Viruses take over part of the immune system and use it against us
Viruses take over part of the immune system and use it against us
.Some viruses are capable of seizing an enzyme that supposedly prevents autoimmune diseases in order to avoid detection. This discovery by the Mayo Clinic researchers and their collaborators is published in PLOS Biology. However, there is also a positive side to this, as the same investigative team defined how much genetic material the virus needs to reverse the process and, rather, activate the immune system against the virus.
The genetic material of the virus takes the form of RNA, a chemical related to DNA. The RNA can be single-stranded, similar to a thread, or a complex structure known as double-stranded. Several immune proteins from humans recognize viral RNA, because the genetic material of the virus contains long double-stranded stretches. Human cells create their own RNA to fulfill vital functions and, sometimes, that RNA has short double-stranded stretches. When the double-stranded RNA activates the immune system, an autoimmune disorder can occur, that is, an erroneous attack of the immune system against the body itself.
In order to avoid this autoimmunity, a protein called "ADAR1" (adenosine deaminases that act on RNA) was developed in humans. Aicardi-Goutières syndrome is a rare and debilitating autoimmune disorder that may be the consequence of a deleterious mutation in the ADAR1 gene. Patients suffering from Aicardi-Goutières syndrome produce inflammatory reactions against their own bodies and this causes damage to tissues, especially in the brain.
So, how does ADAR1 prevent this autoimmunity?
The ADAR1 recognizes short double-stranded stretches of human RNA and switches them to single strands so that they do not activate the immune system.
However, "the ADAR is a double-edged sword," says the director of the Mayo Clinic-based study group, Dr. Roberto Cattaneo. This researcher explains that while the ADAR1 protein consists of a balance between detecting viruses and preventing autoimmunity, viruses have evolved to take advantage of this balance.
ADAR1 acts on double-stranded viral RNA with the same urgency as on human RNA; that is, the protein changes the double-stranded RNA of single-stranded viruses and, in that way, protects some viruses from immune detection.
The Mayo Clinic-based group was able to demonstrate that there is a threshold for double-stranded RNA, in which the ADAR1 is no longer able to change enough single-stranded RNA, and then the presence of that double-stranded viral RNA unchanged activates the immune system.
"There were already works on the use of the ADAR, but now we can give figures: a threshold, that is, we have a quantitative evaluation of what is happening," says Dr. Cattaneo.
The study mentions that the threshold for immune activation is a figure of about 1000 double strands of RNA. The researchers discovered the threshold by the following process: first, they made the deletion of the ADAR1 gene in the cells; then, they collected and sequenced the human RNA from these experiments; then, they compared the human RNA of normal cells with that of cells with ADAR1 deficiency, which allowed them to determine which genes are affected by ADAR1; subsequently, they took the cells with ADAR1 deletion and infected them with the measles virus or another mutant measles virus that produced more RNA. Neither virus could develop well without the ADAR1; but by re-introducing ADAR1, the normal measles virus was able to develop well, unlike the mutant virus that was not able to do so. By comparing the amount of double-stranded RNA of the mutant virus with that of the normal virus, they were able to calculate the threshold of double-stranded RNA that the ADAR1 changed.
"This is fascinating from the evolutionary point of view, it's an interferon-inducible gene that nobody thought could be a favorable factor for viruses, because that's not how you think about it," says Dr. Cattaneo.
The group's discovery of how viruses take over ADAR and the threshold of RNA can lead to new antiviral therapies directed against ADAR1 so that viruses can not use it to hide from the immune system. (Source: Mayo Clinic)
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