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Tick-Pathogen Interactions and Vector Competence: Identification of Molecular Drivers for Tick-Borne Diseases

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ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

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.
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Figure 2: 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.

Mentions: Intracellular bacteria induce cytoskeletal rearrangement to establish infection (Ireton, 2013). In I. scapularis, A. phagocytophilum remodels tick cytoskeleton by altering the ratio between monomeric globular G actin and filamentous F actin to facilitate infection through selective regulation of gene transcription in association with the RNA polymerase II and the TATA-binding protein (Sultana et al., 2010). In I. scapularis midgut cells, the up-regulation of Spectrin alpha chain or Alpha-fodrin in response to infection results in cytoskeleton remodeling that is used by A. phagocytophilum to facilitate infection (Ayllón et al., 2013, Figure 2A). Although not functionally characterized, a proteomics analysis in I. ricinus tick salivary glands showed the under-representation of cytoskeleton proteins in response to Borrelia infection, suggesting that some Borrelia strains promote a cytoskeleton rearrangement in ticks (Cotté et al., 2014, Figure 2B).


Tick-Pathogen Interactions and Vector Competence: Identification of Molecular Drivers for Tick-Borne Diseases
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.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5383669&req=5

Figure 2: 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.
Mentions: Intracellular bacteria induce cytoskeletal rearrangement to establish infection (Ireton, 2013). In I. scapularis, A. phagocytophilum remodels tick cytoskeleton by altering the ratio between monomeric globular G actin and filamentous F actin to facilitate infection through selective regulation of gene transcription in association with the RNA polymerase II and the TATA-binding protein (Sultana et al., 2010). In I. scapularis midgut cells, the up-regulation of Spectrin alpha chain or Alpha-fodrin in response to infection results in cytoskeleton remodeling that is used by A. phagocytophilum to facilitate infection (Ayllón et al., 2013, Figure 2A). Although not functionally characterized, a proteomics analysis in I. ricinus tick salivary glands showed the under-representation of cytoskeleton proteins in response to Borrelia infection, suggesting that some Borrelia strains promote a cytoskeleton rearrangement in ticks (Cotté et al., 2014, Figure 2B).

View Article: PubMed Central - PubMed

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus