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Arthropod-borne virus

ABSTRACT: Genome sequencing of vector-borne viruses to understand genetic diversity and evolutionary dynamics.

PROVIDER: PRJNA289885 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7588753.fastq.gz	Fastqsanger.gz
	SRR7588753_1.fastq.gz	Fastqsanger.gz
	SRR7588753_2.fastq.gz	Fastqsanger.gz
	SRR7588754.fastq.gz	Fastqsanger.gz
	SRR7588754_1.fastq.gz	Fastqsanger.gz

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Induction and suppression of Haemaphysalis longicornis ticks antiviral RNA interference responses by arthropod-borne RNA viruses (RNA-Seq)

Project description:Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne bunyavirus that causes severe clinical symptoms and mortality in humans. Haemaphysalis longicornis tick has been identified as the competent vector for SFTSV transmission. Although antiviral RNA interference (RNAi) in insects has been well documented, the degree to which RNAi contributes to antiviral defense in ticks is still largely elusive. In this study, utilizing arthropod-borne RNA viruses, including SFTSV, we find abundant virus-derived small interfering RNAs (vsiRNAs) are induced in H. longicornis after infection through either microinjection or natural blood-feeding. Furthermore, we identify a Dicer2-like homolog, the core protein of antiviral RNAi pathway, in H. longicornis and knocking down this gene exacerbated virus amplification. To counteract this antiviral RNAi of ticks, viruses have evolved suppressors of RNAi (VSRs). Here, we show that reduced viral replication inversely correlated with the accumulation of vsiRNAs in ticks after infection with recombinant sindbis virus (SINV) expressing heterologous VSR proteins. Elucidating the antiviral RNAi pathway of ticks by model arthropod-borne RNA viruses in vivo is critical to understanding the virus-host interaction, providing a feasible intervention strategy to control tick-borne arbovirus transmission.

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Project description:Beet necrotic yellow vein virus (BNYVV) and Beet soil-borne mosaic virus (BSBMV) belong to the genus Benyvirus. Both viruses share a similar genome organization, but disease development induced in their major host plant sugar beet displays striking differences. BNYVV induces excessive lateral root (LR) formation by hijacking auxin-regulated pathways; whereas BSBMV infected roots appear asymptomatic. To elucidate transcriptomic changes associated with the virus-specific disease development of BNYVV and BSBMV, we performed a comparative transcriptome analysis of a virus infected susceptible sugar beet genotype.

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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.

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