of scientists at the University of California successfully modified the genome on stem cells to simulate a rare natural mutation that activates the body's resistance mechanism. fight HIV virus. If the mutant cells are safely implanted in the patient's body, the researchers believe that the approach could create a viable HIV treatment. The study has been published in the journal of the National Academy of Sciences, the latest issue.

A few weeks ago, a shocking medical news was published: Timothy Ray Brown, a Berlin patient infected with HIV since 2008, was cured after receiving stem cells from donor owners. Natural mutations with resistance to HIV virus. This type of mutation is called CCR5Δ32 , the main essence is the lack of 32 pairs of nucleotides on chromosomes that regulate the type 5 chemokine receptor . People with mutations CCR5Δ32 possess the ability to self-produce an important receptor in the activity of HIV virus called CCR5 .

Although the HIV virus primarily uses a receptor named CD4 in white blood cells to attack targeted cells, the process requires the presence of another receptor called CCR5 . And the CCR5Δ32 mutation has created an abnormal form of CCR5 receptors that prevent HIV from attacking the target cell. Therefore, HIV cannot change and store genetic information into the human genome. However, only individuals who possess the mutant chromosome can be immune to HIV.

Picture 1 of Simulation of mutations that support HIV treatment

In the case of Brown's patient, by transplanting mutant stem cells CCR5Δ32 , doctors successfully treated HIV for this patient. However, this impressive treatment is just one of many risky and very expensive options. Doctors call this as light at the end of the tunnel.

Inspired by this impressive case, the team of scientists led by Dr. Yuet Kan from the University of California proposed the idea of mutating CCR5Δ32 by artificial methods without having to directly take cells stem from donors with congenital mutations.

To do that, the researchers switched to modifying a gene system called CRISPR-Cas9 based on the immune system used by a variety of different bacteria and generally have antiviral properties. Genetic information after editing will be cut and grafted into the induced pluripotent stem cell genome (iPSC) to accurately copy the CCR5Δ32 mutation in nature.

Next, mutated induced pluripotent stem cells are differentiated into two different types of immune cells, and according to researchers, these cells are fully immune to HIV. in the laboratory.

If the technique continues to be tested clinically, the patient's cells will be used as an iPSC source to form a natural drug for HIV treatment and this "drug" will feature each Different patients. In an interview with NewScientist, Dr. Kan said he did not intend to differentiate the mutated iPSCs into white cells that would be infected with HIV, named CD4 + T. Instead, he would differentiate them into the form of Transitional cells have the ability to separate further into any type of blood cell.

If mutant cells can be safely transplanted into HIV patients in the same way as Brown's, this is, in theory, a radical treatment for HIV. However, this does not mean that transplantation will take place easily and simply. Doctors need to perform a lot of preclinical tests before officially applying them to the patients.

So far, the research team has taken a long research path to produce the aforementioned approach. However, a lot of verifiable research and testing needs to be strictly followed by the team in order to reach a final conclusion. But clearly, this is a promising and promising method that will bring about HIV treatment in the future. One thing is certain: with the current level of medical development, the successful development of HIV treatment is only a matter of time.

Update 15 December 2018
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