Flavivirus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA394139 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Flavivirus infection is tightly connected to host lipid metabolism. Here, we performed shotgun lipidomics of cells infected with neurotropic Zika, West Nile, and tick-borne encephalitis viruses, as well as dengue and yellow fever virus. Early in infection specific lipids accumulated, e.g., neutral lipids in Zika and some lyso-phospholipids in all infections. Ceramide levels increased following infection with viruses that cause a cytopathic effect. In addition, fatty acid desaturation as well as glycerophospholipid metabolism were significantly altered. Importantly, depletion of enzymes involved in phosphatidylserine metabolism as well as phosphatidylinositol biosynthesis reduced orthoflavivirus titers and cytopathic effects while inhibition of fatty acid monounsaturation only rescued from virus-induced cell death. Interestingly, interfering with ceramide synthesis had opposing effects on virus replication and cytotoxicity depending on the targeted enzyme. Thus, lipid remodeling by orthoflaviviruses includes distinct changes but also common patterns shared by several viruses that are needed for efficient infection and replication.
2024-09-03 | GSE264306 | GEO
Project description:<p>Flavivirus infection is tightly connected to host lipid metabolism. Here, we performed shotgun lipidomics of cells infected with neurotropic Zika, West Nile and tick-borne encephalitis viruses, as well as dengue and yellow fever virus. Early in infection specific lipids accumulated, e.g., neutral lipids in Zika and some lyso-phospholipids in all infections. Ceramide levels increased following infection with viruses that cause a cytopathic effect. In addition, fatty acid desaturation as well as glycerophospholipid metabolism were significantly altered. Importantly, depletion of enzymes involved in phosphatidylserine metabolism as well as phosphatidylinositol biosynthesis reduced orthoflavivirus titers and cytopathic effects while inhibition of fatty acid monounsaturation only rescued from virus-induced cell death. Interestingly, interfering with ceramide synthesis had opposing effects on virus replication and cytotoxicity depending on the targeted enzyme. Thus, lipid remodeling by orthoflaviviruses includes distinct changes but also common patterns shared by several viruses that are needed for efficient infection and replication.</p>
2025-02-24 | MTBLS11030 | MetaboLights
Project description:To identify novel host factors essential for flavivirus replication, we performed proteomic profiling of endoplasmic reticulum (ER) fractions isolated from cells infected with Dengue virus (DENV) or Zika virus (ZIKV)
2025-10-09 | PXD069297 |
Project description:To search for host factors regulating Zika virus infection, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of enrichment of their mutant clones within a pooled loss-of-function library upon Zika virus infection.
2023-05-31 | E-MTAB-11945 | biostudies-arrayexpress
Project description:West Nile virus (WNV) is an emerging mosquito-borne flavivirus, related to dengue virus and Zika virus. To gain insight into host pathways involved in WNV infection, we performed a systematic affinity-tag purification mass spectrometry (AP-MS) study to identify 259 WNV-interacting human proteins. RNAi screening revealed 26 genes that both interact with WNV proteins and influence WNV infection. We found that WNV, dengue and Zika virus capsids interact with a conserved subset of proteins that impact infection. These include the exon-junction complex (EJC) recycling factor, PYM1, which is antiviral against all three viruses. The EJC has roles in nonsense-mediated decay (NMD), and we found that both the EJC and NMD are antiviral. Mechanistically, we found that the EJC protein RBM8A directly binds WNV RNA. To counteract this antiviral defense, flavivirus infection inhibits NMD and the interaction of capsid with PYM1 interferes with EJC protein function and localization. Moreover, depletion of PYM1 attenuates RBM8A binding to viral RNA, suggesting that WNV sequesters PYM1 to protect viral RNA from decay. Together, these data suggest a complex interplay between the virus and host in regulating NMD and the EJC complex.
2019-11-14 | PXD011728 | Pride
Project description:Zika virus (ZIKV) is a mosquito-transmitted positive-sense RNA virus in the family Flaviviridae. Live attenuated vaccines have been successfully used to combat infection by flaviviruses, such as yellow fever and Japanese encephalitis viruses. A Zika virus harboring combined mutations in the envelope protein glycosylation site and in the nonstructural 4B protein amino acid 36 (ZE4B-36) was generated and assessed for stability, attenuation, and protection against infection. To determine the genetic stability of its RNA genome, ZE4B-36 was serially passaged in vitro in Vero cells. Virus harvested from passages (P)1 to P6 was subjected to next generation sequencing and downstream analysis to determine its nucleotide sequence variability. Specifically, single nucleotide variant analysis showed that the ZE4B-36 genome decreased its genetic diversity and resulted in a more stable nucleotide sequence. Thus, in addition to showing attenuation and protection, ZE4B-36 is a stable live attenuated virus that possesses characteristics important for a vaccine to combat Zika disease.
