The joint La Jolla Institute for Immunology study has discovered how certain herpes viruses evade immune system detection.
New research from the University of Pittsburgh School of Medicine and La Jolla Institute for Immunology, published June 30 in Nature Microbiology, may lead to development of a therapy against cytomegalovirus (CMV), the leading infectious cause of birth defects in the US.
Researchers discovered a mechanism by which CMV, a herpes virus that infects the majority of the world’s adult population, enters cells in blood vessels and contributes to vascular disease.
CMV uses molecular machinery common to all herpes viruses, but the new study found CMV also employs another molecular “key,” allowing the virus to “sneak in” and bypass the body’s natural immune defenses.
The finding highlights new potential for the development of future antiviral drugs and suggests that other viruses of the herpes family, such as Epstein-Barr and chickenpox, could use similar molecular structures to spread from one infected cell to the next while avoiding immune detection.
In the US, approximately one in every 200 babies is born with congenital CMV infection. Of the babies infected, one in five will have birth defects, such as hearing loss, or go on to have long-term health challenges.
For most adults, CMV infections are asymptomatic. But a CMV infection during pregnancy means significant health risks for the developing child and could be deadly for people who are immunosuppressed.
CMV uses a protein called gH to enter cells. But unlike other herpes viruses, the new study found, CMV replaces a protein partner called gL with another partner called UL116 and recruits a protein called UL141 to facilitate infection.
This complex of gH-UL116-UL141, called GATE by the researchers, becomes an alternative tool for breaking into cells lining the blood vessels and causing internal damage while simultaneously preventing the body’s own immune system from recognizing the signs of infection.
The newly-discovered GATE could become a potential vaccine target for CMV and other herpes viruses.
“Previous attempts to generate a CMV vaccine have failed, but that was before we identified the GATE complex,” LJI associate professor and co-senior author of the study Chris Benedict said in a press release.
“We hope that new strategies targeting GATE will improve our chances to combat CMV infection, and also perhaps cleanse our bodies of this lifelong infection.”
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