Age distribution of latent herpes simplex virus 1 and varicella-zoster virus genome in human nervous tissue

Abstract

Latency in nervous tissue caused by herpes simplex virus 1 (HSV-1) and by varicella-zoster virus (VZV) is an intriguing feature of herpes-virus' neurotropism. HSV-1 and VZV latency are the causes of ophthalmic zoster and recurrent HSV infections in the distributions of the trigeminal branches. HSV-1 neuronal latency may play a role in the etiopathogenesis of HSV encephalitis. We attempted to determine the prevalence and age distribution of VZV and HSV latency. We applied nested polymerase chain reaction (PCR) assays to detect HSV-1 and VZV genome in trigeminal ganglia and olfactory bulbs which were obtained from 109 human corpses at forensic postmortems. HSV-1 latency was found in 72.5% of trigeminal ganglia and in 15.5% of olfactory bulbs. VZV latency was 63.3% in trigeminal ganglia and 1% in olfactory bulbs. Simultaneous latency of VZV and HSV genome occurs in 48.8% of trigeminal ganglia. The age-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% between 21–30 years, fell to 50% for 40–50 years, and rose to 89% for 71–80 years. If the latent trigeminal ganglion HSV-1 genome were the source of endogenously acquired encephalitis, the peak incidence of HSV encephalitis in older subjects correlates with our findings. Increased VZV latency prevalence in nervous tissue of younger people without subsequent disease indicates sufficient immune surveillance.