Scientists have revealed a herpes infection plan for humans: it looks like a game with bets

Cytomegalovirus is a common virus in the same family as herpes simplex, chickenpox and

mononucleosis.More than half of all people will become infected with cytomegalovirus during their lifetime. Once infection occurs, the virus often goes into a dormant state, leaving the person infected for life. However, in some cases the virus breaks dormancy; for example, in children and in transplant recipients. This not only leads to serious health problems, but can also result in death. Indeed, cytomegalovirus is a leading cause of birth defects in children and a leading cause of graft failure after transplantation.

In a new study, scientists describe in detailhow cytomegalovirus goes into a dormant state: changing the levels of certain proteins in its viral particles. This gives some of them a greater ability to cause disease, and others - a tendency to a latent state. This is the viral version of the “safe bet” that allows the virus to persist throughout the patient’s life.

Cytomegalovirus is a devastating diseasecausing serious birth defects. We now have a new understanding of how the virus establishes latency, which we believe will help pave the way for new treatments.

Laure Weinberger, first author of the study and director of the Gladstone Institutes' Center for Cellular Circuitry

Under a microscope, scientists noticed that somecytomegalovirus particles have a very high level of pp71 protein, while others do not. Protein pp71 is involved in the replication of viral DNA, and also helps the virus evade the immune response of the human body. However, the researchers wondered why some particles contain much more protein than others.

Some particles had 40 times more protein. Other viral proteins changed the concentration only twice between the individual particles of cytomegalovirus. Scientists then discovered that particles with more pp71 protein were more contagious and reproduce more of their DNA than particles with less pp71.

When pp71 protein was present at higherlevels, the virus had an advantage and could undergo faster replication. But the discovery posed an interesting question: if high protein levels provide an evolutionary advantage for the virus by enhancing replication, why does the virus still create some particles with relatively few pp71?

Scientists have suggested that particles are lowpp71 must also have an evolutionary advantage in various conditions. And, indeed, the researchers found that a low level of pp71 was needed by the virus to establish latency.

A better understanding of how virusesestablish latency could help researchers develop more effective treatments that eliminate not only all the active virus in someone's body, but also hidden copies of it.

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