AGE DISTRIBUTION OF LATENT HERPES-SIMPLEX VIRUS-1 AND VARICELLA-ZOSTER VIRUS GENOME IN HUMAN NERVOUS-TISSUE

Latency in nervous tissue caused by herpes simplex virus 1 (HSV-1) and by varicella-zoster virus (VZV) is an intriguing feature of herpes-vi rus' neurotropism. HSV-1 and VZV latency are the causes of ophthalmic zoster and recurrent HSV infections in the distributions of the trigem inal branches. HSV-1 neuronal latency may play a role in the etiopatho genesis of HSV encephalitis. We attempted to determine the prevalence and age distribution of VZV and HSV latency. We applied nested polymer ase chain reaction (PCR) assays to detect HSV-1 and VZV genome in trig eminal ganglia and olfactory bulbs which were obtained from 109 human corpses at forensic postmortems. HSV-1 latency was found in 72.5% of t rigeminal ganglia and in 15.5% of olfactory bulbs. VZV latency was 63. 3% in trigeminal ganglia and 1% in olfactory bulbs. Simultaneous laten cy of VZV and HSV genome occurs in 48.8% of trigeminal ganglia. The ag e-group specific prevalence of HSV neuronal latency increases from 18. 2% in 0-20 years to reach finally 100% in persons older than 60 years. Age specific prevalences of VZV peaked for a first time with 82% betw een 21-30 years, fell to 50% for 40-50 years, and rose to 89% for 71-8 0 years. If the latent trigeminal ganglion HSV-1 genome were the sourc e of endogenously acquired encephalitis, the peak incidence of HSV enc ephalitis in older subjects correlates with our findings. Increased VZ V latency prevalence in nervous tissue of younger people without subse quent disease indicates sufficient immune surveillance.