Antiviral RNA interference in disease vector (Asian longhorned) ticks
| Autor: | Yang Li, Liting Ma, Yan Xu, Chuang Gao, Yanxin Ren, Zhi Ye, Jingwen Wang, Zhengwei Zhong |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Molecular biology
Physiology viruses Disease Vectors Biochemistry Mice RNA interference Sequencing techniques Medical Conditions Ticks RNA Virus Infections Medicine and Health Sciences Nodaviridae RNA Small Interfering Biology (General) Gene knockdown Mammalian Genomics biology Drosophila Melanogaster Eukaryota RNA sequencing Genomics Animal Models Small interfering RNA Body Fluids Nucleic acids Insects Infectious Diseases Blood Genetic interference Experimental Organism Systems Tick-Borne Diseases Host-Pathogen Interactions Epigenetics Drosophila Haemaphysalis longicornis Anatomy Research Article Nodamura virus Sindbis virus Arthropoda Severe Fever with Thrombocytopenia Syndrome QH301-705.5 Immunology Tick Microbiology Virus Model Organisms Virology Arachnida parasitic diseases Genetics Animals Non-coding RNA Biology and life sciences Ixodes Organisms RC581-607 biology.organism_classification bacterial infections and mycoses Invertebrates Viral Replication Gene regulation Research and analysis methods Species Interactions Disease Models Animal Molecular biology techniques Viral replication Animal Genomics Animal Studies RNA Parasitology Gene expression Sindbis Virus Immunologic diseases. Allergy Zoology Entomology |
| Zdroj: | PLoS Pathogens, Vol 17, Iss 12, p e1010119 (2021) PLoS Pathogens |
| ISSN: | 1553-7374 1553-7366 |
| Popis: | Disease vectors such as mosquitoes and ticks play a major role in the emergence and re-emergence of human and animal viral pathogens. Compared to mosquitoes, however, much less is known about the antiviral responses of ticks. Here we showed that Asian longhorned ticks (Haemaphysalis longicornis) produced predominantly 22-nucleotide virus-derived siRNAs (vsiRNAs) in response to severe fever with thrombocytopenia syndrome virus (SFTSV, an emerging tick-borne virus), Nodamura virus (NoV), or Sindbis virus (SINV) acquired by blood feeding. Notably, experimental acquisition of NoV and SINV by intrathoracic injection also initiated viral replication and triggered the production of vsiRNAs in H. longicornis. We demonstrated that a mutant NoV deficient in expressing its viral suppressor of RNAi (VSR) replicated to significantly lower levels than wildtype NoV in H. longicornis, but accumulated to higher levels after knockdown of the tick Dicer2-like protein identified by phylogeny comparison. Moreover, the expression of a panel of known animal VSRs in cis from the genome of SINV drastically enhanced the accumulation of the recombinant viruses. This study establishes a novel model for virus-vector-mouse experiments with longhorned ticks and provides the first in vivo evidence for an antiviral function of the RNAi response in ticks. Interestingly, comparing the accumulation levels of SINV recombinants expressing green fluorescent protein or SFTSV proteins identified the viral non-structural protein as a putative VSR. Elucidating the function of ticks’ antiviral RNAi pathway in vivo is critical to understand the virus-host interaction and the control of tick-borne viral pathogens. Author summary 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. |
| Databáze: | OpenAIRE |
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