HSV is a somewhat obscure acronym for a very common virus. HSV is short for Herpes Simplex Virus, and it is one of the most prevalent diseases in America.  Roughly 80% of adults in the nation are estimated to have a form of HSV infection. In fact, you’re likely familiar with many of the members of the herpesvirus family, which encompasses Epstein Barr (which causes mononucleosis), Varicella Zoster (chicken pox), CMV (the most common cause for congenital birth defects in children).

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

Since HSV is so prevalent in the population, especially as the age of individuals increase, it is a great danger to the general immune system. Studies have shown the body devotes T cells (immune system agents) to the constant stalemate with HSV. Over time, researchers believe this essentially tires the immune system, and increases susceptibility to other infections.

Chris Benedict, Ph.D., has spent his career examining these viruses and trying to find ways to convert them and their methods into techniques that the body can use to increase and better direct its immune responses to outside agents. His recent research is focusing on how HSV binds itself to a substance known as HVEM, a cytokine-receptor (proteins used to signal other cells) in the human body that can either boost or suppress the immune response. HVEM can communicate with the cytokines LIGHT and BTLA, which have very different immune system roles. LIGHT will boost the response of the immune system, whereas BTLA suppresses it. The way HSV interacts with these items may be one very important key to discovering how it can remain, seemingly untouched, in the body.

Benedict’s work aims to discover not only how HSV harnesses these cytokines, but also to learn how these cytokines can be used to affect a broad array of  human diseases. Particularly, he is interested in harnessing the suppression caused by BTLA to dampen effects of inflammatory auto-immune conditions such as arthritis. HSV is a highly complex disease and working with mutated versions of the virus to study its changes in behavior is a difficult process, but one that the latest advances in technology is making this possible for researchers.