The Herpes Virus Manipulates Our DNA To Replicate: What Those Infected Can Do About It
The herpes simplex virus (HSV) causes what we know as genital herpes, a sexually transmitted disease the Centers for Disease Control and Prevention (CDC) reported affects 776,000 new Americans each year. But how exactly does the virus work? A new study from The Wilstar Institute in Philadelphia published ahead of print in the journal Cell Reports sheds some light.
First, some background: There are two types of HSV, type 1 and type 2. The primary difference between the two has to do with where the virus lies dormant in the body. This is also known as a “site of preference.” HSV-1 prefers a group of nerve cells near the ear, recurring on the lower lip or face. And HSV-2, which is more common in woman than men, prefers the base of the spine, thus recurring in the genital area. The focus of the present study was HSV-1.
Turns out, HSV-1 rearranges telomeres, the small, protective ends of chromosomes. In fact, experts often compare telomeres to the clear tips of shoelaces because they prevent chromosomes from fraying and breaking, preserving their ability to pass on genetic information. When the virus inhibits and manipulates a telomere protein called TPP1, it results in the loss of the telomere repeat DNA signal and makes it more efficient for HSV-1 to replicate. This suggests TPP1 normally provides some sort of protective function against this virus.
"This study expands our knowledge of telomeres further in two very important ways. First, it gives us an indication that some viruses are able to manipulate telomeres specifically in order to replicate, said Dr. Paul Lieberman, of The Wilstar Institute, in a press release. “Second, it appears that proteins like TPP1 provide very specific protective functions. These findings allow us to ask additional questions and better understand just how telomeres may protect cells from viral infection."
HSV-1 often causes cold sores, but the CDC reported it could also cause serious conditions such as blindness, encephalitis (inflammation of the brain), and aseptic meningitis (inflammation of the linings of the brain). There’s currently no vaccine to prevent infection and reactivation, only a few effective treatments.
While more research will need to be done to determine how to protect against this manipulation — perhaps in the form of new medication or therapy — prior research suggests the length of telomeres can generally increase a person’s risk for disease. One study published in the Journal of the American Medical Association found a shorter telomere length made people more susceptible to rhinovirus or the common cold. "Our work suggests the possibility that telomere length is a relatively consistent marker across the life span and that it can start predicting disease susceptibility in young adulthood," said Sheldon Cohen, lead study author, said in a statement.
And as far as the length of our telomeres, some studies suggest a healthy lifestyle can stimulate growth. This includes a healthy diet, moderate exercise, and yoga and meditation for reduced stress.
Source: Zhong Deng, et al. HSV-1 Remodels Host Telomeres to Facilitate Viral Replication. Cell Reports. 2014.