HSV-1 BRAIN INFECTION BY THE OLFACTORY NERVE ROUTE AND VIRUS LATENCY AND REACTIVATION MAY CAUSE LEARNING AND BEHAVIORAL DEFICIENCIES AND VIOLENCE IN CHILDREN AND ADULTS - A POINT-OF-VIEW

Two recent studies provided new evidence on the latency of HSV-1 DNA i n 15.5% of olfactory bulbs and in 72.5% of trigeminal nerves from huma n corpses at forensic postmortems (I) and in 35% of 40 autopsied human brains (2). In the latter brains, latent HSV-1 DNA was found in the o lfactory bulbs, amygdala, hippocampus, brain stem, and trigeminal gang lia. Although in these studies it is not known by which route HSV-1 en tered the olfactory bulbs and brain, experimental studies in mice (3) revealed that injection of HSV-1 into the olfactory bulbs leads to vir us migration into the brain amygdala and hippocampus via the olfactory nerve and locus coeruleus. If the olfactory ciliary nerve epithelium is the port of entry of HSV-1 into the olfactory bulbs and brain in hu mans as well, protection of the nose against HSV-I infection may be ne eded to prevent virus latency in neurons in the amygdala and hippocamp us (3). Infection of humans by HSV-1 was estimated to increase from 18 .2% in the 0-20 year population group to 100% in persons older than 60 years (1), indicating that worldwide human populations at all ages ar e at risk of brain infection by the olfactory nerve route. In addition , both primary infection and reactivation of latent DNA in the brain m ay lead to damage of neurons in the brain involved in memory, learning , and behavior, as observed in infected, acyclovir-treated mice (3). T he current introduction of a live apathogenic varicella-zoster virus ( VZV) vaccine to immunize children against chickenpox (4) may suggest t hat the time is ripe for immunization of children and adults against H SV-I infections, especially infections by the olfactory nerve route, t o prevent potential brain damage.