Coxiella burnetii protein CBU2016 supports CCV expansion

• Published in: Pathogens and disease Vol. 82
• Main Authors: Thomas, David R, Garnish, Sarah E, Khoo, Chen Ai, Padmanabhan, Bhavna, Scott, Nichollas E, Newton, Hayley J
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 07.02.2024
• Subjects: Animals; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Cell Line; Coxiella burnetii - genetics; Coxiella burnetii - metabolism; Coxiella burnetii - pathogenicity; Gene Knockout Techniques; HeLa Cells; Host-Pathogen Interactions; Humans; Moths - microbiology; Q Fever - microbiology; THP-1 Cells; Vacuoles - metabolism; Vacuoles - microbiology; Virulence Factors - genetics; Virulence Factors - metabolism; Dot/Icm secretion system; replicative vacuole; Coxiella burnetii; intracellular bacterial pathogen
• ISSN: 2049-632X; 2049-632X
• DOI: 10.1093/femspd/ftae018

Coxiella burnetii is a globally distributed obligate intracellular pathogen. Although often asymptomatic, infections can cause acute Q fever with influenza-like symptoms and/or severe chronic Q fever. Coxiella burnetii develops a unique replicative niche within host cells called the Coxiella-containing vacuole (CCV), facilitated by the Dot/Icm type IV secretion system translocating a cohort of bacterial effector proteins into the host. The role of some effectors has been elucidated; however, the actions of the majority remain enigmatic and the list of true effectors is disputable. This study examined CBU2016, a unique C. burnetii protein previously designated as an effector with a role in infection. We were unable to validate CBU2016 as a translocated effector protein. Employing targeted knock-out and complemented strains, we found that the loss of CBU2016 did not cause a replication defect within Hela, THP-1, J774, or iBMDM cells or in axenic media, nor did it affect the pathogenicity of C. burnetii in the Galleria mellonella infection model. The absence of CBU2016 did, however, result in a consistent decrease in the size of CCVs in HeLa cells. These results suggest that although CBU2016 may not be a Dot/Icm effector, it is still able to influence the host environment during infection.