Sunday, December 14, 2014
How Herpes Virus Alters Our DNA
A new study has revealed one of the mechanisms Herpes Simplex Virus I (HSV-1) uses to replicate effectively in a host cell. As a reminder, HSV is a widespread virus in the U.S., which is known to cause cold sores. A latent infection, HSV remains in the body (residing in nerve cells near the ear, lower lip, or face) even after symptoms subside, and symptoms may reemerge periodically.
The study found that HSV-1 is able to interfere in telomere functioning. Telomeres flank the ends of chromosomes and consist of repeated DNA units that prevent a chromosome from damage during mitosis, since replication normally results in the loss of a few nucleotides on the ends of a chromosome. HSV-1 specifically inhibits and alters TPP1, resulting in a loss of one of these repeating units. This inhibition increases the effectiveness of HSV-1 replication.
The implications of this study are that telomeres can be targets that viruses use to more effectively replicate, and that telomere proteins such as TPP1 can have a protective effect during viral infection. Combined with the fact that telomere length has already been implicated in disease risk, this study raises the possibility that novel drugs or treatments that preserve telomere length during viral infection may hamper the ability of a virus to replicate.