Fig 1.
Tick–host–pathogen interactions: conflict and cooperation.
(A) Conflict. Ticks produce a feeding lesion and inhibit host hemostatic, immune, and inflammatory responses to complete feeding, while hosts react locally and systemically to tick infestation. Ticks react to pathogen infection by activating different mechanisms to limit pathogen infection, while pathogens manipulate tick biological processes such as innate immune response and apoptosis to facilitate infection, multiplication, and transmission. Pathogens inhibit host immune response, among other mechanisms, to facilitate infection, but at the same time, hosts react to pathogen infection by activating different mechanisms to control pathogen infection. (B) Cooperation. Ticks benefit from hosts by promoting feeding after deviation of host response to tick bite, while hosts may benefit from tick infestation by increased resistance to pathogen infection. Ticks benefit from pathogen infection by increased survival at low and high temperatures and fitness, while pathogens manipulate tick biological processes to facilitate infection but without affecting tick feeding and reproduction. Pathogens benefit from host response to facilitate infection, while hosts may benefit from pathogen infection by interference with and reduced susceptibility to infection with other more lethal pathogens or by bacterial-induced epigenetic deregulations that could promote host defense to infection.
Table 1.
Examples of the conflict and cooperation events acting on tick–host–pathogen interactions.
Fig 2.
Ixodes scapularis tick–A. phagocytophilum coevolution.
The pathogen inhibits apoptosis by reducing porin levels to increase infection but without affecting tick feeding and reproduction, as illustrated after gene knockdown to maintain tick vector capacity. However, the pathogens do not manipulate subolesin levels because, as shown after gene knockdown, it can affect infection and tick performance. These results illustrate coevolutionary mechanisms by which pathogens manipulate tick protective responses to facilitate infection while preserving tick feeding and vector capacity to guarantee survival of both pathogens and ticks.