Antiviral antibiotics

When antibiotics act on viruses

Kirill Stasevich, "Science and Life", based on the materials of Yale University: Topical antibiotic triggers unexpected antiviral response

We know that antibiotics do not work on viruses. Antibiotics target a cell – bacterial, fungal, or, say, cancerous; in it they spoil important molecular processes, without which the cell cannot live. But viruses are not cells, they are just a complex of proteins and nucleic acids. It is clear why they are insensitive to antibiotics.

But this is if we consider the virus and the antibiotic separately from everything. However, the virus does not live in a vacuum: in order for it to multiply, it needs to penetrate into the cell, and its cell lives surrounded by other cells, very different, which together make up tissues and organs. Could it be that the virus will feel the antibiotic, let's say, indirectly, because of the changed environmental conditions?

Researchers have repeatedly tried to find out how viruses perceive antibiotics, and the results were very different: sometimes cells and animals became more sensitive to viral infection, sometimes, on the contrary, it became more difficult for the virus to infect the host.

So, a few years ago, Akiko Iwasaki and her colleagues from Yale published an article in the journal PNAS, which stated that the flu virus only benefits from antibiotics. The whole point turned out to be that without bacteria that live on the mucous membrane of the respiratory tract, but do not harm us in any way, the immune system cannot properly turn on the antiviral protection system. The antibiotics we use to treat the throat destroy these bacteria, making the cells of the respiratory tract more sensitive to the virus.

In a new article by the same researchers, which was published in Nature Microbiology, we are talking about another virus – the herpes simplex virus – and about a completely different effect. The herpes virus penetrates through any mucous membrane, and this time the vaginal mucosa of mice was treated with antibiotics. It turned out that antibiotics suppressed the reproduction of the virus, and although the number of viral particles in the treated mice in the first days of the experiment was the same as in untreated mice, their symptoms of the disease were weaker – because of antibiotics, the virus could not unfold in full force.

At first, a mixture of antibiotics was used in the experiments, but then we decided to find out which one of them has an antiviral effect – so that we could then understand the mechanism of action. It turned out that the viral activity was suppressed by neomycin. As for the mechanism, the first thing one could think of was bacteria – that the death of bacteria somehow has a bad effect on viruses. However, the bacteria had nothing to do with it: in mice devoid of microbes, neomycin acted in the same way.

In fact, everything was different: neomycin activated genes in cells that control antiviral protection, those that encode interferon proteins. (Moreover, neomycin stimulated antiviral protection not only in mouse cells, but also in human cells.) Exactly how he did it remains to be seen, however, it is already clear that the effect of antibiotics on the body is not limited to the extermination of bacteria – an antibiotic may well directly affect the molecular and cellular cuisine.

Neomycin was also tested on another virus – the flu virus, which, as mentioned above, only benefited from antibiotics. However, now everything was different: when neomycin was injected into the mice's nose, they became quite resistant even to a very virulent strain of the virus - without an antibiotic, the flu killed all the mice, whereas after neomycin, as many as 40% survived.

Of course, this does not mean that antibiotics should be used immediately against viral infections now. Firstly, as we can see, it all depends on what kind of antibiotic and against what kind of virus is used.

Secondly, if we talk about clinical use, then we still need to understand whether there is really a significant benefit here: antibiotics also kill our bacterial symbionts, without which we would have to be very, very bad, and if we also start to be treated with antibiotics against viruses, we can ruin all the beneficial microflora altogether.

So far, experiments with "antiviral antibiotics" tell us more that even such familiar substances as antibiotics may well surprise us, and that when studying the effect of some substances, it is necessary to take into account all possible mechanisms by which this substance can affect the body.

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