摘要 :
Zika virus belongs to family of viruses 'Flaviviridae' and spreads mostly by daytime-active Aedes mosquitoes. The resulting infection is known as Zika fever. It is usually asymptomatic or often causes mild symptoms, which are very...
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Zika virus belongs to family of viruses 'Flaviviridae' and spreads mostly by daytime-active Aedes mosquitoes. The resulting infection is known as Zika fever. It is usually asymptomatic or often causes mild symptoms, which are very similar to dengue fever. The Aedes aegypti mosquito is also responsible for dengue and chikungunya viruses. Zika virus can spread by crossing the placental barrier from a pregnant mother to a fetus, which can result in microcephaly, severe brain malformations including Guillain-Barre syndrome (GBS), and other birth defects. Until now, there is no specific treatment of Zika fever disease, and Zika virus illness cannot be prevented by medications or vaccines. According to WHO, no vaccine is likely to be available until 2020. The only way of preventing this disease is to prevent the mosquito bites. This article presents the history of Zika virus, its reported cases including microcephaly and GBS, and a comparison of its symptoms with those of dengue and chikungunya diseases, as well as preventive measures. With advances in research and technology, knowledge about the Zika virus has grown, yet some questions remain unanswered regarding Zika virus's genetic diversity, pathophysiology, transmission vectors and reservoirs, potential synergetic of coinfection with other related arboviruses, and treatment. These problems highlight the need for further research to achieve adequate the surveillance, infection management, optimized treatment, and public health mediations in Zika virus outbreaks. This article contributes to our understanding of the disease mechanism, genome structure, diagnosis, transmission, and preventive strategies to combat Zika virus infection.
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Objective: To comprehensively review the available evidence and existing consensus reports and guidelines regarding the pregnancy and reproductive implications of the mosquito-transmitted Zika virus (ZIKV) infection. A primary foc...
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Objective: To comprehensively review the available evidence and existing consensus reports and guidelines regarding the pregnancy and reproductive implications of the mosquito-transmitted Zika virus (ZIKV) infection. A primary focus was to provide pertinent information to aid clinicians in the management of pregnancies at risk for, exposed to, or with confirmed ZIKV infection.
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The spread of Zika virus to the Americas was accompanied by surge in the number of infants with CNS abnormalities leading to a declaration of a health emergency by the WHO. This was accompanied by significant responses from govern...
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The spread of Zika virus to the Americas was accompanied by surge in the number of infants with CNS abnormalities leading to a declaration of a health emergency by the WHO. This was accompanied by significant responses from governmental health agencies in the United States and Europe that resulted in significant new information described in the natural history of this perinatal infection in a very short period of time. Although much has been learned about Zika virus infection during pregnancy, limitations of current diagnostics and the challenges for accurate serologic diagnosis of acute Zika virus infection has restricted our understanding of the natural history of this perinatal infection to infants born to women with clinical disease during pregnancy and to Zika exposed infants with obvious clinical stigmata of disease. Thus, the spectrum of disease in infants exposed to Zika virus during pregnancy remains to be defined. In contrast, observations in informative animal models of Zika virus infections have provided rational pathways for vaccine development and existing antiviral drug development programs for other flaviviruses have resulted in accelerated development for potential antiviral therapies. This brief review will highlight some of the current concepts of the natural history of Zika virus during pregnancy. (C) 2018 Elsevier Inc. All rights reserved.
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La enfermedad o fiebre del Zika es una enfermedad febril, zoonótica, transmitida por vectores, de curso agudo, emergente, autolimitada y benigna, causada por el virus Zika (ZIKAV), Se reportó inicialmente en Africa y Asia, pero ...
