Synergy in viral-bacterial co-infection expedites algal bloom demise.
Algal bloom demise, often caused by viruses, is a major driver of carbon cycling in the surface ocean 1,2 . However, although blooms collapse synchronously, fewer than 30% of algal cells are actively infected by viruses 3 , indicating the involvement of additional mortality agents. Here we quantified tripartite interactions within a synthetic community composed of the abundant coccolithophore Gephyrocapsa huxleyi, bacteria and viruses isolated during a bloom. We found that bacteria significantly
Algal bloom demise, often caused by viruses, is a major driver of carbon cycling in the surface ocean 1,2 . However, although blooms collapse synchronously, fewer than 30% of algal cells are actively infected by viruses 3 , indicating the involvement of additional mortality agents. Here we quantified tripartite interactions within a synthetic community composed of the abundant coccolithophore Gephyrocapsa huxleyi, bacteria and viruses isolated during a bloom. We found that bacteria significantly enhanced virus-induced algal mortality in G. huxleyi as well as in three other globally widespread microalgae. We quantified this interaction using two new metrics: the synergy index, which measures viral-bacterial interaction strength, and the benefit index, which assesses changes in bacterial fitness. We identified Alteromonas bacteria as drivers of viral-bacterial co-infection, with consistently high synergy index and benefit index. We found that during algal blooms, Alteromonas displayed high chemoattraction towards infected cell extracts, accumulated in aggregates derived from bloom demise, and increased in abundance during oceanic bloom collapse. Viral-bacterial synergy represents a previously unrecognized mortality agent that controls bloom termination, modulating the balance between the carbon-recycling viral shunt and the carbon-exporting viral shuttle pathways, which influence global carbon cycling 4-6 .
