Anaplasma phagocytophilum Inhibits Apoptosis and Promotes Cytoskeleton Rearrangement for Infection of Tick Cells

Anaplasma phagocytophilum causes human granulocytic anaplasmosis. Infection with this zoonotic pathogen affects gene expression in both the vertebrate host and the tick vector, Ixodes scapularis. Here, we identified new genes, including spectrin alpha chain or alpha-fodrin (CG8) and voltage-dependen...

Full description

Bibliographic Details
Authors: Ayllón, Nieves, Villar, Margarita, Busby, Ann T., Kocan, Katherine M., Blouin, Edmour F., Bonzón Kulichenko, Elena, Galindo, Ruth C., Mangold, Atilio Jose, Alberdi, Pilar, José M. Pérez de la Lastra, Vázquez, Jesús, De la Fuente, José
Format: article
Status:Published version
Publication Date:2013
Country:Argentina
Institution:Consejo Nacional de Investigaciones Científicas y Técnicas
Repository:CONICET Digital (CONICET)
Language:English
OAI Identifier:oai:ri.conicet.gov.ar:11336/26072
Online Access:http://hdl.handle.net/11336/26072
Access Level:Open access
Keyword:Anaplasma Phagocytophilum
Human Granulocytic Anaplasmosis
Equine Granulocytic Anaplasmosis
Ixodes Scapularis
Description
Summary:Anaplasma phagocytophilum causes human granulocytic anaplasmosis. Infection with this zoonotic pathogen affects gene expression in both the vertebrate host and the tick vector, Ixodes scapularis. Here, we identified new genes, including spectrin alpha chain or alpha-fodrin (CG8) and voltage-dependent anion-selective channel or mitochondrial porin (T2), that are involved in A. phagocytophilum infection/multiplication and the tick cell response to infection. The pathogen downregulated the expression of CG8 in tick salivary glands and T2 in both the gut and salivary glands to inhibit apoptosis as a mechanism to subvert host cell defenses and increase infection. In the gut, the tick response to infection through CG8 upregulation was used by the pathogen to increase infection due to the cytoskeleton rearrangement that is required for pathogen infection. These results increase our understanding of the role of tick genes during A. phagocytophilum infection and multiplication and demonstrate that the pathogen uses similar strategies to establish infection in both vertebrate and invertebrate hosts.

Similar Items