Antibiotics such as sulfonamides are ubiquitous environmental contaminants that pose severe ecological risks globally. Constructed wetlands are critical systems for mitigating these pollutants, where diverse microbial communities drive complex biogeochemical transformations. Within these ecosystems, bacteriophages are the most abundant biological entities, capable of shaping bacterial community structure and function through lytic infection and gene transfer. Virus-encoded auxiliary metabolic genes (AMGs) can specifically modulate host metabolism to enhance survival under chemical stress. However, the precise role of viruses in regulating both the degradation of antibiotics and the dissemination of antibiotic resistance genes (ARGs) remains poorly understood. Here we show that positive bacteria-phage interactions significantly improve sulfamethoxazole (SMX) removal while concurrently restricting the transfer of ARGs. Using sediment microcosm experiments, we demonstrate that the addition of phage-concentrated solutions increases SMX removal efficiency by up to 35%. Viruses achieve this by enriching specific SMX-degrading bacteria and augmenting bacterial metabolic capacity through the expression of AMGs related to energy production and extracellular polymeric substance synthesis. Furthermore, lytic viruses act as biological blockers, significantly reducing the total relative abundance of ARGs by directly lysing antibiotic-resistant host cells rather than promoting transduction. Our findings highlight the profound ecological influence of viruses in shaping microbial responses to pollutant stress. Regulating these viral communities presents a promising biological strategy to enhance the bioremediation of emerging contaminants and mitigate the global health risks of antibiotic resistance. • Viruses shape microbial community responses to environmental pollutant stress. • Phage addition increases sulfamethoxazole removal efficiency by up to 35.0%. • Virus-encoded auxiliary metabolic genes enhance bacterial degradation capacity. • Lytic viruses reduce antibiotic resistance genes via host cell lysis.
Liu et al. (Wed,) studied this question.