scholarly journals CImP: Cellular Imprinting Proteomics applied to ocular disorders elicited by Congenital Zika virus Syndrome

2019 ◽  
Author(s):  
Livia Rosa-Fernandes ◽  
Raquel Hora Barbosa ◽  
Maria Luiza B. dos Santos ◽  
Claudia B. Angeli ◽  
Thiago P. Silva ◽  
...  
Keyword(s):  
Zika Virus ◽  
Ocular Surface ◽  
Molecular Mechanisms ◽  
Membrane Filter ◽  
Neurological Diseases ◽  
Specific Protein ◽  
Protein Markers ◽  
Impression Cytology ◽  
Zikv Infection ◽  
Molecular Alterations

AbstractIMPORTANCEOcular complications in infants with Congenital Zika Syndrome (CZS) have been reported. However, the molecular mechanisms underlying of eye dysfunctions are presently unknown.OBJECTIVEA method (termed Cellular Imprinting Proteomics, CImP) for the identification and quantification of the ocular surface proteome using a minimally invasive membrane filter device is described. Moreover, The CImP method was applied to profile the molecular alterations in the eyes of infants exposed to Zika virus (ZIKV) infection during gestation.DESIGN, SETTINGS AND PARTICIMPANTSThe CImP method was applied to a cohort divided into three conditions: 1) Ctrl (infants with no infectious diseases, n=5). 2) Zikv (infants exposed to ZIKV gestation, with no microcephaly, n=5). 3) ZikvCZS(infants exposed to ZIKV, with microcephaly, n=3). All conditions were age and sex-matched. An improved impression cytology method was used to capture the outermost ocular surface cells. The number of impression cytology membrane collected was: Ctrl (12), Zikv (14) and ZikvCZS(8). Proteins were extracted and analysed using mass spectrometry-based proteomics technology followed by statistical analysis. Parallel reaction monitoring was performed to validate the expression of specific protein markers.RESULTSUsing the CImP method, 2209 proteins were identified on the membrane-captured conjunctiva epithelial cells. Modulation of neutrophil degranulation, cell death, ocular and neurodevelopment pathways are reported in infants with CZS compared to matched controls. Moreover, the molecular pattern of ocular surface cells retrieved from infants infected during the gestation but with no CZS was different from matched controls.CONCLUSIONS AND PERSPECTIVESMolecular alterations in the ocular cell surface associated to ZIKV infection with and without CZS complications are reported for the first time. We predict that this method will be introduced successfully in the study of several neurological diseases with the aim to identify novel diagnostic and therapeutic biomarkers.

#71: Single-cell RNA Sequencing Analysis of Zika Virus Infection in Human Stem Cell-Derived Neuroprogenitor Cells and Cerebral Organoids

2021 ◽  
Vol 10 (Supplement_1) ◽  
pp. S14-S14
Author(s):  
K E Ocwieja ◽  
T K Hughes ◽  
J M Antonucci ◽  
A L Richards ◽  
A C Stanton ◽  
...  
Keyword(s):  
Stem Cell ◽  
Single Cell ◽  
Rna Sequencing ◽  
Zika Virus ◽  
Molecular Mechanisms ◽  
Sequencing Analysis ◽  
Human Stem Cell ◽  
Zikv Infection ◽  
Single Cell Sequencing ◽  
Single Cell Rna Sequencing

Abstract Background The molecular mechanisms underpinning the neurologic and congenital pathologies caused by Zika virus (ZIKV) infection remain poorly understood. It is also unclear why congenital ZIKV disease was not observed prior to the recent epidemics in French Polynesia and the Americas, despite evidence that the Zika virus has actively circulated in parts of Africa and Asia since 1947 and 1966, respectively. Methods Due to advances in stem cell-based technologies, we can now model ZIKV infections of the central nervous system in human stem cell-derived neuroprogenitor cells and cerebral organoids, which recapitulate complex three-dimensional neural architecture. We apply Seq-Well—a simple, portable platform for massively parallel single-cell RNA sequencing—to characterize these neural models infected with ZIKV. We detect and quantify host mRNA transcripts and viral RNA with single-cell resolution, thereby defining transcriptional features of both uninfected and infected cells. Results In neuroprogenitor cells, single-cell sequencing reveals that while uninfected bystander cells strongly upregulate interferon pathway genes, these are largely suppressed in cells infected with ZIKV within the same culture dish. In our organoid model, single-cell sequencing allows us to identify multiple cellular populations, including neuroprogenitor cells, intermediate progenitor cells, and terminally differentiated neurons. In this model of the developing brain, we identify preferred tropisms of ZIKV infection. Our data additionally reveal differences in cell-type frequencies and gene expression within organoids infected by historic and contemporary ZIKV strains from a variety of geographic locations. Conclusions These findings may help explain phenotypic differences attributed to the viruses, including variable propensities to cause microcephaly. Overall, our work provides insight into normal and diseased human brain development and suggests that both virus replication and host response mechanisms underlie the neuropathology of ZIKV infection.

