Does Zika virus suppress the antiviral host response in neuronal cells?

10.18258/6968 ◽  
2016 ◽  
Author(s):  
Dr. Husni Elbahesh Dr. Husni Elbahesh
Keyword(s):  
Zika Virus ◽  
Host Response ◽  
Neuronal Cells

Zika Virus NS5 Forms Supramolecular Nuclear Bodies That Sequester Importin-α and Modulate the Host Immune and Pro-Inflammatory Response in Neuronal Cells

2019 ◽  
Vol 5 (6) ◽  
pp. 932-948 ◽  
Author(s):  
Ivan H. W. Ng ◽  
Kitti Wing-Ki Chan ◽  
Min Jie Alvin Tan ◽  
Chin Piaw Gwee ◽  
Kate M. Smith ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Zika Virus ◽  
Neuronal Cells ◽  
Nuclear Bodies ◽  
Importin Α

scholarly journals Zika virus infection differentially affects genome-wide transcription in neuronal cells and myeloid dendritic cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (4) ◽  
pp. e0231049
Author(s):  
Tamina Park ◽  
Myung-gyun Kang ◽  
Seung-hwa Baek ◽  
Chang Hoon Lee ◽  
Daeui Park
Keyword(s):  
Dendritic Cells ◽  
Virus Infection ◽  
Zika Virus ◽  
Neuronal Cells ◽  
Myeloid Dendritic Cells ◽  
Zika Virus Infection ◽  
Genome Wide

scholarly journals Host response: Cross-fit T cells battle Zika virus

2017 ◽  
Vol 2 (6) ◽  
Author(s):  
Matthew Collins ◽  
Aravinda de Silva
Keyword(s):  
T Cells ◽  
Zika Virus ◽  
Host Response

scholarly journals A Novel Mechanism for Zika Virus Host-Cell Binding

Viruses ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1101
Author(s):  
Courtney A. Rieder ◽  
Jonathan Rieder ◽  
Sebastién Sannajust ◽  
Diana Goode ◽  
Ramaz Geguchadze ◽  
...  
Keyword(s):  
Zika Virus ◽  
Neuronal Cells ◽  
Annexin V ◽  
Vero Cells ◽  
Western Hemisphere ◽  
Host Cells ◽  
E Protein ◽  
Clinical Presentations ◽  
Secondary Mechanism ◽  
Protein Cell

Zika virus (ZIKV) recently emerged in the Western Hemisphere with previously unrecognized or unreported clinical presentations. Here, we identify two putative binding mechanisms of ancestral and emergent ZIKV strains featuring the envelope (E) protein residue asparagine 154 (ASN154) and viral phosphatidylserine (PS). Synthetic peptides representing the region containing ASN154 from strains PRVABC59 (Puerto Rico 2015) and MR_766 (Uganda 1947) were exposed to neuronal cells and fibroblasts to model ZIKV E protein/cell interactions and bound MDCK or Vero cells and primary neurons significantly. Peptides significantly inhibited Vero cell infectivity by ZIKV strains MR_766 and PRVABC59, indicating that this region represents a putative binding mechanism of ancestral African ZIKV strains and emergent Western Hemisphere strains. Pretreatment of ZIKV strains MR_766 and PRVABC59 with the PS-binding protein annexin V significantly inhibited replication of PRVABC59 but not MR_766, suggesting that Western hemisphere strains may additionally be capable of utilizing PS-mediated entry to infect host cells. These data indicate that the region surrounding E protein ASN154 is capable of binding fibroblasts and primary neuronal cells and that PS-mediated entry may be a secondary mechanism for infectivity utilized by Western Hemisphere strains.

scholarly journals Correction to: Zika Virus and the Metabolism of Neuronal Cells

2018 ◽  
Vol 56 (4) ◽  
pp. 2558-2558
Author(s):  
Hussin A. Rothan ◽  
Shengyun Fang ◽  
Mahesh Mohan ◽  
Siddappa N. Byrareddy
Keyword(s):  
Zika Virus ◽  
Neuronal Cells

scholarly journals Favipiravir (T-705) Protects IFNAR−/− Mice against Lethal Zika Virus Infection in a Sex-Dependent Manner

2021 ◽  
Vol 9 (6) ◽  
pp. 1178
Author(s):  
Keesha Matz ◽  
Jackson Emanuel ◽  
Julie Callison ◽  
Don Gardner ◽  
Rebecca Rosenke ◽  
...  
Keyword(s):  
Zika Virus ◽  
Host Response ◽  
Combined Treatment ◽  
Nucleoside Analogs ◽  
Dependent Manner ◽  
Zikv Infection ◽  
Specific Host ◽  
Improved Outcomes ◽  
Dose Dependent

