Pf bacteriophage are temperate phages that infect the bacterium Pseudomonas aeruginosa, a major cause of chronic lung infections in cystic fibrosis (CF) and other settings. Pf and other temperate phages have evolved complex, mutualistic relationships with their bacterial hosts that impact both bacterial phenotypes and chronic infection. We and others have reported that Pf phages are a virulence factor that promote the pathogenesis of P. aeruginosa infections in animal models and are associated with worse skin and lung infections in humans. Here we review the biology of Pf phage and what is known about its contributions to pathogenesis and clinical disease. First, we review the structure, genetics, and epidemiology of Pf phage. Next, we address the diverse and surprising ways that Pf phages contribute to P. aeruginosa phenotypes including effects on biofilm formation, antibiotic resistance, and motility. Then, we cover data indicating that Pf phages suppress mammalian immunity at sites of bacterial infection. Finally, we discuss recent literature implicating Pf in chronic P. aeruginosa infections in CF and other settings. Together, these reports suggest that Pf bacteriophage have direct effects on P. aeruginosa infections and that temperate phages are an exciting frontier in microbiology, immunology, and human health.

Lytic viruses kill almost 20% of marine bacteria every day, re-routing nutrients away from the higher trophic levels of the marine food web and back in the microbial loop. Importantly, the effect of this inflow of key elements on the ecosystem depends on the nutrient requirements of bacteria as well as on the elemental composition of the viruses that infect them. Therefore, the influence of viruses on the ecosystem could vary depending on which nutrient is limiting. In this paper, we considered an existing multitrophic model (nutrient, bacteria, zooplankton, and viruses) that accounts for nitrogen limitation, and developed a phosphorus-limited version to assess whether the limiting nutrient alters the role of viruses in the ecosystem. For both versions, we evaluated the stationary state of the system with and without viruses. In agreement with existing results, nutrient release increased with viruses for nitrogen-limited systems, while zooplankton abundance and export to higher trophic levels decreased. We found this to be true also for phosphorus-limited systems, although nutrient release increased less than in nitrogen-limited systems. The latter supports a nutrient-specific response of the ecosystem to viruses. Bacterial concentration decreased in the phosphorus-limited system but increased in most nitrogen-limited cases due to a switch from mostly bottom-up to entirely top-down control by viruses. Our results also show that viral concentration is best predicted by a power-law of bacterial concentration with exponent different from 1. Finally, we found a positive correlation between carbon export and viruses regardless of the limiting nutrient, which led us to suggest viral abundance as a predictor of carbon sink.

Filamentous phages are a frontier in bacterial pathogenesis, but the impact of these phages on bacterial fitness is unclear. In particular, Pf phages produced by Pa promote antibiotic tolerance but are metabolically expensive to produce, suggesting that competing pressures may influence the prevalence of Pf+ versus Pf− strains of Pa in different settings.