scholarly journals Zika Virus Production Is Resistant to RNase L Antiviral Activity

2019 ◽  
Vol 93 (16) ◽  
Author(s):  
Jillian N. Whelan ◽  
Yize Li ◽  
Robert H. Silverman ◽  
Susan R. Weiss
Keyword(s):  
Antiviral Activity ◽  
Zika Virus ◽  
Viral Genome ◽  
Molecular Mechanisms ◽  
Virus Production ◽  
Type I ◽  
Rnase L ◽  
Oligoadenylate Synthetase ◽  
Zikv Infection ◽  
Initial Report

SUMMARYThere is currently no knowledge of how the emerging human pathogen Zika virus (ZIKV) interacts with the antiviral endoribonuclease L (RNase L) pathway during infection. Since activation of RNase L during infection typically limits virus production dramatically, we used CRISPR-Cas9 gene editing technology to knockout (KO) targeted host genes involved in the RNase L pathway to evaluate the effects of RNase L on ZIKV infection in human A549 cells. RNase L was activated in response to ZIKV infection, which degraded ZIKV genomic RNA. Surprisingly, despite viral genome reduction, RNase L activity did not reduce ZIKV infectious titers. In contrast, both the flavivirus dengue virus and the alphavirus Sindbis virus replicated to significantly higher titers in RNase L KO cells compared to wild-type (WT) cells. Using MAVS/RNase L double KO cells, we demonstrated that the absence of increased ZIKV production in RNase L KO cells was not due to compensation by enhanced type I interferon transcripts to thus inhibit virus production. Finally, when synthetic double-stranded RNA was detected by OAS3 to induce RNase L antiviral activity prior to ZIKV infection, we observed reduced ZIKV replication factory formation, as well as a 42-fold reduction in virus yield in WT but not RNase L KO cells. This study proposes that ZIKV evades RNase L antiviral activity by generating a viral genome reservoir protected from RNase L cleavage during early infection, allowing for sufficient virus production before RNase L activation is detectable.IMPORTANCEWith the onset of the 2015 ZIKV outbreak, ZIKV pathogenesis has been of extreme global public health interest, and a better understanding of interactions with the host would provide insight into molecular mechanisms driving the severe neurological outcomes of ZIKV disease. Here is the initial report on the relationship between ZIKV and the host oligoadenylate synthetase-RNase L (OAS-RNase L) system, a potent antiviral pathway effective at restricting replication of diverse viruses. Our study elucidated a unique mechanism whereby ZIKV production is impervious to antiviral RNase L activity, through a mechanism of viral RNA protection that is not mimicked during infection with numerous other RNase L-activating viruses, thus identifying a distinct replication strategy potentially important for ZIKV pathogenesis.

scholarly journals MOMC-1. Employing the Zika Virus to kill paediatric nervous system tumour cells

2021 ◽  
Vol 3 (Supplement_2) ◽  
pp. ii3-ii3
Author(s):  
Matthew Sherwood ◽  
Robert Ewing ◽  
Carolini Kaid ◽  
Thiago Giove Mitsugi ◽  
Keith Okamoto
Keyword(s):  
Nervous System ◽  
Zika Virus ◽  
Molecular Mechanisms ◽  
Neuroblastoma Cell ◽  
Tumour Cells ◽  
Host Protein ◽  
Oncolytic Virotherapy ◽  
Motor Deficits ◽  
Zikv Infection ◽  
Tumour Metastasis

