Chlamydia are successful obligate intracellular bacteria highly adapted to survive and propagate within host cells. As such, these pathogens have evolved many strategies to acquire nutrients and manipulate cell pathways to evade the anti-bacterial responses elicited by the host. Technical advances in imaging, high-throughput “omics”, sequencing, and genetic tools have contributed to unraveling some of the chlamydial adaptive mechanisms and virulence factors. The ability to manipulate the chlamydial genome, which has been an unreachable challenge until only a few years ago, opened the door to elucidate at the molecular level, the chlamydial factors relevant for the intracellular life-style, the pathogenic mechanisms and immune evasion that these bacteria use in order to establish acute or chronic persistent infections. To know how Chlamydia exploit host cell signaling, vesicular transport, and metabolism will help understanding bacterial survival mechanisms. Cut-on-edge information about these critical aspects of Chlamydia biology will contribute to address current challenges for controlling chlamydial infections and to the development of novel anti-chlamydial agents and preventive vaccines.
This Research Topic aims to gather the most recent breakthroughs in Chlamydia biology, pathogenesis, interactions with host cells, strategies for intracellular survival, persistence, and mechanisms for immune response evasion. Advances in these topics are key for the generation of novel preventive and therapeutic anti-chlamydial approaches.
As such, this Research Topic will focus on:
-The availability of new tools for genetic manipulation that is pivotal to address unknown aspects of Chlamydia biology
-A detailed assessment of bacterial proteins and enzymes involved in cell invasion, inclusion development, replication and exit from host cells
-Characterization of Chlamydia persistence to expand current information about chronic infections and relapse after treatment.
-Advances in critical knowledge of Chlamydia-host cell interactions to develop novel anti-chlamydial agents directed against host targets.
-Studies oriented to increase available data about chlamydial strategies to subvert adaptive and innate immune responses for designing preventive vaccines.
This collection will include manuscripts within the areas of research described above to give the reader an overview of the latest discoveries and new findings on Chlamydia.
We welcome the submission of Original Research, Reviews and mini-Reviews, which include, but are not limited to, the following topics:
1. Bacterial effectors and mechanisms of invasion and host cell exit.
2. Chlamydia-host cell interactions: the hijacking of host signaling, vesicular transport and metabolism.
3. Evasion of host innate and adaptive immune response
4. New tools for Chlamydia genetic manipulation and high-throughput omics
5. Improvements in infection treatment and new anti-chlamydial agents
6. Development of vaccines and preventive approaches
All article types accepted by Frontiers are encouraged.
Chlamydia are successful obligate intracellular bacteria highly adapted to survive and propagate within host cells. As such, these pathogens have evolved many strategies to acquire nutrients and manipulate cell pathways to evade the anti-bacterial responses elicited by the host. Technical advances in imaging, high-throughput “omics”, sequencing, and genetic tools have contributed to unraveling some of the chlamydial adaptive mechanisms and virulence factors. The ability to manipulate the chlamydial genome, which has been an unreachable challenge until only a few years ago, opened the door to elucidate at the molecular level, the chlamydial factors relevant for the intracellular life-style, the pathogenic mechanisms and immune evasion that these bacteria use in order to establish acute or chronic persistent infections. To know how Chlamydia exploit host cell signaling, vesicular transport, and metabolism will help understanding bacterial survival mechanisms. Cut-on-edge information about these critical aspects of Chlamydia biology will contribute to address current challenges for controlling chlamydial infections and to the development of novel anti-chlamydial agents and preventive vaccines.
This Research Topic aims to gather the most recent breakthroughs in Chlamydia biology, pathogenesis, interactions with host cells, strategies for intracellular survival, persistence, and mechanisms for immune response evasion. Advances in these topics are key for the generation of novel preventive and therapeutic anti-chlamydial approaches.
As such, this Research Topic will focus on:
-The availability of new tools for genetic manipulation that is pivotal to address unknown aspects of Chlamydia biology
-A detailed assessment of bacterial proteins and enzymes involved in cell invasion, inclusion development, replication and exit from host cells
-Characterization of Chlamydia persistence to expand current information about chronic infections and relapse after treatment.
-Advances in critical knowledge of Chlamydia-host cell interactions to develop novel anti-chlamydial agents directed against host targets.
-Studies oriented to increase available data about chlamydial strategies to subvert adaptive and innate immune responses for designing preventive vaccines.
This collection will include manuscripts within the areas of research described above to give the reader an overview of the latest discoveries and new findings on Chlamydia.
We welcome the submission of Original Research, Reviews and mini-Reviews, which include, but are not limited to, the following topics:
1. Bacterial effectors and mechanisms of invasion and host cell exit.
2. Chlamydia-host cell interactions: the hijacking of host signaling, vesicular transport and metabolism.
3. Evasion of host innate and adaptive immune response
4. New tools for Chlamydia genetic manipulation and high-throughput omics
5. Improvements in infection treatment and new anti-chlamydial agents
6. Development of vaccines and preventive approaches
All article types accepted by Frontiers are encouraged.