Zika virus (
ZIKV) has recently caused a
pandemic disease, and many cases of
ZIKV infection in
pregnant women resulted in
abortion,
stillbirth, deaths and
congenital defects including
microcephaly, which now has been proposed as
ZIKV congenital syndrome. This study aimed to investigate the in situ
immune response profile and mechanisms of neuronal
cell damage in fatal Zika
microcephaly cases.
Brain tissue samples were collected from 15 cases, including 10 microcephalic
ZIKV-positive
neonates with
fatal outcome and five neonatal control
flavivirus-negative
neonates that died due to other causes, but with preserved
central nervous system (CNS)
architecture. In
microcephaly cases, the histopathological features of the
tissue samples were characterized in three CNS areas (
meninges, perivascular space, and parenchyma). The changes found were mainly calcification,
necrosis, neuronophagy,
gliosis, microglial nodules, and inflammatory infiltration of mononuclear
cells. The in situ
immune response against
ZIKV in the CNS of
newborns is complex. Despite the predominant expression of Th2
cytokines, other
cytokines such as Th1, Th17, Treg, Th9, and Th22 are involved to a lesser extent, but are still likely to participate in the immunopathogenic mechanisms of neural
disease in fatal cases of
microcephaly caused by
ZIKV.