Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611, USA.
Viruses. 2024 Aug 23;16(9):1348. doi: 10.3390/v16091348.
Prophages can alter their bacterial hosts to prevent other phages from infecting the same cell, a mechanism known as superinfection exclusion (SIE). Such alterations are facilitated by phage interactions with critical bacterial components involved in motility, adhesion, biofilm production, conjugation, antimicrobial resistance, and immune evasion. Therefore, the impact of SIE extends beyond the immediate defense against superinfection, influencing the overall fitness and virulence of the bacteria. Evaluating the interactions between phages and their bacterial targets is critical for leading phage therapy candidates like , a Gram-negative bacterium responsible for persistent and antibiotic-resistant opportunistic infections. However, comprehensive literature on the mechanisms underlying SIE remains scarce. Here, we provide a compilation of well-characterized and potential mechanisms employed by phages to establish SIE. We hypothesize that the fitness costs imposed by SIE affect bacterial virulence, highlighting the potential role of this mechanism in the management of bacterial infections.
噬菌体可以改变其细菌宿主，以防止其他噬菌体感染同一细胞，这种机制被称为超感染排除（SIE）。这种改变是由噬菌体与参与运动、粘附、生物膜生成、共轭、抗菌耐药性和免疫逃避的关键细菌成分相互作用而促进的。因此，SIE 的影响超出了对超感染的直接防御，影响了细菌的整体适应性和毒力。评估噬菌体与其细菌靶标的相互作用对于像噬菌体这样的噬菌体治疗候选物至关重要，噬菌体是一种革兰氏阴性菌，负责持续性和抗生素耐药性机会性感染。然而，关于 SIE 背后的机制的全面文献仍然很少。在这里，我们提供了一组经过充分表征和潜在的机制，由噬菌体用来建立 SIE。我们假设 SIE 带来的适应性成本会影响细菌的毒力，突出了这种机制在细菌感染管理中的潜在作用。
