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Uncovering CMV’s Secret Weapon: A Breakthrough in Developing Therapy Against a Leading Cause of Birth Defects

Scientists have discovered a stealthy mechanism that cytomegalovirus (CMV)—the leading infectious cause of birth defects in the U.S.—uses to infiltrate blood vessel cells while evading immune detection. The virus forms a hidden protein complex that acts like a molecular “backdoor,” allowing it to bypass the immune system’s defenses. This newly identified pathway may explain why vaccine efforts have failed for decades and opens the door to targeted therapies that could finally prevent CMV-linked birth defects in newborns and protect vulnerable patients.
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New research from the University of Pittsburgh School of Medicine and La Jolla Institute for Immunology has made a groundbreaking discovery in understanding the mechanism by which cytomegalovirus (CMV), a herpes virus that infects millions worldwide, enters cells lining the blood vessels and contributes to vascular disease.

The study, published in Nature Microbiology, reveals that CMV employs an alternative molecular “key” called GATE (gH-UL116-UL141 complex) to sneak through a side door and evade the body’s natural immune defenses. This finding may explain why efforts to develop prophylactic treatments against CMV have been unsuccessful.

In the United States, approximately one in every 200 babies is born with congenital CMV infection, which can result in birth defects such as hearing loss or long-term health challenges. For most adults, CMV infections are asymptomatic, but a CMV infection during pregnancy presents significant health risks to the unborn child and could be deadly for people who are immunosuppressed.

The researchers suggest that targeting the GATE complex could become a potential vaccine target for CMV and other herpes viruses, which have also been linked to various diseases. This breakthrough has far-reaching implications for developing antiviral drugs and vaccines to combat CMV infection and its consequences.

“If we don’t know what weapons the enemy is using, it’s hard to protect against it,” said senior author Jeremy Kamil, Ph.D., associate professor of microbiology and molecular genetics at Pitt. “We found a missing puzzle piece that represents one possible reason why immunization efforts against CMV have been unsuccessful.”

The research was supported by the National Institutes of Health and ARPA-H APECx contract. Other authors of this study include researchers from the University of Toronto, Louisiana State University Health Shreveport, and La Jolla Institute for Immunology.

This discovery has the potential to revolutionize our understanding of CMV infection and its impact on human health, leading to the development of more effective treatments and a better chance at combating this widespread virus.

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