Abstract Malignant paediatric nervous system tumours, such as Medulloblastoma, Neuroblastoma and ATRT commonly harbour tumour cells with stem-like features which are highly tumorigenic and resistant to conventional cancer therapies. These tumours can exhibit high lethality and may result in severe sequelae, including cognitive and motor deficits that significantly affect patients’ quality of life. Oncolytic virotherapy is a novel therapy class that exploits viruses that preferentially infect and destroy tumour cells. These viruses present a unique advantage in targeting highly heterogeneous cancers, such as nervous system tumours, as they possess a secondary mechanism of action through which they induce a tumour-specific immune response. Clinical studies employing oncolytic virotherapy have in general reported low toxicity and minimal adverse effects, deeming oncolytic virotherapy as a potentially attractive and safer intervention against paediatric tumours. The Zika virus (ZIKV) is capable of infecting and destroying neural stem-like cancer cells from human embryonal Central Nervous System (CNS) tumours in vitro and in vivo. Infection of CNS tumour cells with ZIKV effectively inhibits tumour metastasis in mice and, in some cases, induces complete tumour remission. Neuroblastoma arises from immature nerve cells and multiple Neuroblastoma cell lines are susceptible to ZIKV infection and oncolysis. These initial findings have demonstrated the potential for a ZIKV-based virotherapy against paediatric nervous system tumours and warrants examination into the molecular mechanisms through which ZIKV executes its oncolytic ability. My research goal is to elucidate the mechanisms which are of paramount importance for ZIKV-induced oncolysis of brain tumour and Neuroblastoma cells. Utilising global expression omics profiling of ZIKV infection and mapping of viral protein-host protein interactions will identify these mechanisms both at the cellular pathway and molecular levels. These collectively will inform our understanding of how we can employ a future ZIKV-based virotherapy against paediatric nervous system tumours.

scholarly journals Zika virus epidemiology: from Uganda to world pandemic, an update

2018 ◽  
Vol 146 (6) ◽  
pp. 673-679 ◽  
Author(s):  
C. Talero-Gutiérrez ◽  
A. Rivera-Molina ◽  
C. Pérez-Pavajeau ◽  
I. Ossa-Ospina ◽  
C. Santos-García ◽  
...  
Keyword(s):  
Public Health ◽  
Health Problem ◽  
Zika Virus ◽  
Mosquito Control ◽  
Neurological Diseases ◽  
Local Population ◽  
Public Health Problem ◽  
Control Measures ◽  
Control Treatment ◽  
Zikv Infection

AbstractZika virus (ZIKV) infection is an emergent worldwide public health problem. Historically, 84 countries have reported vector-borne ZIKV transmission, 61 of which report on-going transmission. It is a Flavivirus transmitted through arthropods belonging to the Aedes genus. Since 2015, ZIKV infections have increased dramatically; with 1.3 million people infected during 2015 in Brazil alone. This paper's objective is to highlight the conjectural epidemiological points of the virus’ dissemination. The digital archives Pubmed, MEDLINE, EMBASE and Cochrane were searched for papers that assessed aspects of ZIKV transmission and epidemiology. The first isolation occurred in Uganda in 1947. Since then, important outbreaks were documented globally. Consequently, an emergent public health problem arose from a rapidly increasing incidence and its association with the development of neurological diseases such as microcephaly and Guillain–Barré syndrome. Key factors in the successful containment of outbreaks include surveillance of mosquitos in the neighbourhood, an early mosquito control treatment, an assertive information campaign, and the involvement of the local population and healthcare workers. As such, while ZIKV seems to be spreading globally in a similar manner to other arboviruses, such as Dengue and Chikungunya viruses, it can also be rapidly contained due to the pre-existing availability of necessary resources and regulatory tools as control measures. This review aims to provide a description of those characteristics of ZIKV infection that may be useful in the construction of effective outbreak control strategies.

scholarly journals Integrated MicroRNA and mRNA Profiling in Zika Virus-Infected Neurons

Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 162 ◽  
Author(s):  
Francine Azouz ◽  
Komal Arora ◽  
Keeton Krause ◽  
Vivek Nerurkar ◽  
Mukesh Kumar
Keyword(s):  
Zika Virus ◽  
Wide Spectrum ◽  
Neurological Diseases ◽  
Critical Role ◽  
Inverse Correlation ◽  
Viral Immunity ◽  
Zikv Infection ◽  
Processing Enzymes ◽  
Functional Studies ◽  
Primary Mouse

