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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 guards against viral infections.
A team of scientists led by Leor S. Weinberger, PhD, the William and Ute Bowes Distinguished Professor and director of the Gladstone-UCSF Center for Cell Circuitry, uncovered the mechanism that allows the virus to replicate. When a virus enters 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 PP71 proteins are needed for the virus to replicate. But they actually die after a few hours, while it takes days to create new virus. 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 new virus.
Researchers 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. They noticed that when the IE1 protein degrades slowly, as it normally does, the virus can replicate very efficiently. If the protein breaks down faster, the virus can’t multiply as well, the virus needs the IE1 protein to successfully replicate.