Ticks and the pathogens they transmit constitute a growing burden for human and animal health worldwide. Vector competence is a component of vectorial capacity and depends on genetic determinants affecting the ability of a vector to transmit a pathogen. These determinants affect traits such as tick-host-pathogen and susceptibility to pathogen infection. Therefore, the elucidation of the mechanisms involved in tick-pathogen interactions that affect vector competence is essential for the identification of molecular drivers for tick-borne diseases. In this review, we provide a comprehensive overview of tick-pathogen molecular interactions for bacteria, viruses, and protozoa affecting human and animal health. Additionally, the impact of tick microbiome on these interactions was considered. Results show that different pathogens evolved similar strategies such as manipulation of the immune response to infect vectors and facilitate multiplication and transmission. Furthermore, some of these strategies may be used by pathogens to infect both tick and mammalian hosts. Identification of interactions that promote tick survival, spread, and pathogen transmission provides the opportunity to disrupt these interactions and lead to a reduction in tick burden and the prevalence of tick-borne diseases. Targeting some of the similar mechanisms used by the pathogens for infection and transmission by ticks may assist in development of preventative strategies against multiple tick-borne diseases.

• MeSH
• arachnida jako vektory mikrobiologie   parazitologie   virologie   MeSH
• interakce hostitele a patogenu * MeSH
• klíšťata mikrobiologie   parazitologie   fyziologie   virologie   MeSH
• lidé MeSH
• nemoci přenášené klíšťaty epidemiologie   MeSH
• přenos infekční nemoci * MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

• MeSH
• Anaplasma phagocytophilum MeSH
• biologická adaptace genetika   fyziologie   MeSH
• biologická evoluce MeSH
• ekologie * MeSH
• genetická transkripce genetika   MeSH
• interakce hostitele a patogenu genetika   MeSH
• klíšťata mikrobiologie   MeSH
• klíště mikrobiologie   MeSH
• molekulární evoluce MeSH
• regulace genové exprese genetika   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

The obligate intracellular pathogen, Anaplasma phagocytophilum, is the causative agent of human, equine, and canine granulocytic anaplasmosis and tick-borne fever (TBF) in ruminants. A. phagocytophilum has become an emerging tick-borne pathogen in the United States, Europe, Africa, and Asia, with increasing numbers of infected people and animals every year. It has been recognized that intracellular pathogens manipulate host cell metabolic pathways to increase infection and transmission in both vertebrate and invertebrate hosts. However, our current knowledge on how A. phagocytophilum affect these processes in the tick vector, Ixodes scapularis is limited. In this study, a genome-wide search for components of major carbohydrate metabolic pathways was performed in I. scapularis ticks for which the genome was recently published. The enzymes involved in the seven major carbohydrate metabolic pathways glycolysis, gluconeogenesis, pentose phosphate, tricarboxylic acid cycle (TCA), glyceroneogenesis, and mitochondrial oxidative phosphorylation and β-oxidation were identified. Then, the available transcriptomics and proteomics data was used to characterize the mRNA and protein levels of I. scapularis major carbohydrate metabolic pathway components in response to A. phagocytophilum infection of tick tissues and cultured cells. The results showed that major carbohydrate metabolic pathways are conserved in ticks. A. phagocytophilum infection inhibits gluconeogenesis and mitochondrial metabolism, but increases the expression of glycolytic genes. A model was proposed to explain how A. phagocytophilum could simultaneously control tick cell glucose metabolism and cytoskeleton organization, which may be achieved in part by up-regulating and stabilizing hypoxia inducible factor 1 alpha in a hypoxia-independent manner. The present work provides a more comprehensive view of the major carbohydrate metabolic pathways involved in the response to A. phagocytophilum infection in ticks, and provides the basis for further studies to develop novel strategies for the control of granulocytic anaplasmosis.

• MeSH
• Anaplasma phagocytophilum patogenita   fyziologie   MeSH
• anaplasmóza metabolismus   MeSH
• buněčné linie MeSH
• citrátový cyklus genetika   MeSH
• glukoneogeneze genetika   MeSH
• glykolýza genetika   MeSH
• interakce hostitele a patogenu genetika   MeSH
• klíště enzymologie   genetika   metabolismus   mikrobiologie   MeSH
• metabolické sítě a dráhy genetika   MeSH
• metabolismus sacharidů genetika   MeSH
• mitochondrie genetika   metabolismus   MeSH
• pentózofosfátový cyklus genetika   MeSH
• proteiny členovců chemie   genetika   metabolismus   MeSH
• proteomika metody   MeSH
• regulace genové exprese fyziologie   MeSH
• sacharidy MeSH
• slinné žlázy mikrobiologie   MeSH
• terciární struktura proteinů MeSH
• transkriptom genetika   MeSH
• zvířata MeSH
• Check Tag
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH