Molecular epidemiological study on Infectious Pancreatic Necrosis Virus isolates from aquafarms in Scotland over three decades

The Infectious Pancreatic Necrosis Virus (IPNV) and its Virulence Determinants: What is Known and What Should be Known

“…This supported previous results by Santi et al [54]; however, in their paper they recognized that the mutations observed in putatively important locations in the domain of the strains under study could be an explanation for the lack of activity. Therefore, IPNV-VP5 is still accepted as an antiapoptotic protein [58,59], which also has a strong inhibition of the interferon (IFN) signaling [48,60]. Finally, in IBDV, in addition to this antiapoptotic activity at early stages of infection, VP5 has been demonstrated to activate cell apoptosis in late stages, possibly constituting a mechanism for progeny release [61], something that could be similar in IPNV.…”

“…Marjara et al [68] also recently demonstrated-in persistently infected cells-the upregulation of genes involved in transcription repression, which suggests that IPNV persistence could be due to the reduction of viral replication as a result of a reduced transcription capacity. Other authors [59,69] have added that the persistence status could be due to the virus and host reaching a balance in such a manner that the virus reduces its level of replication so as not to harm the host and thus not triggering the host defenses.…”

“…There are two possible explanations for all of these discrepancies. On the one hand, Ulrich et al [59] suggested that VP5 could be a de novo gene, generated by overprinting on segment A, and providing an anti-apoptotic capacity and hence an advantage for the virus to be able to adapt to farmed vaccinated hosts and maintain a low level of replication in that environment. On the other hand, it has been demonstrated that not only VP5, but also the remaining viral proteins, except VP1, inactivate IFN signaling by antagonizing IFNa1 promoter activation [48] and it is well known [110] that the IFN system is involved in the activation of apoptosis.…”

Discrete virus factories form in the cytoplasm of cells co-infected with two strains of the segmented dsRNA virus, infectious bursal disease virus (IBDV), that subsequently coalesce

“…As well as causing severe morbidity and mortality, the virus is immunosuppressive, leaving birds that recover with an increased susceptibility to secondary infection and a reduced response to vaccination programs [2, 3]. Infectious Pancreatic Necrosis Virus (IPNV) is responsible for high mortalities in farmed salmon and trout and some strains can cause persistent infection, with fish spreading the virus by vertical or horizontal transmission [4]. In addition, more recently described birnaviruses, for example chicken proventriculus necrosis virus (CPNV) [5] and blotched snakehead virus (BSNV) [6] cause production loses that are only just beginning to be understood, and birnaviruses of insects such as Drosophila X virus (DXV) and Culex Y virus (CYV) are useful as tools for studying cellular antiviral responses [7].…”

“…As the Birnaviridae genome is divided into two segments, reassortment is a problem in the field. Reassortment of IBDV has been observed to occur between field strains and vaccine strains [28], between different serotypes [29], and is thought to be responsible for the emergence of very virulent strains [30], and reassortment has also been observed during IPNV infections [4, 31], complicating the epidemiology of the diseases. However, despite the importance of reassortment, the molecular mechanisms involved remain unknown.…”