Zika virus (ZIKV) infections have caused a wide spectrum of neurological diseases, such as Guillain-Barré syndrome, myelitis, meningoencephalitis, and congenital microcephaly. No effective therapies currently exist for treating patients infected with ZIKV. MicroRNAs (miRNAs) are a group of small RNAs involved in the regulation of a wide variety of cellular and physiological processes. In this study, we analyzed digital miRNA and mRNA profiles in ZIKV-infected primary mouse neurons using the nCounter technology. A total of 599 miRNAs and 770 mRNAs were examined. We demonstrate that ZIKV infection causes global downregulation of miRNAs with only few upregulated miRNAs. ZIKV-modulated miRNAs including miR-155, miR-203, miR-29a, and miR-124-3p are known to play critical role in flavivirus infection, anti-viral immunity and brain injury. ZIKV infection also results in downregulation of miRNA processing enzymes. In contrast, ZIKV infection induces dramatic upregulation of anti-viral, inflammatory and apoptotic genes. Furthermore, our data demonstrate an inverse correlation between ZIKV-modulated miRNAs and target host mRNAs induced by ZIKV. Biofunctional analysis revealed that ZIKV-modulated miRNAs and mRNAs regulate the pathways related to neurological development and neuroinflammatory responses. Functional studies targeting specific miRNA are warranted to develop therapeutics for the management of ZIKV neurological disease.

scholarly journals Zika Virus sfRNA Plays an Essential Role in the Infection of Insects and Mammals

Proceedings ◽  
2020 ◽  
Vol 50 (1) ◽  
pp. 112
Author(s):  
Andrii Slonchak ◽  
Leon E. Hugo ◽  
Morgan Freney ◽  
Alberto A Amarilla ◽  
Sonja Hall-Mendelin ◽  
...  
Keyword(s):  
Human Brain ◽  
Brain Development ◽  
Zika Virus ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Nuclear Translocation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Rnai Pathway ◽  
Type I ◽  
Zikv Infection

Similar to other flaviviruses, Zika virus (ZIKV) produces abundant subgenomic flavivirus RNA (sfRNA) derived from the 3’ untranslated region. The molecular mechanisms that determine the functions of sfRNA are currently not completely understood. Here, we created ZIKV mutants deficient in sfRNA production and employed them to investigate the role of this RNA in virus interactions with mammalian and insect hosts. We found that in mosquitoes, sfRNA facilitates virus replication and is required for ZIKV dissemination into saliva and virus transmission. The production of sfRNA was found to have no effect on the RNAi pathway, but instead downregulated the expression of genes involved in the regulation of apoptosis. The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) of histological sections from infected mosquitoes confirmed that sfRNA prevents the apoptotic death of infected cells, thus identifying inhibition of apoptosis as a novel mechanism of sfRNA action in mosquitoes. We also found that sfRNA facilitates ZIKV replication in mammalian cells, mice, and human brain organoids. Moreover, ZIKV mutants deficient in sfRNA production were unable to form plaques, cause the death of human brain organoids, or establish infection in the mouse foetal brain. We then found that the proviral activity of sfRNA in mammalian cells relies on its ability to suppress type I interferon signalling. We showed that this is achieved via the inhibition of phosphorylation and the nuclear translocation of STAT1. In addition, we found that the production of sfRNA in the ZIKV infection of human brain organoids is associated with the suppression of multiple genes involved in brain development, indicating that sfRNA can be involved in the disruption of brain development associated with ZIKV infection.

scholarly journals Impression cytology is a non-invasive and effective method for ocular cell obtention from babies with Congenital Zika Syndrome: perspectives in OMIC studies

2019 ◽  
Author(s):  
Raquel Hora Barbosa ◽  
Maria Luiza B. dos Santos ◽  
Thiago P. Silva ◽  
Liva Rosa-Fernandes ◽  
Ana Pinto ◽  
...  
Keyword(s):  
Zika Virus ◽  
Ocular Surface ◽  
Clinical Signs ◽  
Impression Cytology ◽  
Morphological Alterations ◽  
Non Invasive ◽  
Viable Cells ◽  
Congenital Zika Syndrome ◽  
Microscopic Features ◽  
Conjunctival Epithelial Cells

