BioProject

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. More...

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. Overall design: Comparison of differential gene expression in infected tick cell lines (Ixodes scapularis [ISE6] and Ixodes ricinus [IRE/CTVM20]) at 7 days post-infection, following infection with tick-borne flaviviruses, and Anaplasma phagocytophilum. Differential gene expression determined through comparison with mock-treated (uninfected) cells. Less...