From one host to another: adaptation of a phage infecting avian pathogenic Escherichia coli to the laboratory strain K-12.

Avian colibacillosis is an infectious disease that causes significant economic losses worldwide in the poultry industry. The bacterium avian pathogenic Escherichia coli (APEC) is the etiological agent of the disease and is primarily treated with antibiotics. Unfortunately, due to antibiotic resistance in APEC, therapeutic options for treating this disease are becoming increasingly limited. Bacteriophages-viruses that infect bacteria-represent promising therapeutic candidates; however, understanding how these viruses adapt is essential before considering them for commercial applications. This study investigated the adaptation of an APEC-infecting phage to a laboratory strain E. coli K-12 host. Successive passages of the phage on the K-12 strain resulted in clear adaptation to this new host, with only a slight fitness cost on APEC. The adapted phages also exhibited smaller capsids. Genomic comparison between the adapted phages and the wild-type phage revealed three mutations that may explain the adaptation to the K-12 strain: two point mutations located in a gene encoding a hypothetical protein and a 42-bp in-frame deletion in a homologue of the gene encoding the tail spike protein TSP4. This study, in addition to identifying molecular determinants involved in the adaptation of an APEC-infecting phage, further highlights the remarkable capacity of viruses to evolve.