New way to attack herpes virus discovered by scientists
Normally, when a virus enters your cell, that cell blocks the virus’s DNA and prevents it from performing any actions.
A team of scientists have uncovered the mechanism that allows the herpes virus to replicate. Their study could open new therapeutic avenues to treat not only cytomegalovirus but other viruses as well.
Human cytomegalovirus is a leading cause of birth defects and transplant failures. As it’s evolved over time, this virus from the herpes family has found a way to bypass the body’s defense mechanisms that usually guard against viral infections. Until now, scientists couldn’t understand how it manages to do so.
Normally, when a virus enters your cell, that cell blocks the virus’s DNA and prevents it from performing any actions. The virus must overcome this barrier to effectively multiply.
To get around this obstacle, cytomegalovirus doesn’t simply inject its own DNA into a human cell. Instead, it carries its viral DNA into the cell along with proteins called PP71. After entering the cell, it releases these PP71 proteins, which enables the viral DNA to replicate and the infection to spread.
The researchers found that, while PP71 is still present in the cell, it activates another protein known as IE1. This happens within the first few hours of the virus entering the cell, allowing the IE1 protein to take over after PP71 dies and continue creating a new virus.
To confirm their findings, the team created a synthetic version of the virus that allowed them to adjust the levels of the IE1 proteins using small molecules. With this technique, they could let the virus infect the cell while controlling how quickly the IE1 protein would break down in the cell.
The first author of the new study Noam Vardi said, “We noticed that when the IE1 protein degrades slowly, as it normally does, the virus can replicate very efficiently. But if the protein breaks down faster, the virus can’t multiply as well. So, we confirmed that the virus needs the IE1 protein to successfully replicate.”
This study could have broad implications for the scientific community, which has been struggling to determine how cells maintain their identity over time. During development, for instance, stem cells choose a path based on the proteins that surround them. But even after these initial proteins disappear, the specialized cells don’t change.
So, stem cells that turn into neurons during development continue to be neurons long after those proteins are gone. The new study could lead to a new therapeutic target to attack cytomegalovirus and other herpesviruses, such as Epstein-Barr virus that causes mononucleosis and herpes simplex virus 1 and 2 that produce most cold sores and genital herpes. The full findings are present in the journal- Proceedings of the National Academy of Sciences.
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