.....herpes & autism.....
An association between herpes simplex virus (HSV) and autism has long been
known (eg, 1). Writing in 1981, DeLong and colleagues could identify
elevated "serum herpes simplex titers" and found similar phenotype in two
other patients in whom elevated titers were not found (1), but newer
techniques are increasing the rates at which HSV sequences are being found
in temporal lobe tissues (2-3), ie locales likely to be substrates for
various aspects of autism.
.....the good old days.....
In 1995, a pathology article described tissue samples from herpes-related
encephalitis, and the authors wrote: "Although a viral etiology has long
been considered, to date there has been no successful isolation of viruses
from the brain samples of patients with epilepsy and chronic
An interesting contrast to that "old" 1995 article describes findings of
far more HSV signs in tissues from epileptic foci. Among tissues taken
from temporal lobes of persons with monofocal epilepsy, "Twenty (40%) of
the 50 epilepsy cases and 2 (4%) of the 48 control cases had at least one
sample that tested positive for HSV (P<.001). Sixty-seven percent (8 or
12) of the epilepsy cases with heterotopia were positive for HSV." (3)
.....questions & possibilities.....
In immunocompetent kids with focal CNS herpes simplex colonizations that
originated early in life, might some brain areas related to autism-
spectrum traits have become sufficiently damaged so as to have led to
permanent traits, with or without residual seizures? Might some such kids
have worsening of symptoms during periods of immunosuppression (eg, during
a time of extreme stress and related adrenal activation), ie, a time
during which the herpes virus might temporarily re-activate?
Herpes simplex virus in humans has long been known to prefer temporal lobe
and limbic sites; and not only are olfactory nerves a possible route for
infection, but so too might oral cavities provide entry: "Innoculation of
murine tooth pulp with HSV selectively infected the mandibular division
of the trigeminal nerve and caused encephalitis predominantly affecting
the temporal cortex and limbic system, a pattern of disease similar to
human HSE [herpes simplex encephalitis]..." (4)
Furthermore, "In the study by Baringer and Pisani..., HSV genomic material
was detected by PCR in the trigeminal ganglia of 65% of a group of 40
postmortem specimens... HSV genomic sequences could also be detected in
cerebral tissue of 35%, including medulla, olfactory bulbs, pons, gyrus
rectus, amygdala, and hippocampus... The finding that in one third of
cases of recurrent HSV encephalitis the virus isolated from the pharynx is
different from that in the CNS supports the theory of reactivation of
latent HSV from within the CNS..." And, the range of herpes phenotypes can
range from mild to severe. (4)
How small can an HSV-lesion temporal-lobe be? Might such a lesion occur
early in life in language areas and/or in memory areas and/or in areas
dedicated to processing of social-interaction stimuli and/or emotions? I
do not know, but the HSV data seem to be pointing in that direction. If
such localizations can occur, then (at least speculationally) some cases
of autism might be the result of highly localized HSV colonizations in
one or several parts of the temporal lobe.
Other viruses, too, have been found to be capable of CNS residence, with
varying traits and epileptiform patterns as associated features (4).
1) DeLong GR et al. Acquired reversible autistic syndrome in acute
encephalopathic illness in children. Arch Neurol 38.191-4 1981.
2) Jay V et al. Pathology of chronic herpes infection associated with
seizure disorder... Ped Pathol Lab Med 15.131-46 1995.
3) Sanders VJ et al. Presence of herpes simplex DNA in surgical tissue
from human epileptic seizure foci detected by polymerase chain reaction.
Arch Neurol 54.9554-60 1997.
4) O'Meara M et al. Viral encephalitis in children. Current Opinion in
Pediatrics 8.11-15 1996.