Yellow fever virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA548475 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9597072.fastq.gz | Fastqsanger.gz | |||
| SRR9597073.fastq.gz | Fastqsanger.gz |
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Project description:Host cells produce interferon (IFN) in response to viral infections. Secreted interferon results in the transcription and production of hundreds of interferon-stimulated genes (ISGs). A genome-wide CRISPR screen using IFN alpha-treated Huh7.5 cells was performed to determine which ISGs were required in order for host cells to suppress yellow fever virus (YFV) infection.
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Project description:In this study, we describe a viral suppressor of RNA silencing encoded by the prototype flavivirus, yellow fever virus (YFV). We show that the YFV capsid protein inhibits RNA silencing in the mosquito Aedes aegypti by interfering with Dicer. These results suggest a molecular arms race between vector and pathogen underlies the continued existence of flaviviruses in nature.
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Project description:Central questions regarding the origin of memory CD8 T cells, their turnover and longevity in vivo are not well-defined in humans. Here, we have used the highly efficacious live yellow fever virus vaccine (YFV-17D) to address these issues in the context of a primary acute viral infection. We interrogated genome-wide CpG methylation of YFV tetramer-specific CD8 T cells. These findings provide a better understanding of how memory CD8 T cells are formed and maintained in humans.
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Project description:Yellow fever virus Genome sequencing and assembly
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Project description:Yellow fever (YF) is a life-threatening mosquito-borne disease prevalent in South America and Africa, accounting for up to 60,000 annual deaths. Between December 2016 and May 2018, Brazil reported its worst YF outbreak this century with a fatality rate of 33.6%. While YF vaccines have shown protective capabilities, the genetic profile of those infected with the wild-type YF virus (YFV) remains uncharacterized. Building on recent findings by Kallas et al. (2019), which discerned clinical and immunological determinants of YF mortality, we conducted a comprehensive transcriptional profiling of blood samples from YFV-infected patients. Our investigation integrated omics data with clinical and immunological metrics, contrasting the wild-type YFV acute infection signature against the response triggered by the YF17D vaccine strain and the signature linked to severe COVID-19. Our analyses revealed key molecular mechanisms of YFV infection and determinants of disease severity. Notably, a comparative assessment elucidated distinct gene expression patterns between wild-type YFV infections, YF17D vaccination, and severe COVID-19. This study offers pivotal insights into the molecular underpinnings of YFV infection and its severity, potentially enhancing our comprehension of viral infections at large.
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Project description:The yellow fever virus 17D (YFV-17D) live attenuated vaccine is considered one of the successful vaccines ever generated associated with high antiviral immunity, yet the signaling mechanisms that drive the response in infected cells are not understood. Here, we provide a molecular understanding of how metabolic stress and innate immune responses are linked to drive type I IFN expression in response to YFV-17D infection. Comparison of YFV-17D replication with its parental virus, YFV-Asibi, and a related dengue virus revealed that IFN expression requires RIG-I-like Receptor signaling through MAVS, as expected. However, YFV-17D uniquely induces mitochondrial respiration and major metabolic perturbations, including hyperactivation of electron transport to fuel ATP synthase. Mitochondrial hyperactivity generates reactive oxygen species (ROS) including peroxynitrite, blocking of which abrogated MAVS oligomerization and IFN expression in non-immune cells without reducing YFV-17D replication. Scavenging ROS in YFV-17D-infected human dendritic cells increased cell viability yet globally prevented expression of IFN signaling pathways. Thus, adaptation of YFV-17D for high growth imparts mitochondrial hyperactivity to meet energy demands, resulting in generation of ROS as the critical messengers that convert a blunted IFN response into maximal activation of innate immunity essential for vaccine effectiveness.
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Project description:Yellow fever virus full genome sequencing and assembly
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Project description:Yellow fever virus, a prototypical member of the Flaviviridae family, is a small single-stranded, positive sense enveloped RNA virus causing viscerotropic, frequently fatal disease. Serial passaging of the virulent YFV Asibi strain in the 1930s yielded the YFV17D strain which remains one of the most effective vaccines ever developed. Remarkably, YFV17D and the virulent parental genome differ only by 68 nucleotides leading to 32 amino acid changes. However, it remains largely unknown which of these sequence differences are responsible for attenuation. Here, we demonstrate that while synonymous mutations are highly conserved across pathogenic YFVs they do not contribute to the characteristic host responses elicited by 17D or virulent viruses. Using a highly modular combinatorial genetic approach we identified key genetic elements in the YFV envelope and non-structural 2A (NS2A) proteins that govern the virus’ ability to spread and suppress host responses.. Introducing these mutations into infectious clones of other YFV genomes results in viral attenuation in vitro and in vivo. Collectively, our results define the genetic basis for YFV17D attenuation and highlight a general approach for creating live-attenuated vaccines for other pathogenic viruses.
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Project description:Yellow fever virus, a prototypical member of the Flaviviridae family, is a small single-stranded, positive sense enveloped RNA virus causing viscerotropic, frequently fatal disease. Serial passaging of the virulent YFV Asibi strain in the 1930s yielded the YFV17D strain which remains one of the most effective vaccines ever developed. Remarkably, YFV17D and the virulent parental genome differ only by 68 nucleotides leading to 32 amino acid changes. However, it remains largely unknown which of these sequence differences are responsible for attenuation. Here, we demonstrate that while synonymous mutations are highly conserved across pathogenic YFVs they do not contribute to the characteristic host responses elicited by 17D or virulent viruses. Using a highly modular combinatorial genetic approach we identified key genetic elements in the YFV envelope and non-structural 2A (NS2A) proteins that govern the virus’ ability to spread and suppress host responses.. Introducing these mutations into infectious clones of other YFV genomes results in viral attenuation in vitro and in vivo. Collectively, our results define the genetic basis for YFV17D attenuation and highlight a general approach for creating live-attenuated vaccines for other pathogenic viruses.
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