Neuroinfection and neurological pathologies by the Zika virus. A review
Abstract
The pathogenesis of the Zika Virus (ZIKV) is currently not well understood. However, studies have suggested that it begins when dendritic cells are infected near the site of inoculation of the bite of the mosquito infected with the virus; later it spreads through the lymph nodes and finally to the bloodstream, through which it comes to exert its action. The objective of this article is to describe the mechanism of neuroinfection and neurological pathologies caused by the Zika virus, for which a systematic bibliographic review was carried out. Within this pathogenic action, its predilection for nervous tissues stands out, accepting flavivirus as highly neurotropic. The main route is neuroinvasion as a process that involves multiple steps in the disruption of hermetic intercellular junctions, through the alteration of claudin and its passage through the blood-brain barrier, the choroid plexuses and the glia; this favors the neurological alterations produced as a result of in utero infection. Of these alterations, microcephaly is the most important, which is why the suspicion that there is a relationship between Zika virus infection and microcephaly, as well as Guillain-Barre syndrome, myelitis and viral meningoencephalitis, which locates the virus as the neurotrope par excellence. In conclusion, the data point to an important association between Zika infection and neurological pathology, which is why it represents a target of study in order to prevent its transmission and reduce development during pregnancy.
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