New research from University of Pittsburgh School of Medicine and La Jola Institute for Immunology, published today Nature microbiologyThe major infectious cause of birth defects in the United States reveals an opportunity to develop an therapy against Cytomegalovirus (CMV).

Researchers discovered an already unpounted mechanism, by which CMV, a herpes virus that infects most of the world’s adult population, enters cells that line blood vessels and contribute to vascular disease. In addition to using molecular machinery, which is shared by all herpes viruses, CMV appoints another molecular “key” that allows the virus to secretly sneak through a side door and avoid the body’s natural immune prevention.

The discovery may understand why there are efforts to develop anti -pathological remedies against CMV, so far, have been unsuccessful. This research also highlights a new potential avenue for the development of future antiviral drugs and suggests that other viruses of the herpes family, such as Epstein Bar and chicken pocksOne can use similar molecular structures to spread from one infected cell to another while avoiding immunity.

If we do not know which weapon the enemy is using, then it is difficult to protect against it. We found a missing puzzle piece that represents a possible cause that vaccination attempts against CMV have failed. ,

Jeremy Kamil, PhD, Senior Author, Associate Professor of Microbiology and Molecular Genetics in Pit

In the United States, almost a congenital CMV infection in every 200 infants. One of one of the infected infants will have to go for birth defects, such as hearing loss, or long -term health challenges. For most adults, CMV transitions are touching. But during pregnancy, a CMV infection offers significant health risks for the unborn child and can be fatal to those who are immunospressed, including the recipient of organ transplantation.

Due to the large size of its genome and its complex molecular machinery, CMV develops efforts to develop reluctant remedies for a long time. Similar to other herpes viruses, CMV depends on a protein that is said to enter the cells of the vessel lining called GH. But unlike other herpes viruses, which use a protein partner called GL to facilitate the infection, the new study found that CMV reverses GL with another partner called UL116 and recruits a protein called UL141. As a result of GH-Hul116-Hul141, complex, called gate by authors, then becomes an alternative tool for breaking blood vessels into lining cells and also prevents the body’s immune system from recognizing signs of infection.

The newly discovered gates can become a possible vaccine target for CMV and other herpes viruses.

“Previous attempts to generate a CMV vaccine have failed, but before we identify the gate complex. Erica Olmon Saifier, PhD, MBA.” If we can develop antiviral drugs or vaccines that disrupt CMV entry, it will allow us to fight children and to fight many diseases due to immune-surrendered people.

Other writers of this research are Michael Noris of the University of Toronto, PhD; Lauren Henderson, Mohammad Siddiqui, PhD, both Louisiana State University Health Shrewport; And Giyun Yin, PhD, Quangsun U, PhD, Simon Brunel, PhD, Michael Peacock, PhD, and Erica Olmann Saifier, PhD, all of all of La Jola Institute for Immunology.

The research was supported by the National Institute of Health (Grants AI11685, AI139749, AI101423 and T32hl155022222) and APECX Contract 1ay1AX0000555.