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La enfermedad o fiebre del Zika es una enfermedad febril, zoonótica, transmitida por vectores, de curso agudo, emergente, autolimitada y benigna, causada por el virus Zika (ZIKAV), Se reportó inicialmente en Africa y Asia, pero actualmente se ha propagado ampliamente a gran parte de los países americanos. El diagnóstico confirmatorio de la enfermedad requiere pruebas especializadas, y su tratamiento es solamente sintomático, siendo la prevención de la picadura del mosquito la mejor estrategia para disminuir su presentación. A pesar de ser una enfermedad que puede cursar asintomática o con una manifestaciones clínicas muy benignas y muy raramente mortal, ha prendido las alertas en salud por su progresiva y rápida propagación además de estar asociada a malformaciones congénitas neurológicas, oftálmicas y articulares, en algunos casos irreversibles.
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In this chapter, we first briefly review the history of Zika virus (ZIKV) over the past 70 years since its discovery. We then focus on the ZIKV NS2B/NS3 protease, a major potential target for anti-ZIKV therapeutics. We describe th...
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In this chapter, we first briefly review the history of Zika virus (ZIKV) over the past 70 years since its discovery. We then focus on the ZIKV NS2B/NS3 protease, a major potential target for anti-ZIKV therapeutics. We describe the structure of the complex between Zika virus NS2B-NS3 protease and a peptide boronic-acid inhibitor that we determined in early 2016. We then review other structural studies on the Zika virus protease, which have been published in the past few months. Three different types of construct for the protease have been investigated by X-ray crystallography and NMR spectroscopy: the traditional "linked" construct comprising the NS2B cofactor, a Gly(4)SerGly(4) linker, and the NS3(Pro) chain; a construct where the linker has been replaced by LysThr-Gly-Lys-Arg, which leads to autocleavage; and the bimolecular "unlinked" protease consisting of the NS2B cofactor segment and NS3(pro). In complex with an inhibitor, the protease adopts a closed, "active" conformation with the NS2B chain wrapped around the NS3(Pro) and contributing to the S2 pocket. In the ligand-free state, the Gly(4)SerGly(4)-linked enzyme adopts an open or relaxed conformation, with the C-terminal half of the NS2B cofactor highly flexible and disordered. Very surprisingly, however, the "unlinked", bimolecular protease has been reported to adopt the closed conformation in the crystal, even though, apparently, no peptide was bound to the substrate-binding site. The Gly(4)SerGly(4)-linked enzyme has been used successfully in drug discovery efforts.
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Abstract Maternal infections are among the main risk factors for cognitive impairments in the offspring. Zika virus (ZIKV) can be transmitted vertically, causing a set of heterogeneous birth defects, such as microcephaly, ventricu...
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Abstract Maternal infections are among the main risk factors for cognitive impairments in the offspring. Zika virus (ZIKV) can be transmitted vertically, causing a set of heterogeneous birth defects, such as microcephaly, ventriculomegaly and corpus callosum dysgenesis. Nuclear distribution element like‐1 (Ndel1) oligopeptidase controls crucial aspects of cerebral cortex development underlying cortical malformations. Here, we examine Ndel1 activity in an animal model for ZIKV infection, which was associated with deregulated corticogenesis. We observed here a reduction in Ndel1 activity in the forebrain associated with the congenital syndrome induced by ZIKV isolates, in an in utero and postnatal injections of different inoculum doses in mice models. In addition, we observed a strong correlation between Ndel1 activity and brain size of animals infected by ZIKV, suggesting the potential of this measure as a biomarker for microcephaly. More importantly, the increase of interferon (IFN)‐beta signaling, which was used to rescue the ZIKV infection outcomes, also recovered Ndel1 activity to levels similar to those of uninfected healthy control mice, but with no influence on Ndel1 activity in uninfected healthy control animals. Taken together, we demonstrate for the first time here an association of corticogenesis impairments determined by ZIKV infection and the modulation of Ndel1 activity. Although further studies are still necessary to clarify the possible role(s) of Ndel1 activity in the molecular mechanism(s) underlying the congenital syndrome induced by ZIKV, we suggest here the potential of monitoring the Ndel1 activity to predict this pathological condition at early stages of embryos or offspring development, during while the currently employed methods are unable to detect impaired corticogenesis leading to microcephaly. Ndel1 activity may also be possibly used to follow up the positive response to the treatment, such as that employing the IFN‐beta that is able to rescue the ZIKV‐induced brain injury.
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