Tick-borne pathogens induce differential expression of genes promoting cell survival and host resistance in Ixodes ricinus cells
Abstract
[Background]: 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 vectors implicated are hard ticks of the genus Ixodes. 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 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. [Results]: Infection and transcriptional analysis of the Ixodes ricinus tick cell line IRE/CTVM20 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, putative anti-pathogen genes, and genes that influence the tick innate immune response, including selective activation of toll genes. [Conclusion]: These data provide an insight into potential key genes involved in the tick cellular response to viral or bacterial infection, which may promote cell survival and host resistance. ; This work was jointly funded by the European Commission Seventh Framework Programme under ANTIGONE (project 278976), the Department for Environment, Food and Rural Affairs (Defra), Scottish Government and Welsh Government under project SE4112, EUH2020-funded Research Infrastructure Grant 'European Virus Archive Global (EVAg)' (H2020 grant agreement number 653316) and the INIA grant E-RTA2013-C04-04 (FEDER cofunded, Spain). Lesley Bell-Sakyi is supported by the United Kingdom Biotechnology and Biological Sciences Research Council's Institute Strategic Programme Grant (BBS/E/I/0000174) to the Pirbright Institute. ; Peer Reviewed
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