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.
2024-01-16 | GSE165139 | GEO
Project description:Meta-transcriptomics for the diversity of tick-borne virus in Nujiang, Yunnan Province
| PRJNA1041966 | ENA
Project description:Meta-transcriptomics for virus diversity in patients with fever with thrombocytopenia syndrome in Shandong
Project description:Tick-borne diseases (TBDs) are the most common illnesses transmitted by ticks, and the annual number of reported TBD cases continues to increase. The Asian longhorned tick, a vector associated with at least 30 human pathogens, is native to eastern Asia and recently reached the USA as an emerging disease threat. Newly identified tick-transmitted pathogens continue to be reported, raising concerns about how TBDs occur. Interestingly, tick can harbor pathogens without being affected themselves. For viral infections, ticks have their own immune systems that protect them from infection. Meanwhile, tick-borne viruses have evolved to avoid these defenses as they establish themselves within the vector. Here, we show in detail that infecting longhorned ticks with distinct arthropod-borne RNA viruses through two approaches natural blood feeding and injection, all induce the production of vsiRNAs. Dicer2-like homolog plays a role in regulating antiviral RNAi responses as knocking down of this gene enhanced viral replication. Furthermore, we demonstrate that tick antiviral RNAi responses are inhibited through expression heterologous VSR proteins in recombinant SINV. We identify both the virus and tick factors are critical components to understanding TBDs. Importantly, our study introduces a novel, in vivo virus-vector-mouse model system for exploring TBDs in the future.