Scientists Intend To Destroy HIV By Disabling Certain Genes In Immune Cells - Alternative View

Scientists Intend To Destroy HIV By Disabling Certain Genes In Immune Cells - Alternative View
Scientists Intend To Destroy HIV By Disabling Certain Genes In Immune Cells - Alternative View

Video: Scientists Intend To Destroy HIV By Disabling Certain Genes In Immune Cells - Alternative View

Video: Scientists Intend To Destroy HIV By Disabling Certain Genes In Immune Cells - Alternative View
Video: HIV - Curing the Incurable | Daniel Aaron Donahue | TEDxTUM 2024, May
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Thanks to the genomic editor CRISPR / Cas9, biologists have been able to find three genes by which HIV enters immune cells. These genes can be turned off without causing significant harm to human health.

According to Bruce Walker of the Massachusetts Institute of Technology, viruses are inherently very small and contain few genes. For example, the genetic code of HIV contains only nine genes, while there are more than 19 thousand of them in the human genome. Very often, viruses borrow genes to make proteins vital for reproduction. Scientists have made an attempt to isolate these genes, and determine which of them can be destroyed without killing a person.

It should be noted that the CRISPR / Cas9 genomic editor was recognized as a major breakthrough in science in 2015. Its creator is the American scientist Fen Zhang together with a group of molecular biologists about three years ago. At that time, the editor was modernized several times, which allows scientists to use the editor to modify the genome with almost one hundred percent accuracy.

Scientists say that the fight against HIV is a kind of return to the beginning for the editor, since the system originally developed hundreds of millions of years ago inside bacteria precisely to protect against retroviruses. And only in 2012, scientist Zhang and his colleagues adapted CRISPR / Cas9 for editing the genome of multicellular objects.

Currently, some scientists are trying to use this genomic editor in order to cut the HIV code from the DNA of infected cells, thereby clearing them from infection, or mutate them so that they become invulnerable to HIV.

The scientists, led by Walker, decided to go the other way - they transformed the editor in such a way as to be able to turn off genes in human immune cells into which this system was inserted, in a completely random way. Scientists alternately turned off all 19,000 genes, obtaining a small group of immune cells that successfully survived such a procedure. Then biologists tried to infect these cells with HIV.

Thanks to this experiment, scientists were able to isolate a small set of genes that do not play a big role in the survival of immune cells, but whose work is extremely important for HIV. This set also included two genes that are well known to scientists - CD4 and CCR5, which are responsible for the formation of protein molecules that HIV clings to when cells are infected. Disabling or deleting these genes, as shown by previous experiments, can cause serious side effects. All this makes this procedure very undesirable.

In addition to these two genes, Walker and colleagues identified three other genes that are not clearly associated with HIV - these are SLC35B2, TPST2, and ALCAM. According to scientists, the first two DNA genes could theoretically help HIV enter the cell by altering the way the CCR5 protein works. The third gene, in turn, affects the tendency of cells to connect with each other, therefore, if the ALCAM gene is removed, immune cells become, at a practically low concentration of viral particles in the nutrient medium or blood, invisible to HIV.

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According to the assumptions of virologists, this may be due to the fact that when this gene is removed, the cells contact each other less often, and this does not contribute to the spread of the virus into uninfected cells and tissues.

Scientists have not yet been able to determine whether the removal of these three genes will have the same negative effect on the human body as the elimination of the CCR5 and CD4 genes. The researchers plan to find the answers to their questions in subsequent experiments.