Abstract
Zika virus (ZIKV) infection was historically considered a disease with mild symptoms and no major consequences to human health. However, several long-term, late onset, and chronic neurological complications, both in congenitally-exposed babies and in adult patients, have been reported after ZIKV infection, especially after the 2015 epidemics in the American continent. The development or severity of these conditions cannot be fully predicted, but it is possible that genetic, epigenetic, and environmental factors may contribute to determine ZIKV infection outcomes. This reinforces the importance that individuals exposed to ZIKV are submitted to long-term clinical surveillance and highlights the urgent need for the development of therapeutic approaches to reduce or eliminate the neurological burden of infection. Here, we review the epidemiology of ZIKV-associated neurological complications and the role of factors that may influence disease outcome. Moreover, we discuss experimental and clinical evidence of drugs that have shown promising results in vitro or in vitro against viral replication and and/or ZIKV-induced neurotoxicity.
Highlights
Zika virus (ZIKV) has been known since 1947 [1], and was historically regarded as a geographically restricted virus causing minor symptoms in humans
Reports using in silico and in vitro approaches suggested the potential of sofosbuvir (SFB), an antiviral prodrug clinically used against hepatitis C virus (HCV), to inhibit ZIKV replication [100,101]
While one group reported no effect on viral replication in either cortical neurons, motor neurons or astrocytes derived from induced-pluripotent stem cells [90], another study showed that FAV induced efficient reduction in ZIKV protein expression in human neural progenitor cells derived from human embryonic stem cells [91]
Summary
Zika virus (ZIKV) has been known since 1947 [1], and was historically regarded as a geographically restricted virus causing minor symptoms in humans. One study found that 40% of patients still showed some kind of neurological alteration after 1 year of symptom onset, and after two years some patients had not yet fully recovered [25] These reports demonstrate that ZIKV infection is detrimental to the mature nervous system and is associated with a spectrum of neurological syndromes that may culminate in long-term consequences and even mortality. Trophoblasts, placental barrier cells, are permissive to ZIKV only during a narrow time-frame, likely in the first trimester of gestation [48,53,68,69,70] This is probably one of the reasons why infection during this stage of pregnancy is usually associated to the birth of babies with more severe neurological outcomes. Additional population-based and experimental studies should be performed in order to determine whether and how any of these factors has contributed to determine the higher rate of neurological complications due to ZIKV infection in specific geographical regions
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