Abstract
Reactivation of herpes simplex virus (HSV) is a leading cause of fatal encephalitis in the USA and recurrent herpetic keratitis is a major infectious cause of blindness. There is no effective vaccine and no cure for HSV latency. While current antiviral drugs reduce viral replication, none prevent the initiation of reactivation in the nervous system and, thus, chronic inflammatory damage proceeds. The discovery that HSV VP16 is necessary for the exit from latency represents the first potential target for preventing the chronic inflammatory insult associated with HSV reactivation. Blocking VP16 transactivation would reduce the spread of the virus in the population and, importantly, presumably reduce or prevent the pathological long term chronic inflammation in the nervous system.
Financial & competing interests disclosure
The authors are supported by NIH ROI AI32121 and ROI EY13168. The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.