General Information:

Id: 2,024 (click here to show other Interactions for entry)
Diseases: Q fever
pathogen-host system
Coxiella burnetii/mammalia
review
Reference: Oyston PC and Davies C(2011) Q fever: the neglected biothreat agent J. Med. Microbiol. 60: 9-21 [PMID: 21030501]

Interaction Information:

Comment Coxiella burnetii is the causative agent of Q fever, a disease with a spectrum of presentations from the mild to fatal, including chronic sequelae.
Formal Description
Interaction-ID: 16087

process

Coxiella burnetii infection

increases_activity of

disease

Q fever, acute

Comment C. burnetii can infect a range of cells, including monocytes and macrophages, and cell lines, including macrophages, fibroblast and epithelial cells.
Formal Description
Interaction-ID: 16141

process

Coxiella burnetii infection

increases_activity of

Comment C. burnetii can infect a range of cells, including monocytes and macrophages, and cell lines, including macrophages, fibroblast and epithelial cells.
Formal Description
Interaction-ID: 16142

process

Coxiella burnetii infection

increases_activity of

Comment The uterus and mammary glands are sites of chronic C. burnetii infection in females, and this is associated with abortions in goats and sheep, and infertility in cattle.
Formal Description
Interaction-ID: 16143

process

Coxiella burnetii infection

is localized in

tissue/cell line

mammary gland

during chronic infection
Comment The uterus and mammary glands are sites of chronic C. burnetii infection in females, and this is associated with abortions in goats and sheep, and infertility in cattle.
Formal Description
Interaction-ID: 16144

process

Coxiella burnetii infection

is localized in

tissue/cell line

uterus

during chronic infection
Comment The alveolar macrophage has been proposed as the primary target.
Formal Description
Interaction-ID: 16149

process

Coxiella burnetii infection

is localized in

tissue/cell line

alveolar macrophage

Comment Although IFN-gamma is key to controlling Q fever, apoptosis is closely controlled by the invading Coxiella to maintain viability of the host cell during the lengthy inhabitation. Infected host cells show decreased caspase activity, induction of a pro-survival transcriptional response, including Akt and Erk 1/2 activation, and decreased release of cytochrome c.
Formal Description
Interaction-ID: 16241

process

Coxiella burnetii infection

decreases_activity of

process

host cell apoptosis

in infected host cells
Comment Although IFN-gamma is key to controlling Q fever, apoptosis is closely controlled by the invading Coxiella to maintain viability of the host cell during the lengthy inhabitation. Infected host cells show decreased caspase activity, induction of a pro-survival transcriptional response, including Akt and Erk 1/2 activation, and decreased release of cytochrome c.
Formal Description
Interaction-ID: 16242

process

Coxiella burnetii infection

increases_activity of

in infected host cells
Comment Although IFN-gamma is key to controlling Q fever, apoptosis is closely controlled by the invading Coxiella to maintain viability of the host cell during the lengthy inhabitation. Infected host cells show decreased caspase activity, induction of a pro-survival transcriptional response, including Akt and Erk 1/2 activation, and decreased release of cytochrome c.
Formal Description
Interaction-ID: 16243

process

Coxiella burnetii infection

increases_activity of

in infected host cells
Comment Coxiella burnetii is the causative agent of Q fever, a disease with a spectrum of presentations from the mild to fatal, including chronic sequelae.
Formal Description
Interaction-ID: 17575

process

Coxiella burnetii infection

increases_activity of

disease

Q fever, chronic