Zika virus (ZIKV), a member of the Flaviviridae family, is an important human pathogen that has caused epidemics in Africa, Southeast Asia, and the Americas. No licensed treatments for ZIKV disease are currently available. Favipiravir (T-705; 6-fluoro-3-hydroxy-2-pyrazinecarboxamide) and ribavirin (1-(β-D-Ribofuranosyl)-1H-1,2,4-triazole-3-carboxamide) are nucleoside analogs that have exhibited antiviral activity against a broad spectrum of RNA viruses, including some flaviviruses. In this study, we strengthened evidence for favipiravir and ribavirin inhibition of ZIKV replication in vitro. Testing in IFNAR−/− mice revealed that daily treatments of favipiravir were sufficient to provide protection against lethal ZIKV challenge in a dose-dependent manner but did not completely abrogate disease. Ribavirin, on the other hand, had no beneficial effect against ZIKV infection in this model and under the conditions examined. Combined treatment of ribavirin and favipiravir did not show improved outcomes over ribavirin alone. Surprisingly, outcome of favipiravir treatment was sex-dependent, with 87% of female but only 25% of male mice surviving lethal ZIKV infection. Since virus mutations were not associated with outcome, a sex-specific host response likely explains the observed sex difference.

scholarly journals Zika Virus and the Metabolism of Neuronal Cells

2018 ◽  
Vol 56 (4) ◽  
pp. 2551-2557 ◽  
Author(s):  
Hussin A. Rothan ◽  
Shengyun Fang ◽  
Mohan Mahesh ◽  
Siddappa N. Byrareddy
Keyword(s):  
Zika Virus ◽  
Neuronal Cells

scholarly journals Differential Neuronal Susceptibility and Apoptosis in Congenital Zika Virus Infection

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S56-S56
Author(s):  
Cheng-Ying Ho ◽  
Heather Ames ◽  
Ashley Tipton ◽  
Gilbert Vezina ◽  
Judy Liu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Infection Rate ◽  
Zika Virus ◽  
Neuronal Cells ◽  
Infection Frequency ◽  
Zikv Infection ◽  
High Infection ◽  
Mature Neurons ◽  
Neuronal Lineage

Abstract Background Zika virus (ZIKV) infection during pregnancy may result in severe neurologic injury to the fetus. The mechanisms by which ZIKV injures fetal brain are not fully characterized. Although cell culture and animal models shed valuable insight into pathogenesis, they do not fully recapitulate human disease. Methods To characterize the mechanism of ZIKV-induced human brain injury, we performed immunolabeling on brain tissue from a 20-week fetus with intrauterine ZIKV infection. Formalin-fixed sections of brain tissue were co-immunostained with ZIKV envelope antibody, as well as neuronal and non-neuronal lineage cell markers to assess infection within populations. Apoptosis was assessed by quantifying activated caspase 3 -positive staining cells. Minimum 3–5 random microscopic fields per brain region were photographed and quantified in an automated fashion using the ImageJ Cell Counter plug-in. GraphPad Prism and Microsoft Excel software were used for data analysis. Results ZIKV demonstrated a wide range of neuronal and non-neuronal tropism. However, infection rate was highest in Tbr2+ - Intermediate Progenitor Cells (IPC; 81.4±12%) and DCX+ Immature Neurons (IN; 51.5±13.9%), followed by SOX2+/ Nestin+ Neural Precursor Cells (NPC; 26.6±13.4%). NeuN+ Mature Neurons had the lowest frequency of infection (MN; 10.0±7.0 %) (Figure). Apoptosis was observed in both infected and uninfected bystander cortical neurons. A high infection frequency was also observed in non-neuronal cells (astrocytes, microglia, macrophages, lymphocytes). Conclusion Our study provides valuable insights into ZIKV pathogenesis in the fetus; it is the first to demonstrate differential infectivity/susceptibility of neuronal lineage cells to ZIKV, and evidence of apoptosis in and around these cells. The high frequency of ZIKV+ IPC and IN implies that that infection can be supported until the immature stage of neuronal differentiation. The resistance of mature neurons to ZIKV infection may also explain why ZIKV infection in the third trimester poses less risk of microcephaly in infants. The high infection rate of non-neuronal cells also suggests potential contribution of immune-mediated mechanisms of brain injury in the setting of congenital ZIKV infection. Disclosures All authors: No reported disclosures.

scholarly journals Type A botulinum neurotoxin complex proteins differentially modulate host response of neuronal cells

Toxicon ◽  
2014 ◽  
Vol 82 ◽  
pp. 52-60 ◽  
Author(s):  
Lei Wang ◽  
Yi Sun ◽  
Weiping Yang ◽  
Paul Lindo ◽  
Bal Ram Singh
Keyword(s):  
Host Response ◽  
Botulinum Neurotoxin ◽  
Neuronal Cells ◽  
Type A ◽  
Neurotoxin Complex

scholarly journals Replication of the Zika virus in different iPSC-derived neuronal cells and implications to assess efficacy of antivirals

2017 ◽  
Vol 145 ◽  
pp. 82-86 ◽  
Author(s):  
Kristina Lanko ◽  
Kristel Eggermont ◽  
Abdulsamie Patel ◽  
Suzanne Kaptein ◽  
Leen Delang ◽  
...  
Keyword(s):  
Zika Virus ◽  
Neuronal Cells
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