The persistence of infectious pancreatic necrosis virus (IPNV) in Atlantic salmon was examined with particular emphasis on the association of IPNV with leucocytes. Atlantic salmon were infected with IPNV via the water and via the feed. Despite relatively low mortalities, a high prevalence of IPNV was demonstrated particularly when the virus was introduced via the water. No virus-specific pathology or reduction in the growth performance of infected populations was evident. The conditions for the stimulation of Atlantic salmon leucocytes with the mitogen, phytohemagglutinin (PHA) were optimised and utilized in a co-stimulation assay. In this assay, leucocytes were infected with IPNV and simultaneously stimulated with PHA. It was demonstrated that the ability of IPNV to infect and replicate in leucocytes was enhanced when the cells were stimulated with mitogen. DNA synthesis was inhibited in the infected leucocytes. The inhibition was dependent upon the presence of infectious virus; inactivated virus failed to inhibit DNA synthesis. Three groups of salmon were examined to investigate the <i>in vivo</i> relationship of IPNV with leucocytes. Group A were the control group. IPNV was not isolated from these fish and the leucocytes responded to stimulation with PHA. Group B were experimentally infected IPNV carriers; virus was isolated from 6% of the fish using standard diagnostic methods but was not isolated from the supernatants of leucocyte cultures. The leucocytes of most fish responded to PHA stimulation. Neutralising antibody titres were variable and did not correlate with virus isolation. Group C were also IPNV carriers; virus could not be isolated using standard diagnostic methods but was isolated from the supernatants of stimulated leucocyte cultures of 44% of the fish. A significant inhibition of DNA synthesis in response to PHA stimulation was observed. The persistence of IPNV in Atlantic salmon is discussed in the light of the data presented here and existing knowledge of the persistence of mammalian viruses.