Researchers from the University of Leeds have found a new target for treating herpesvirus infections. By inhibiting the activity of a specific enzyme, the team was able to prevent herpesvirus replication. The treatment should work for all forms of herpesvirus. The details are in a paper that was just published in the journal Nature Microbiology.
The herpesviruses are a diverse family of DNA viruses that can infect most animals, including humans. They are responsible for everything from cold sores to genital herpes and over 90% of human adults have been infected at least once in their lifetime. All herpesviruses hijack a protein complex called human TREX when invading cells and replicating. This protein activity was the focus of the new study.
The research team found that an important component of the human TREX complex was an enzyme called UAP56. Scientists believed that inhibiting this enzyme would prevent herpesviruses from hijacking TREX pathways, slowing or completely stopping infections. The team collaborated with chemists to identify chemicals that would target UAP56.
Chemicals called small-molecule inhibitors were identified and tested. The researchers found that some of these compounds could inhibit UAP56 and halt viral replication while leaving cells undamaged. The team first tested their new method on a Kaposi’s sarcoma-associated herpesvirus but quickly found that the technique worked on other herpesviruses. This is because all viruses in the Herpesviridae family use similar methods when taking over cells and reproducing.
Herpesvirus infections range from mild to serious and affect hundreds of millions of people each year. As viruses become resistant to common medications, it becomes more necessary to develop alternative treatments. All viruses in the Herpesviridae family hijack a protein complex called human TREX; compounds that inhibit this activity show promise in the treatment of herpesvirus infections. Researchers have now identified possible targets and will be conducting further research to determine the best drug candidates.
Schumann et al. Targeting the ATP-dependent formation of herpesvirus ribonucleoprotein particle assembly as an antiviral approach. Nature Microbiology (2016).