Virus-like drug stops bacteria

Kirill Stasevich, "Science and Life" based on the materials of The Scientist: Virus-Mimicking Drug Boosts Resistance to Antibiotic-Resistant Bacteria.

Everyone knows about the benefits of gastrointestinal microflora, but this microflora can include not only bacteria, but also viruses. And if you can't surprise us with useful bacteria anymore, then useful viruses still look pretty amazing.

Two years ago we wrote about how mouse norovirus (MNV) helps the immune system to work properly: if bacteria are removed from the intestine, then inflammation will begin in it due to a malfunction of the immune settings, but in the presence of the virus, inflammation in the intestine subsides, and intestinal lymphocytes begin to work properly.

Eric G. Pamer and his colleagues from Memorial Sloan and Kettering Cancer Center, interested in these results, tried to use norovirus against the antibiotic-resistant bacterium Enterococcus faecium. Normally, the conditionally pathogenic E.faecium, which lives in the gastrointestinal tract, behaves decently, since it is kept within the framework of other bacteria. But if we have to take antibiotics, then part of the microflora dies, and E.faecium gets the opportunity to show its worst qualities – especially if it has drug resistance.

In an article in Science Translational Medicine (Abt et al., TLR-7 activation enhances IL-22–mediated colonization resistance against vancomycin-resistant enterococcus), researchers write that in mice treated with an antibiotic, norovirus was able to suppress the reproduction of opportunistic bacteria. The virus acted through the immune system, stimulating the synthesis of the immune protein – toll-like receptor 7 (TLR7). Toll-like receptors sit in the cell membrane, their task is to recognize foreign molecules that have entered the body together with bacteria, viruses, fungi, etc.; recognizing such a molecule, the receptor triggers the innate mechanism of cellular immune response. Indeed, mice after the introduction of the virus began to actively synthesize antimicrobial peptides that weakened the population of E.faecium.

However, if you just inject norovirus, it may not take root. Other microflora bacteria help him stay in the intestine, and they, as we remember, die out under the action of an antibiotic. But on the other hand, you can use some kind of molecule that will represent such a virus and which will not care whether bacteria support it or not.

It turned out that a synthetic substance that mimics the genomic RNA of mouse norovirus acts in the same way: it directly interacts with the immune receptor, triggering the synthesis of signaling proteins, and through them antimicrobial peptides. In mice that ate a molecule that mimicked the virus, the level of E.faecium in the intestine decreased, despite the fact that the animals had been treated with an antibiotic before.

Given that the drug resistance of bacteria is becoming an increasing problem, such virus-like remedies may come in very handy. The sequence of molecular signals that is triggered by a virus or a virus-like molecule is known, and therefore it would be possible to act here not from the very beginning, but from the middle, that is, to stimulate the synthesis of a certain immune protein.

This approach may be easier and safer, because toll-like receptors have a very strong effect on the immune system, and therefore, acting through them, you can provoke some side effects that will manifest a little later. But, again, using viral activation of immunity to fight resistant bacteria seems to be an effective and ingenious approach – especially since some viruses are ready to tell us how it is done themselves.

Portal "Eternal youth" http://vechnayamolodost.ru 02.03.2016