CMV RESEARCH
cell-bullet1.jpgThe herpesvirus family of viruses is, to say the least, a stealthy group. It’s an odd statement to make of a group that contains Cytomegalovirus (CMV). CMV is recorded as being present in nearly 60% of the population of the United States aged six and up and in over 90% of adults over the age of 80. Due to the common nature of the virus, you likely have heard of or had a herpesvirus in your lifetime.    The family of viruses encompasses Epstein Barr (which causes mononucleosis), Varicella Zoster (chicken pox), herpes simplex (most commonly, cold sores) and CMV (the most common viral cause for congenital birth defects in children).

These viruses have garnered their reputation for stealth due to the way they have evolved over millions of years to live in balance with the body’s immune response. Herpesviruses manage to thwart both innate (general) and adaptive (disease-specific) immunities in the human body. The manner in which they do so is largely a mystery, but also holds great potential to instruct researchers on ways to signal the human body into performing necessary tasks.

Since CMV is so prevalent in the population, especially as the age of individuals increase, it is potentially a great danger to the general immune system. Studies have shown that as much as 30% of the body’s T cells (immune system agents) can be devoted to maintaining the constant stalemate with CMV. Over time, researchers believe this may “tire” the immune system, and increase susceptibility to other infections.

Chris Benedict, Ph.D., has spent his career examining these viruses, uncovering their strategies to try and find ways to convert them into techniques that the body can use to increase and better direct its immune responses to fight disease. One topic of his recent research is focusing on how CMV makes use of a specific cytokine receptor (a protein used to signal other cells) called UL144. UL144 is a clever product of CMV: it mimics the behavior of a molecule known as HVEM, a receptor in the human body that can either boost or suppress the immune response. UL144, however, only suppresses, and is used by CMV to dampen the body’s response to its presence.

Benedict’s work aims both to determine how UL144 contributes to CMVs ability to exist peacefully in the human body, and also to discover more far-reaching uses for UL144. If UL144’s suppression characteristics can be harnessed, it could be used to target unwanted immune responses from the body, and Benedict’s lab is testing this in inflammation models, such as arthritis.

Benedict’s goal for the future is to one day utilize information gained from studying viral proteins such as UL144, molecules that have evolved over millions of years and potentially more effective than anything science can create on its own, to develop new therapies to more efficiently battle human disease.  Additionally, his research should help to unlock the key of the latent nature of herpesvirus infection in the human body.
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