Persistent Infection with Infectious Pancreatic Necrosis Virus Mediated by Defective-interfering (DI) Virus Particles in a Cell Line Showing Strong Interference but Little DI Replication

Abstract

SUMMARYThe characteristics of chinook salmon embryo cells persistently infected with infectious pancreatic necrosis virus were consistent with defective-interfering (DI) particle-mediated persistence. All the cells were infected and were slowly releasing virus, but they could be cured of virus in the presence of antiserum. Immunofluorescence showed that the amount of virus antigen in persistently infected cells was low. This fact, coupled with the observation that few DI particles were released by these cells, indicated that DI particles were not replicated to excess in this cell line.

Differentially expressed genes following persistent infection with infectious pancreatic necrosis virus in vitro and in vivo

“…In accordance with result reported earlier [17] cell culture supernatant from the persistently infected cultures were infective to freshly prepared cultures of CHSE cells. Extracellular virus could be detected at a concentration of approx.…”

“…The mechanism behind a persistent infection in vitro is to a large extent unknown. It has been proposed that formation of defective interfering (DI) particles is one possible explanation while others have found that CHSE cells to a little extent supported the replication of DI particles [17]. Obviously, persistently infected cells have activated responses to suppress the viral load which is balanced against the replication rate of the virus, thus keeping the number of virus particles low.…”

Cardiomyopathy Syndrome of Atlantic Salmon (Salmo salar L.) Is Caused by a Double-Stranded RNA Virus of the Totiviridae Family

“…While the general understanding would be that naked viruses release their progeny through cell lysis (38), our findings support virus release occurring without CPE being found by visual inspection of the cell cultures. This observation is not unique, and release of another fish pathogenic virus, infectious pancreatic necrosis virus, into cell culture supernatants at high copy numbers without obvious CPE has been observed (19,22). Further, release of rotavirus from polarized epithelial cells in vitro has also been observed to occur without cell lysis (17).…”

Viral Polypeptides and RNA of Defective Interfering Particles of IPN Virus Generated by Serial Undiluted Passaging in TO-2 Cells.

“…Several studies indicated that marine bivalves are also common hosts of IPNV (Dobos et al, 1979;Lo et al, 1988 , 1978;Kennedy and MacDonald, 1982;Lo et al, 1990;MacDonald, 1978;MacDonald and Kennedy, 1979;MacDonald and Yamamoto, 1978;Malsberger and Cerini, 1963;Nicholson and Dunn, 1974). Most of the above studies indicated that defective interfering (DI) par ticles were involved in IPNV viral interference.…”