Page 91
allied
academies
Ann Biol Sci, 2017
ISSN: 2348-1927
August 23-24, 2017 | Toronto, Canada
Annual Conference on
MICROBIAL PATHOGENESIS, INFECTIOUS DISEASE,
ANTIMICROBIALS AND DRUG RESISTANCE
T
here is increasing evidences that favor the prenatal
beginning of schizophrenia. These evidences point toward
intra-uterine environmental factors that act specifically
during the second pregnancy trimester producing a direct
damage of the brain of the fetus. The current available
technology doesn’t allow observing what is happening
at cellular level?, since the human brain is not exposed to
a direct analysis in that stage of the life in subjects at high
risk of developing schizophrenia. In 1977, we began a direct
electron microscopic research of the brain of fetuses at high
risk fromschizophrenicmothers inorder tofindingdifferences
at cellular level in relation to controls. In these studies we
have observed within the nuclei of neurons the presence
of complete and incomplete viral particles that reacted in
positive formwith antibodies to herpes simplex hominis type
I [HSV1] virus, and mitochondria alterations. The importance
of these findings can have practical applications in the
prevention of the illness keeping in mind its direct relation
to the Aetiology and Physiopathology of schizophrenia. A
study of amniotic fluid cells in women at risk of having a
schizophrenic offspring is considered. Of being observed
the same alterations that those observed previously in the
cells of the brain of the studied foetuses, it would intend to
these women in risk of having a schizophrenia descendant,
previous information of the results, the voluntary medical
interruption of the pregnancy or an early anti HSV1 viral
treatment as preventive measure of the later development
of the illness.
e
:
segundo@infomed.sld.cuDirect evidence of viral infection and mitochondrial alterations in the brain of fetuses at high risk for
schizophrenia
Segundo Mesa Castillo
Psychiatric Hospital of Havana, Cuba
Arch Clin Microbiol, 8:5
DOI: 10.4172/1989-8436-C1-003




