Studies of the pathogenesis of neurobehavioral diseases following Boma dise
ase virus infections have been increasing rapidly over the past ten years.
Recent major advances have included a report of vertical transmission of th
e virus in its natural host, the horse, and a report of isolation of a nove
l variant, No/98, in that same species. In rats infected neonatally with th
e Boma disease virus that lack blood-borne inflammation in the brain, evide
nce of an 'endogenous' brain inflammatory response is abundant, with elevat
ed expression of cytokine and chemokine mRNA. Infection in these rats is al
so associated with abnormal levels of neurotransmitters, including serotoni
n and norepinephrine. Data and debate continue to be forthcoming about the
role of Boma disease virus in human infection and psychiatric disease.