AbstractIMPORTANCENoninvasive techniques for obtaining ocular surface cells (neuroepithelial) from babies with Congenital Zika Syndrome CZS - resulting from infection by zika virus (ZIKV) during gestational period (malformations include ocular abnormalities and microcephaly) - remain to be determined.OBJECTIVESThe aim of this study was to describe an optimized impression cytology method for the isolation of viable cells from babies with CZS in satisfactory amounts and quality to enable the application in the context of genome approaches well as morphological and molecular evaluations.DESIGN, SETTINGS AND PARTICIPANTSIn this observational study, ocular surface samples were obtained with a hydrophilic nitrocellulose membrane (through optimized impression cytology method) from twelve babies referred to the Pediatric Service of the Antonio Pedro Hospital, Universidade Federal Fluminense (UFF), Niteroi, Rio de Janeiro, Brazil. Samples were collected with an authorized informed consent from both eyes of eight ZIKV infected babies according to the CZS diagnostic criteria (4 babies with positive PCR for Zika virus in gestation and presence of clinical signs which included ocular abnormalities and microcephaly and 4 babies with positive PCR for Zika virus during gestation but no clinical signs identified) and four unaffected babies (control samples / negative PCR, without clinical signs). Cells were used for microscopy analyses, transcriptomic and proteomic experiments and molecular procedure.MAIN OUTCOMES AND MEASURESThe microscopic features of the conjunctival epithelial cells were described by both direct analysis of the membrane-attached cells and analysis of cytospinned captured cells using several staining procedures, including viability evaluation. In parallel, molecular approaches were performed.RESULTSOn impression cytology, a considerable amount of viable cells were captured. Epithelial basal, polyhedral and goblet cells were clearly identified in all groups. All cases of ZIKV infected babies showed clear morphological alterations (cell keratinization, piknosis, karyolysis, anucleation and vacuolization). Genomic DNA and RNA were successfully isolated from all samples and allowed the establishment of transcriptomic and proteomic studies. Transcriptome analysis showed 8582 transcripts quantified in all samples and 63 differentially expressed genes in ocular cells from the exposed babies. Proteomics analysis allowed the identification of 2080, 2085 and 2086 high confident and unique proteins with at least one unique peptide in the unaffected, exposed to ZIKV and asymptomatic and CZS babies, respectively, being 2062 in common. Multivariate supervised analysis using the total quantitative protein features revealed a clear discrimination between the groups.CONCLUSIONS AND RELEVANCEOur method proved to be a suitable, fast, and non-invasive tool for detailed and precise morphological analyses with a perspective of application in OMIC studies for clinical and research studies of CZS.Key pointsQuestionAre the ocular surface cells of babies with Congenital Zika Syndrome viable to investigate the association between Zika virus infection during embryogenesis and ocular impairment?FindingsTo this date, this is the first study using an approach with perspectives in morphological, molecular and “OMICs” research from ocular samples captured by impression cytology of ZIKV infected babies during embryogenesis. The microscopic features of the conjunctival epithelial cells from all ZIKV infected babies showed clear morphological alterations.MeaningOcular cell surface capture offers a powerful model for studying the pathways involved in ocular diseases associated with ZIKV.

scholarly journals Zika virus dysregulates the expression of astrocytic genes involved in neurodevelopment

2021 ◽  
Vol 15 (4) ◽  
pp. e0009362
Author(s):  
Muhammad Adnan Shereen ◽  
Nadia Bashir ◽  
Rui Su ◽  
Fang Liu ◽  
Kailang Wu ◽  
...  
Keyword(s):  
Brain Development ◽  
Signaling Pathway ◽  
Glial Cells ◽  
Zika Virus ◽  
Molecular Mechanisms ◽  
French Polynesia ◽  
Health Concern ◽  
Hippo Signaling ◽  
Sequencing Data ◽  
Zikv Infection

