Researchers have found that apoptosis, a natural process of programmed cell death, can reactivate latent herpesviruses in the dying cell. The results of their research, which could have broad clinical significance since many cancer chemotherapies cause apoptosis, was published ahead of print in the Journal of Virology.
Human herpesviruses (HHV) are linked to a range of childhood and adult diseases, including chickenpox, mononucleosis, cold sores, and genital sores, and are of a particular concern for patients who are immunosuppressed due cancer or AIDS. Some HHV types are so common they are nearly universal in humans. A key feature of these viruses is their ability to remain latent for long periods of time, and then reactivate after the latent phase. Previously, reactivation was thought to be primarily due to waning immunity, immunosuppression, or exposure to certain inducing agents.
This study began when principal investigator Steven Zeichner of Children's National Medical Center and George Washington University in Washington, DC, followed up earlier findings that high concentrations of the antibiotic doxycycline can induce apoptosis, and can also activate replication by the Kaposi's Sarcoma-associated Herpesvirus (KSHV), and a study by his former mentor, Bernard Roizman of the University of Chicago, which showed that apoptosis also triggers replication of herpes simplex virus-1, which causes cold sores in the mouth.
"We decided to test- several additional human herpesviruses that cause notable diseases and which have good latent infection cell line models, including human herpesviruses (HHV)-6A, =6B, and -7, and Epstein-Bar virus (EBV)," says Zeichner. That all of these herpesviruses were activated by apoptosis suggested that this mechanism might apply to all herpesviruses.