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Title
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.
AuthorBecker Y
AddressDepartment of Molecular Virology, Faculty of Medicine, Hebrew University of Jerusalem, Israel.
Source
Virus Genes,
10:
3, 1995,
217-26
AbstractTwo recent studies provided new evidence on the latency of HSV-1 DNA in 15.5% of olfactory bulbs and
in 72.5% of trigeminal nerves from human corpses at forensic postmortems (1) and in 35% of 40 autopsied
human brains (2). In the latter brains, latent HSV-1 DNA was found in the olfactory bulbs, amygdala,
hippocampus, brain stem, and trigeminal ganglia. Although in these studies it is not known by which route
HSV-1 entered the olfactory bulbs and brain, experimental studies in mice (3) revealed that injection
of HSV-1 into the olfactory bulbs leads to virus 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 humans as well, protection of the nose against HSV-1 infection
may be needed to prevent virus latency in neurons in the amygdala and hippocampus (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 are at risk of brain infection
by the olfactory nerve route. In addition, both primary infection and reactivation of latent DNA in the
brain may lead to damage of neurons in the brain involved in memory, learning, and behavior, as observed
in infected, acyclovir-treated mice (3). The current introduction of a live apathogenic varicella-zoster
virus (VZV) vaccine to immunize children against chickenpox (4) may suggest that the time is ripe for
immunization of children and adults against HSV-1 infections, especially infections by the olfactory
nerve route, to prevent potential brain damage.