2021-12-31 | E-MTAB-9496 | biostudies-arrayexpress
Project description:Human neural progenitor cell (hNPC) transcriptomic responses to infections with Zika virus (ZIKV), Powassan virus (POWV), or two strains of West Nile virus were analyzed at three times after infection in a single batch of hNPCs differentiated from induced pluripotent stem cells. The WNV infections displayed the fastest replication kinetics but the POWV infection produced the highest viral yield. All four infections upregulated common and unique innate immune and antiviral response genes by 12 hpi and induced upregulation of stress pathway genes by 24 hpi. The WNV infections downregulated cell cycle genes earlier than the ZIKV or POWV infections. Transcription factors regulating gene expression changes were predicted. All four orthoflaviviruses dysregulated the expression of 262 microcephaly-associated genes, with virus-specific differences in the extent of dysregulation. The data suggest that fetal hNPC infection in utero by each of the four orthoflaviviruses studied could induce neurodevelopmental disorders.
2026-04-02 | GSE309623 | GEO
Project description:Flavivirus infection involves extensive remodeling of the endoplasmic reticulum (ER), which is key to both the replication of the viral RNA genome as well as the assembly and release of new virions. Yet, little is known about how viral proteins and host factors cooperatively facilitate such a vast transformation of the ER, and how this influences the different steps of the viral life cycle. In this study, we screened for host proteins that interact with the tick-borne encephalitis virus (TBEV) protein NS4B and found that the top candidates were coupled to trafficking between ER exit sites (ERES) and the Golgi. We characterized the role of ACBD3, one of the identified proteins, in flavivirus infection and show that it interacts with NS4B to promote infection across multiple flavivirus species. Using ACBD3 knockout cells, we found that the depletion of ACBD3 inhibited TBEV replication by preventing the trafficking of virions from the cell. We found that ACBD3 promotes flavivirus infection via a different mechanism than its previously described role in picornavirus infection. ACBD3 was enriched at modified ERES-Golgi contact sites to support virus replication. Therefore, we propose that ACBD3 promotes flavivirus replication by modifying the trafficking between the ERES and the Golgi to enable the release of new virions.
2025-03-31 | PXD051173 | Pride
Project description:<p>Tick-borne encephalitis virus is an enveloped, pathogenic, RNA virus in the family Flaviviridae, genus Flavivirus. Viral particles are formed when the nucleocapsid, consisting of an RNA genome and multiple copies of the capsid protein, buds through the endoplasmic reticulum membrane and acquires the viral envelope and the associated proteins. The coordination of the nucleocapsid components to the sites of assembly and budding are poorly understood. Here, we investigate nucleocapsid assembly by characterizing the interactions of the wild-type and truncated capsid proteins with membranes by using biophysical methods and model membrane systems. We show that capsid protein initially binds membranes via electrostatic interactions with negatively-charged lipids which is followed by membrane insertion. Additionally, we show that membrane-bound capsid protein can recruit viral genomic RNA. We confirm the biological relevance of the biophysical findings by using mass spectrometry to show that purified virions contain negatively-charged lipids. Our results suggest that nucleocapsid assembly is coordinated by negatively-charged membrane patches on the endoplasmic reticulum and that the capsid protein mediates direct contacts between the nucleocapsid and the membrane.</p>
2023-01-06 | MTBLS6076 | MetaboLights
Project description:Zika virus (ZIKV), a mosquito-borne flavivirus, has imposed tremendous global threat to human health and was declared as a public health emergency of international concern by the World Health Organization in 2016. However, the pathogenic mechanism of ZIKV still lacks sufficient understanding. In recent years, the development of single-cell sequencing technology has provided a more precise approach for exploring disease mechanisms. Therefore, in this study, we depicted a high-resolution transcriptomic landscape and functional changes of brain immune and neural cells during disease progression of ZIKV, which will facilitate a better understanding of the underlying pathogenesis of ZIKV-induced microcephaly.
2026-06-01 | GSE233624 | GEO