Herpes Simplex Virus Reactivated by Protein

Herpes simplex virus (HSV) infects an individual for their entire life, but likely remains dormant except for periodic reactivation.

The cycle of dormancy and reactivation has been poorly understood by researchers; however, the authors of a study published by Cell Host & Microbe discovered a set of protein complexes that could play a role in HSV.

The research team from the National Institutes of Health found that these proteins are recruited to viruses, and produce initial infection and reactivation. Environmental stresses also play a role in regulating the proteins and reactivating infection, which may explain why stress may trigger reactivation in some individuals.

The World Health Organization estimates that more than 500 million individuals have been infected with HSV-2, while two-thirds of the global population has been infected by HSV-1. These infections range in symptoms from lesions on various parts of the body to eye conditions that can lead to blindness, according to the study.

Individuals infected with HSV have also been observed to have a higher risk of acquiring and transmitting HIV. Among infants, HSV can result in neurological and developmental issues.

Other studies show that children diagnosed with acute lymphoblastic leukemia were found to be more than 3 times as likely to have had a cytomegalovirus infection—a member of the herpes virus family—at birth compared with children who do not develop the cancer.

Despite lifelong infection and potential complications, there are no preventative or curative treatments for HSV due to a lack of understanding of the virus.

In a previous study, the authors made progress towards understanding how the HCF-1 protein can initiate and reactivate an HSV infection. HCF-1 and associated proteins are recruited to the viral genome to facilitate viral replication and spread. These findings lay the groundwork for the creation of novel drugs to prevent infection and reinfection of HSV.

In the new study, the authors discovered that HCF-1 protein complexes may play an additional role in HSV. They found that compounds that turn on components of HCF-1 protein complexes could reactivate latent HSV in mice.

The authors noted that these findings were especially interesting, since some HCF-1 associated proteins were also involved with HIV reactivation, according to the study.

Much like HSV, HIV infections can remain dormant for many years but reactivate. This suggests that both infections may involve similar pathways.

The authors plan to continue their study into protein complexes that are involved with gene expression, infection, and reactivation of HSV to better understand the mechanisms of the infection. New information about the involved complexes and how they function may lead to additional treatment targets for HSV, the study concluded.