Herpesviruses steal one cell’s protein, use it to infect anothervar abtest_1814480 = new ABTest(1814480, ‘click’);

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One of the defining characteristics of viruses is that they rely on host proteins to reproduce. A host cell will often copy viral genes into RNA and then translate those RNAs into proteins, for example. Typically, a mature virus that is ready to spread to another cell contains little more than viral proteins, the genetic material of the virus, and perhaps some membrane of the host. It doesn’t need any more; All the proteins needed for it to reproduce further must be present in the next cell it infects.

But there may be an exception to this pattern in some of the figures released this week. Members of the herpesvirus family capture a protein in the first cell they infect and then carry this protein with them to the next cell. This behavior may be helpful because of the common targets of herpesviruses—neurons that have very unusual cell structures.

a long way to the nucleus


Like other viruses, herpesviruses begin by infecting cells exposed to the environment. But from there, they move on to the nerve cells where they reside, even when there are no obvious signs of infection. These infected cells serve as a launching point for re-establishing active infections, causing life-long problems for anyone unfortunate enough to become infected.

To establish this type of latent infection, the herpesvirus has to reside in the nucleus of the cell. And it can be a long way from the site of infection, as nerve cells can send out long extensions called axons that allow them to communicate to different areas of the body. The longest of these axons can exceed a meter, so if the virus enters the neuron at the far end of the axon, it has to travel a long way to reach the nucleus.

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Of course, the cell itself has to move things down these long axons, so it has a system in place to manage it. Proteins form long filaments that run the length of the axon; Other proteins (called motors) can attach to these fibers and move up or down the axon, carrying cargo as they go.

Herpes viruses have evolved to take advantage of this mechanism. The virus encodes a protein that is incorporated into its shell, and it has the ability to latch onto a single motor. So once it innervates the nerve cell, it can be carried down the length of the axon as if it were just another piece of cargo. As a result, the cell performs most of the functions required for the virus to reside.

a roadblock

In the new study, a group of US-based researchers was looking at the protein the virus uses to ride on a motor protein. Previous work had shown that proteins could latch onto two different types of motors (dynein and kinesin, for those of you on these things), and researchers were interested in seeing how the protein interacted with kinesin. interacts. So they found out where the interactions took place in the viral proteins.

Turning to the viral gene that encoded this protein, they carried a mutation that lost its ability to capture kinesin. Viruses carrying these mutations were no longer able to spread once the cell was infected. This was little surprise, given that they should still be able to capture the second motor protein.

To get a better understanding of what was happening, the researchers grew the virus in nerve cells that lacked kinesin. The virus easily moved down the axon, possibly because of its interaction with other motors. But once it entered the body of the cell, the virus accumulated near the nucleus, but was not able to enter it efficiently.

But there is a big difference between the low efficiency observed in this experiment and the complete absence of transfection when the protein is mutated. Explanation for this difference: The virus actually carries kinesin with it from the first cell it infects.

It was very hard to figure out, but researchers eventually found a way. They tagged kinesin with an enzyme that would cause a chemical to change color. They then showed that the virus-infected cells also changed color, indicating that the virus could carry the tagged kinesin into the cells.


Combining all this, it appears that the virus hijacks the host’s transport system in two ways. One of its own proteins can bind to the motor that drives the virus down the axon of the nervous system and carries it to the nucleus. The same protein also captures another motor and brings it with it to the cell. This allows the motor virus to transition from “near the nucleus” to “inside it”.

Given that nerve cells also have their own kinesin, it’s unclear why it’s needed—something the authors identify themselves and are probably working on. But the bigger question is whether viruses carrying host proteins around are more common than we thought. Given how difficult it was to detect this process at work in herpesvirus, it is possible that it also occurs in other well-studied viruses, but we have so far missed it.

Nature, 2021. DOI: 10.1038/S41586-021-04106-W (About DOI).

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