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. 2017 Apr 7;7:114. doi: 10.3389/fcimb.2017.00114

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Copyright © 2017 de la Fuente, Antunes, Bonnet, Cabezas-Cruz, Domingos, Estrada-Peña, Johnson, Kocan, Mansfield, Nijhof, Papa, Rudenko, Villar, Alberdi, Torina, Ayllón, Vancova, Golovchenko, Grubhoffer, Caracappa, Fooks, Gortazar and Rego.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Tick-pathogen molecular interactions. (A) A. phagocytophilum (B) B. burgdorferi s.l., (C) TBEV, and (D) B. bovis/B. bigemina activate mechanisms (panel 1) and manipulate tick protective responses and other biological processes in order to facilitate infection (panel 2), while ticks respond to limit pathogen infection and preserve feeding fitness and vector competence for survival of both ticks and pathogens (panel 3). MG, midgut; HE, hemocyte; SG, salivary gland; MSPs, major surface proteins; HSPs, heat shock proteins; ER, endoplasmic reticulum.