By AMERICAN HEART ASSOCIATION NEWS
There’s a common and potentially deadly virus that can make stealthy adjustments to better infect different types of cells. It’s called the human cytomegalovirus, or CMV, and researchers have now discovered an important clue to how it adapts in order to move through the body — a finding that could aid in the creation of a vaccine against it.
“What’s really cool about the findings is that they provide insight into something very basic and fundamental about how this virus goes about its business of infecting humans,” said Jeremy Kamil, Ph.D., senior author of the study, published recently in the Proceedings of the National Academy of Sciences. “This kind of knowledge provides an invaluable foothold that can be used to develop new therapies.”
The virus can be lethal to heart transplant patients, unborn babies and others with weakened immune systems.
Researchers at Louisiana State University Health Sciences Center in Shreveport discovered that a protein called UL148 helps control two “keys” on the virus’ surface that allow it to enter and infect cells. Scientists from the University of Alabama at Birmingham and the University of Montana contributed to the research.
CMV is a type of herpes virus. Infectious mononucleosis, herpes simplex, chickenpox and shingles are also members of the herpes virus family. Like these other herpes infections, CMV stays in the body for life.
About 80 percent of people age 40 and older have CMV, said Kamil, an assistant professor of microbiology at LSU Health Sciences Center. The virus typically remains dormant in healthy people and does not require treatment, he said.
Yet the virus is a strong opponent, even in healthy people, Kamil said. “A huge component of your immune system is directed against this virus,” he said.
For people whose immune systems are weakened — for example, organ transplant recipients taking medicine to prevent organ rejection — CMV is a more serious concern.
“Heart transplant patients get hammered by it,” said Kamil.
Active infections occur in one out of four heart transplant patients, who are twice as likely to die within five years if they have CMV, according to researchers.
CMV is also the most common viral infection at birth, affecting about 30,000 newborns in the U.S. each year, according to the Centers for Disease Control and Prevention. More than 5,000 American children each year suffer permanent problems caused by CMV, including mild hearing loss, impaired vision, developmental disabilities and, in rare cases, death, according to the CDC.
Kamil noted that the discovery of the UL148 protein may also give scientists insights into how the virus makes the necessary adjustments to move through the body and infect different types of cells.
“Heart transplant patients could benefit from therapies that prevent the virus from infecting the full range of cell types,” Kamil said. “These would be based on vaccines, antibody infusions or other novel interventions that block viral entry or prevent infected cells from spreading the virus further.”