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Viruses use their ability to sense the environment to make a ‘replicate and kill’ decision.

One study found that viruses use information from their environment to “decide” when to fit snugly inside their host and when to multiply and explode, killing the host cell.

The study, led by the University of Maryland at Baltimore County (UMBC) in Frontiers in Microbiology, suggests that this work adds a new set of complexity to our understanding of virus- host and may have future implications for antiviral drug development, quoting Evan Earl. , professor of biological sciences and senior author of the new research paper.

Today, viruses use this ability to their advantage. But in the future, Earl said, “We could use it to hurt him.”

The new study focuses on phages, which are viruses that infect bacteria. The phages in the study can infect their hosts only when the bacterial cells have special appendages called “bacterial hairs” and “cilia” that help the bacteria move and mate.

The bacteria produce a protein called CtrA that controls when polyps form. The new paper shows that many polyp-dependent phages have patterns in their DNA (called ‘binding sites’) where the CtrA protein can be cleaved.

Earl said it is unusual for a phage to have a binding site for a protein produced by its host.

Even more surprising, Earl and co-author Dr. Elijah Mascolo found, through detailed genomic analysis, that these binding sites are not unique to a single phage, or even a single group of phage.

Many different phage species contain CtrA binding sites – but all of them require their hosts to have bacterial hairs and/or flagella to infect them. They realized it couldn’t be a coincidence.

The ability to monitor CtrA levels “has been invented many times during the evolution of different phages that infect different bacteria,” Earl said. When distantly related species show a similar trait, this is called convergent evolution, which implies that the trait is definitely beneficial.

One example that scientists are focusing on involves a group of bacteria called Caulobacterales, a well-studied group of bacteria, because they exist in two forms: a free-floating “swarm ” form and a surface-attaching “stalker” form.

While ‘swarms’ have bristles/whips, the ‘follower’ form does not. In these bacteria, CtrA regulates the cell cycle by determining whether a cell will divide equally with two other cells of the same cell type or divide asymmetrically to form a “swarm” and a “stem” cells.

Since phages can only infect “swarm” cells, when there are many “swarm” cells to infect, it is in their interest to burst out of their host.

In general, Caulobacterales live in nutrient-poor environments and are relatively common. “But when they find a good microhabitat, they go on to the following cells and multiply,” said Earl, who later produced large amounts of swimming cells.

So, says Earl: “We hypothesize that phages monitor CtrA levels that rise and fall throughout the cells’ life cycle to detect when a swarm cell becomes a follower cell and becomes a swarm factory .” And at that point, the phages will explode the cell because there are swarms nearby to be infected.”

Unfortunately, the method of proving this hypothesis is very difficult and difficult, so it is not part of this final paper, but Earl and colleagues hope to address this question in the future.

However, the research team could see no other explanation for the duplication of CtrA binding sites in many different phages, all of which require bristles/flags to infect their hosts.

Even more interesting are the effects of viruses that infect other organisms, even humans.

And Earl explained that the main finding from this study is that “the virus uses cellular intelligence to make decisions,” and if it happens in bacteria, it almost certainly happens in plants and animals. , if this is a logical evolutionary approach. , evolution will discover it and use it.”

Professor Earl and colleagues concluded that these remarkable discoveries could open up new therapeutic avenues. “If you’re making an antiviral drug and you know the virus is listening for a certain signal, then maybe you can fool the virus,” he said.

Source: Science Daily

Source: Arabic RT

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