Herpes viruses steal a cell's protein and use it to infect another cell

Without stealing the protein, the virus cannot reach the nucleus of neurons.

One of the distinguishing characteristics of viruses is that they depend on host proteins to reproduce. The host cell often transcribes viral genes into RNAs and then translates these genes into proteins, for example. An adult virus that is ready to spread to another cell usually contains slightly more viral proteins, virus genetic material, and possibly part of the host membrane. You don't need anything else. All the proteins you need to multiply more must be present in the next cell they infect.

But some data released this week may have found an exception to this pattern. Members of the herpes virus family appear to attach to the protein in the first cell they are infected and then carry the protein with them to the next cell. This behavior may be beneficial due to the natural targets of herpes viruses - neurons that have an unusual cellular structure. By infecting cells that are exposed to the environment. But from there they go to the neurons, where they settle and remain there even when there is no visible sign of injury. These infected cells then act as a springboard for replication of active infection, causing lifelong problems for any unlucky person who becomes infected.

To cause this latent infection, the herpes virus must take up residence. In the cell nucleus, this can be far from the site of the injury, because neurons can send out long extensions called axons that allow them to communicate in different parts of the body. The longest of these axons can be more than a meter, so if the virus enters a neuron at the end of the axon, it must travel a long distance to reach the nucleus. The proteins form long fibers that run along the axon. Other proteins (called motors) can attach to these fibers and pass the axon up or down and carry the load into motion.

Herpes viruses have evolved to use this system. The virus encodes a protein embedded in its envelope and has the ability to bind to one of the motors. So when it hits a neuron, it can be carried down the axon, just as if it were just another charge. As a result, the cell does much of the work required to locate the virus.


They were. In the protein that the virus uses to ride motor proteins. Previous work had shown that the protein could bind to two different types of actuators (dyneine and quinine, for whom think those things), and the researchers were interested in seeing how the protein interacted with quinine. So they discovered where this interaction occurs in a viral protein.

By switching to the viral gene that encodes this protein, they made mutations that destroyed its ability to absorb quinine. Viruses that carry these mutations are unable to spread after infecting another cell. This came as a bit of a surprise, given that they still needed to be able to bind to the second motor protein.

To better understand what was going on, the researchers grew the virus in neurons. which lacks Keynesianism. Perhaps due to interaction with another motor, the virus easily moved down the axon. But upon entering the cell body, the virus accumulated close to the nucleus but could not enter it effectively. But there is a big difference between the low efficiency seen in this experiment. Complete absence of infection when the protein is mutated. Explain the difference: the virus actually transmits kinase from the first cell it infects.

It was very difficult to detect, but researchers eventually came up with a way. They named kinsine an enzyme that changes the color of a chemical. They then showed that virus-infected cells also changed color, indicating that the virus could carry the labeled quinine into the cells.


Putting it all together shows. The virus appears to have hijacked the host's transmission system in two ways. One of its proteins could bind to a motor that lowers the virus from the axons of the nervous system and brings it closer to the nucleus. The same protein takes the second motor and introduces it into the cell. This engine allows the virus to move from "near the nucleus" to "inside it".

Since neurons also have their own kinesin, it is not clear why this is needed. - Something the authors themselves said. Diagnose and possibly work on it. But the bigger question is, are viruses that carry host proteins more common than previously thought? Given how difficult this process is to detect in the herpes virus, this may be the case in other well-studied viruses, but we've lost it so far Nature, 2021. DOI. : 10.1038/s41586-021-04106-w (about DOI).

Herpes viruses steal a cell's protein and use it to infect another cell
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