Zika virus (ZIKV) disease has become a global health emergency with devastating effects on public health. Recent evidences implicate the virus as an emergent neuropathological agent promoting serious pathologies of the human nervous system, that include destructive and malformation consequences such as development of ocular and fetal brain lesions,
microcephaly in neonates, and
Guillain-Barré syndrome (GBS) in adults. These
neurological disorders of both central and peripheral nervous systems are thought to be associated to the neurotropic properties of the virus that has ability to infect neural stem cells as well as peripheral neurons, a hallmark of its pathogenicity. The presence of
autoantibodies against
gangliosides plays a pivotal role in the etiogenesis of GBS and a variety of
neurological disorders.
Gangliosides are a class of
galactose-containing
cerebrosides mainly expressed in nervous system tissues playing a critical role in the physiology of neural cells and neurogenesis. Herein, our findings indicate that patients at acute phase of
ZIKV infection without any neurological signs show increased levels of
IgG autoantibody against GD3
gangliosides, a class of
glycolipid found to be highly expressed in neural stem cell acting in the maintenance of their self-renewal cellular capacity. It is possible that a pathological threshold of these
antibodies is only acquired in secondary or subsequent
infections. In the light of these evidences, we propose that the target of GD3 by autoimmune responses may possibly has an effect in the neuropathy and neurogenesis disorder seen during
ZIKV infection.