# Modulation of host cell pathways by Coxiella burnetii Dot/Icm effectors

## TL;DR

This review explores how Coxiella burnetii uses its Dot/Icm system to manipulate host cells, supporting its survival and replication.

## Contribution

The paper provides a comprehensive summary of recent advances in understanding the Dot/Icm system and its effectors in Coxiella burnetii.

## Key findings

- The Dot/Icm system is essential for Coxiella burnetii virulence and intracellular replication.
- Effectors delivered by the Dot/Icm system modulate host cell pathways to form a Coxiella-containing vacuole.
- Understanding these mechanisms is crucial for developing new treatments against Coxiella infections.

## Abstract

Coxiella burnetii, the etiological agent of Q fever, is a significant intracellular bacterial pathogen. C. burnetii is a highly infectious pathogen that primarily targets pulmonary alveolar macrophages during natural infection. It can then disseminate to macrophages in other tissues and organs, leading to chronic infections. C. burnetii is capable of infecting a variety of cultured cells, including primary macrophages, macrophage‐like cells, epithelial cells, and fibroblasts. The virulence of C. burnetii is entirely dependent on the Dot/Icm type IVB secretion system (T4BSS), which delivers effectors into infected cells to modulate cellular pathways for the biogenesis of the Coxiella‐containing vacuole that supports its intracellular replication. A deeper understanding of how C. burnetii exploits host cell processes is essential for developing novel therapeutic strategies to combat infections caused by this important pathogen. This review summarizes the historical milestones and recent advances in our understanding of the structure and function of the C. burnetii Dot/Icm system and its effectors.