Bacterial Strategies to Subvert Innate Immune Defenses and Sustain Persistence

Dear Colleagues, 

Focus

This Special Issue centers on molecular and cellular mechanisms by which persistent bacterial pathogens evade and manipulate innate immune defenses to establish and maintain chronic infections. It highlights bacterial tactics targeting pattern recognition receptors, phagocyte function, inflammatory signaling, and host cell survival pathways.​

Scope

Contributions may address: PAMP modification and immune sensor antagonism; effector-mediated interference with NF-κB, MAPK, and inflammasome signaling; phagosome maturation blockade and intracellular survival strategies; biofilm formation and metabolic adaptation for persistence; cytokine network reprogramming; and links between immune subversion and clinical outcomes like relapsing infections or antibiotic tolerance. Studies spanning in vitro, animal, and human models are welcome.​

Purpose

This Special Issue aims to synthesize cutting-edge insights into bacterial immune evasion, identify therapeutic vulnerabilities in pathogen-host interactions, and inspire novel interventions that restore innate immunity or disrupt persistence niches.​

Relationship with Existing Literature 

Existing reviews comprehensively cover acute bacterial virulence factors and adaptive immunity in chronic infections but leave significant gaps in innate immune subversion mechanisms specific to persistence. While literature documents individual pathways (e.g., Legionella T4SS effectors, Mycobacterium phagosome arrest), no current collection systematically connects these tactics across diverse persistent pathogens to their role in sustaining infection rather than acute virulence.​

This Special Issue supplements the field in the following ways: 

1. Unifying fragmented insights from siloed pathogen-specific studies into a cohesive framework of innate immune modulation. 
2. Emphasizing persistence over acute infection, addressing how bacteria maintain long-term host colonization versus transient killing. 
3. Bridging environmental and host phases, exploring how adaptations precondition pathogens for innate evasion upon host entry. 
4. Highlighting translational gaps, with an emphasis on immunomodulatory therapies and diagnostics targeting evasion mechanisms.

Dr. Rajesh Palanisamy
Guest Editor

Manuscript Submission Information

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