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Tick-borne encephalitis virus

ABSTRACT: Tick-borne encephalitis virus Genome sequencing

PROVIDER: PRJNA1090781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28468905_1.fastq.gz	Fastqsanger.gz
	SRR28468906_1.fastq.gz	Fastqsanger.gz
	SRR28468907_1.fastq.gz	Fastqsanger.gz
	SRR28468908_1.fastq.gz	Fastqsanger.gz
	SRR28468909_1.fastq.gz	Fastqsanger.gz

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Sequential MAVS- and MyD88/TRIF-signaling triggers anti-viral responses of tick-borne encephalitis virus-infected murine astrocytes

Project description:Upon tick borne encephalitis virus exposure of brain-resident cells, astrocytes are important IFN-β producers that followed a biphasic response, which initially depends on MAVS- and later on MyD88/TRIF-signaling

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Genotype-Driven Sensitivity in Mice to Tick-Borne Encephalitis Virus Correlates with Differential Host Responses in Peripheral Macrophages and Brain

Project description:Tick-borne encephalitis (TBE) is the most common tick-borne viral infection in Eurasia, with outcomes ranging from asymptomatic to fatal encephalitis. While the reasons for this variability are unclear, host genetics likely plays a role. Our previous research showed that BALB/c mice have intermediate susceptibility to TBE virus (TBEV), STS mice are highly resistant, and the recombinant congenic strain CcS-11, which has 12.5% of the STS genome on the BALB/c background, is more susceptible than the BALB/c. In this study, we used these three mouse strains to investigate the host response to TBEV infection in both peripheral macrophages, one of the initial target cell populations, and in the brain, the terminal target organ for the virus.

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Project description:There are very few studies exploring the genetic diversity of tick-borne encephalitis complex viruses. Most of the viruses have been sequenced using capillary electrophoresis, however, very few viruses have been analyzed using deep sequencing to look at the genotypes in each virus population. In this study, different viruses and strains belonging to the tick-borne encephalitis complex were sequenced and genetic diversity was analyzed. Shannon entropy and single nucleotide variants were used to compare the viruses. Then genetic diversity was compared to the phylogenetic relationship of the viruses.

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Multi-omics unveils host perturbations by tick-borne encephalitis virus for therapeutic targets

Project description:Multi-omics unveils host perturbations by tick-borne encephalitis virus for therapeutic targets

2024-01-09 | PXD048439 |

Simultaneous Membrane and RNA Binding by Tick-Borne Encephalitis Virus Capsid Protein

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>

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Secreted NS1 proteins of tick-borne encephalitis virus and West Nile virus block dendritic cell activation and effector functions

Project description:Flavivirus non-structural protein 1 (NS1) is secreted from cells in infected individuals and in cell culture and levels correlate with disease severity. Treatment of murine bone marrow–derived dendritic cells (BMDCs) with recombinantly produced solube NS1 (sNS1) of tick-borne encephalitis virus (TBEV) or West Nile virus (WNV) prior to poly(I:C) stimulation revealed two gene clusters that were downregulated by TBEV or WNV sNS1 and that were associated with innate and adaptive immune responses. Especially co-stimulatory molecules and pro-inflammatory cytokines as well as chemokines were found to be downregulated in sNS1 pre-treated BMDCs prior to poly(I:C) stimulation.

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Tick-borne Pathogens Induce Differential Expression of Genes Promoting Cell Survival and Host Resistence in Ixodes ricinus Cells

Project description:There has been an emergence and expansion of tick-borne diseases in Europe, Asia and North America in recent years, including Lyme disease, tick-borne encephalitis, and human anaplasmosis. The primary tick vectors implicated are hard ticks of the Ixodes genera. Although much is known about the host response to these bacterial and viral pathogens, there is limited knowledge of the cellular responses to infection within the tick vector. The bacterium Anaplasma phagocytophilum (A. phagocytophilum), is able to bypass apoptotic processes in ticks, enabling infection to proceed. However, the tick cellular responses to infection with the flaviviruses tick-borne encephalitis virus (TBEV) and louping ill virus (LIV), which cause tick-borne encephalitis and louping ill respectively, are less clear. Infection of an Ixodes ricinus (I. ricinus) tick cell line with the viruses LIV and TBEV, and the bacterium A. phagocytophilum, identified activation of common and distinct cellular pathways. In particular, commonly-upregulated genes included those that modulate apoptotic pathways (HSP70), putative anti-pathogen genes (FKBP and XBL1), and genes that influence the tick innate immune response, including selective activation of toll genes. These data provide an insight into potentially key genes involved in the tick cellular response to viral or bacterial infection.

2017-01-01 | GSE85300 | GEO

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