Guillain-Barré syndrome (GBS) is an autoimmune disease that damages the nerves of the peripheral nervous system, causing paralysis in humans. Several infectious agents including dengue virus, Epstein-Barr virus, and herpes virus have been suggested to be possible factors in the development of GBS however the exact cause is yet to be discovered. Recently, a strong temporal and geographical correlation between Zika virus (ZIKV) outbreaks and an increase in GBS cases within the region has implied that ZIKV could possibly portray a key role in the onset of GBS. This Flaviviridae virus has recently been causing large epidemics and increasing numbers of neurological complications, such as microcephaly, have been reported following outbreaks within the human population. The Asian strain of ZIKV has been shown to be neurovirulent and therefore capable of infecting nerve cells, providing further support for this connection. This article discusses the current evidence available to support the association between ZIKV and GBS, the molecular determinants that increase the neurotropism of specific ZIKV strains, and the putative molecular mechanism of ZIKV pathogenesis that causes the development of GBS. Determining the role of ZIKV in the onset of GBS can allow for the discovery of novel diagnostic biomarkers, which can aid in the early detection and prevention of GBS. The discovery of a possible mechanism of neurovirulent ZIKV strains can aid in understanding the pathogenesis of the virus in not only GBS, but other associated neurological diseases as well. Paper
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Priya Suresh (2026) studied this question.
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