Zika virus (ZIKV) is a kind of flavivirus emerged in French Polynesia and Brazil, and has led to a worldwide public health concern since 2016. ZIKV infection causes various neurological conditions, which are associated with fetus brain development or peripheral and central nervous systems (PNS/CNS) functional problems. To date, no vaccine or any specific antiviral therapy against ZIKV infection are available. It urgently needs efforts to explore the underlying molecular mechanisms of ZIKV-induced neural pathogenesis. ZIKV favorably infects neural and glial cells specifically astrocytes, consequently dysregulating gene expression and pathways with impairment of process neural cells. In this study, we applied a model for ZIKV replication in mouse primary astrocytes (MPAs) and profiled temporal alterations in the host transcriptomes upon ZIKV infection. Among the RNA-sequencing data of 27,812 genes, we examined 710 genes were significantly differentially expressed by ZIKV, which lead to dysregulation of numerous functions including neurons development and migration, glial cells differentiation, myelinations, astrocytes projection, neurogenesis, and brain development, along with multiple pathways including Hippo signaling pathway, tight junction, PI3K-Akt signaling pathway, and focal adhesion. Furthermore, we confirmed the dysregulation of the selected genes in MPAs and human astroglioma U251 cells. We found that PTBP1, LIF, GHR, and PTBP3 were upregulated while EDNRB and MBP were downregulated upon ZIKV infection. The current study highlights the ZIKV-mediated potential genes associated with neurodevelopment or related diseases.

scholarly journals A ‘Furry-Tale’ of Zika Virus Infection: What Have We Learned from Animal Models?

Viruses ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 29 ◽  
Author(s):  
Loulieta Nazerai ◽  
Jan Pravsgaard Christensen ◽  
Allan Randrup Thomsen
Keyword(s):  
Animal Models ◽  
Immune Responses ◽  
Zika Virus ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Zikv Infection ◽  
Infected People ◽  
Collective Effort ◽  
Transplacental Infection

The worldwide attention that the Zika virus (ZIKV) attracted, following its declaration as a Public Health Emergency of International concern by WHO in 2016, has led to a large collective effort by the international scientific community to understand its biology. Despite the mild symptoms caused by ZIKV in most infected people, the virus displays a number of worrying features, such as its ability to cause transplacental infection, fetal abnormalities and vector independent transmission through body fluids. In addition, the virus has been associated with the induction of Guillain-Barre syndrome in a number of infected individuals. With travelling, the virus has spread outside the original ZIKV endemic areas making it imperative to find ways to control it. Thus far, the large number of animal models developed to study ZIKV pathogenesis have proven to be valuable tools in understanding how the virus replicates and manifests itself in the host, its tissue tropism and the type of immune responses it induces. Still, vital questions, such as the molecular mechanisms of ZIKV persistence and the long-term consequences of ZIKV infection in the developing brain, remain unanswered. Here, we reviewed and discussed the major and most recent findings coming from animal studies and their implications for a ZIKV vaccine design.

Inhibition of Neurogenesis by Zika Virus Infection

2018 ◽  
Vol 17 (2) ◽  
pp. 78-86 ◽  
Author(s):  
Fahim Ahmad ◽  
Amna Siddiqui ◽  
Mohammad A. Kamal ◽  
Sayed Sartaj Sohrab
Keyword(s):  
Zika Virus ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Management Strategies ◽  
Neuronal Cell ◽  
The United States ◽  
Causal Link ◽  
Published Data ◽  
Zikv Infection ◽  
First Case

Background & Objective: The link between Zika Virus (ZIKV) epidemic and neurological disorder has raised an urgent global alarm. The current epidemic of ZIKV has triggered quick responses in the scientific world. The first case of ZIKV was reported in 2015 from Brazil and now has spread over 30 countries. Nearly four hundred cases of traveler associated ZIKV infection have also been reported in the United States. ZIKV is primarily transmitted by mosquito belonging to the genus Aedes that are widely distributed throughout the world. Additionally, the virus can also be transmitted from male to female by sexual contact. The epidemiological investigations during the current outbreak found a causal link between infection in pregnant women and the development of microcephaly (MCPH) in their unborn babies. This finding is a cause of grave concern since MCPH is a serious neural developmental disorder that can lead to significant post-natal developmental abnormalities and disabilities. Recently, published data indicates that ZIKV infection severely affects the growth of fetal neural progenitor cells and cerebral neurons resulting in malformation of cerebral cortex leading to MCPH. Recently, it has been reported that ZIKV infection deregulates the signaling pathway of neuronal cell and inhibits the neurogenesis. Conclusion: In this review, we discussed the information about cellular and molecular mechanisms of neurodegeneration of human neuronal cells and inhibition of neurogenesis. The provided information in this review will be very useful further not only in neuro-scientific research but also in the desig and development of management strategies for MCPH and other mosquito-borne diseases.

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