Battling Phages: How Bacteria Defend against Viral Attack

摘要: Bacteriophages (phages) are accomplished, bacteria-specific, viral predators with far-reaching impact: from the food and biotechnology industries [1] to global nutrient cycling [2] human health disease [3]; wherever bacteria thrive, it seems, so do predatory phages. In order survive constant onslaught of phage, have evolved mechanistically diverse defense strategies that act at every stage phage life cycle (Fig 1) [4,5]. Phages rapidly co-evolve overcome these barriers, resulting in a constant, often surprising, molecular arms race [6]. this review, I highlight spectrum “innate” used by evade predation, particular attention paid more recent findings field. For discussion CRISPR-Cas adaptive immune system, readers directed several reviews [4–6]. Fig 1 An overview bacterial systems against phage. Preventing Phage Attachment A successful infection starts adsorption virus specific surface receptor. receptors, typically protein, polysaccharide, or lipopolysaccharide (LPS), must not only be present on cell, but accessible permissive spatial distribution. Therefore, prevent include modifying receptor structure through mutation concealing receptors an additional physical barrier A decrease availability can mediated phase variation which expression is subject heritable, reversible switching, allowing for population heterogeneity effort ensure survival. Bordetella bronchiseptica varies between Bvg+ phase, required pulmonary colonization, Bvg- phase. express numerous virulence colonization factors, including adhesin pertactin. use pertactin as been identified [7]. Not surprisingly, temperate phages associated clinical isolates B. bronchiseptica. Similarly, Vibrio cholerae O1 serogroup strains rely LPS antigen efficient intestinal tract. Prevalent V. samples, although virulent, temperate, relationship, depend wild-type levels expression. The variation, variants protected attenuated [8]. Although classical view its purpose facilitate evasion host system [9], also apply powerful selective forces molecules, high observed many molecules may driven either, both, forces. modulated competing Pseudomonas aeruginosa type IV pilus (TFP), important pathogenesis biofilm formation, lysogenic conversion. D3112 encodes protein called Tip binds TFP ATPase prevents localization, loss piliation protection other [10]. In some cases, hidden behind barrier, such capsule extracellular polymer. K1 Escherichia coli has shown directly interfere T7 attachment [11]. addition hiding attachment, produce decoys. T4 reduced presence outer membrane vesicles (OMVs), leading suggestion shedding OMVs into environment decoy would otherwise lead productive [12].