Herpes simplex
© WikimediaHerpes simplex lesion of lower lip, second day after onset.
Helsinki - Once someone has contracted herpes the virus can emerge again at any time. The re-emergence is linked with periods of stress. Scientists have been looking into how this happens.

The first finding relates to how herpes establishes a life-long association with an infected person. Here the DNA genome of the virus hides within the nucleus of human infected cells.

The second finding relates to how stress triggers a reactivation of the virus. This is connected to human cellular stress responses. For the study, University of Helsinki researchers looked at Kaposi's sarcoma associated herpes virus.

Kaposi's sarcoma associated herpes virus causes Kaposi's sarcoma (an aggressive form of lymphoma), a cancer commonly occurring in AIDS patients. Due to its cancer association, the virus is classified as an oncovirus ,a group that includes both RNA and DNA-based viruses.

There are seven known oncoviruses that can cause cancer in humans. Other examples include human papilloma virus and Epstein-Barr virus.

The study into the virus reactivation mechanism used advanced microscopy technologies and genetic manipulation techniques. The findings revealed that several chemical stresses trigger the activation several cellular "stress-sensors" proteins. These proteins include p53 and p21clip.

The activation of the proteins creates an environment that favors the production of viral lytic genes, which lead to massive damage of cellular DNA and halt cell division. In essence, the virus takes over the human cell and directs all cellular nutrients towards creating new virus particles.

The new finding draws a direct connection between the cell stress response and virus reactivation. Now discovered, this is seen as a straightforward biochemical process. It is hoped that the discovery will lead to a new generation of anti-viral drugs. This is an important research area, given the risk of cancer development.

The research findings are published in the journal PLOS Pathogens. The paper is titled "Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication."