Necrosis of infectious pancreatic necrosis virus (IPNV) infected cells rarely is preceded by apoptosis

Espinoza, Juan Carlos; Cortés-Gutierrez, Marcia; Kuznar, Juan

doi:10.1016/j.virusres.2004.10.014

Cited by 15 publications

(19 citation statements)

References 15 publications

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“…However, the role of necrosis in viral infection is less clear, partly because the necrosis process is less well-studied. Nevertheless, to date, necrosis has been shown to play an important role during viral infection by at least four viruses (An et al, 2000;Espinoza et al, 2005;Miller and Fox, 2004;Ran et al, 1999). Whether or not necrosis is important for SARS-CoV infection remains to be determined.…”

Section: Resultsmentioning

confidence: 99%

Over-expression of severe acute respiratory syndrome coronavirus 3b protein induces both apoptosis and necrosis in Vero E6 cells

et al. 2006

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The genome of the severe acute respiratory syndrome coronavirus encodes for eight accessory viral proteins with no known homologues in other coronaviruses. One of these is the 3b protein, which is encoded by the second open reading frame in subgenomic RNA 3 and contains 154 amino acids. Here, a detailed time-course study was performed to compare the apoptosis and necrosis profiles induced by full-length 3b, a 3b mutant that was deleted by 30 amino acids from the C terminus (3b∆124-154) and the classical apoptosis inducer, Bax. Our results showed that Vero E6 cells transfected with a construct for expressing 3b underwent necrosis as early as 6 h after transfection and underwent simultaneous necrosis and apoptosis at later time-points. At all the time-points analysed, the apoptosis induced by the expression of 3b was less than the level induced by Bax but the level of necrosis was comparable. The 3b∆124-154 mutant behaves in a similar manner indicating that the localization of the 3b protein does not seems to be important for the cell-death pathways since full-length 3b is localized predominantly to the nucleolus, while the mutant is found to be concentrated in the peri-nuclear regions. To our knowledge, this is the first report of the induction of necrosis by a SARS-CoV protein.

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Section: Resultsmentioning

confidence: 99%

Over-expression of severe acute respiratory syndrome coronavirus 3b protein induces both apoptosis and necrosis in Vero E6 cells

et al. 2006

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“…13,21,22 Caspase 3 (CPP32) activation, translocation of phosphatidyl serine (PS), and DNA fragmentation are markers of the early and late phases of apoptosis. 19,23 In this study, we detected the activities of caspase 3/7, phosphatidylserine translocation, DNA fragmentation, and DNA content of HepG2 cells infected with PTV Adames and Balliet strains at different time points after infection. It showed a correlation between the reduction of cell viability and the virus replication (Figures 1 and 2).…”

Section: Discussionmentioning

confidence: 99%

Apoptosis of Hepatocytes Caused by Punta Toro Virus (Bunyaviridae: Phlebovirus) and Its Implication for Phlebovirus Pathogenesis

Ding

Chen

et al. 2005

The American Journal of Pathology

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Experimental infection of hamsters with Punta Toro virus (PTV) produces a disease with clinical and pathological similarities to the severe human hemorrhagic fever caused by Rift Valley fever virus (RVFV), thus providing an animal model for RVFV pathogenesis. In this model, hepatocytic apoptosis is the main pathological component of liver injuries that are responsible for severe hemorrhagic manifestations. To further elucidate whether viral replication in hepatocytes directly causes apoptosis, we studied the morphological and biochemical changes of apoptosis in HepG2 cells at different time points after PTV infection. Cellular viability began to decrease 12 hours after infection compared with controls. Caspases 3/7 were activated significantly at 48 and 72 hours after infection, and phosphatidylserine translocation and DNA fragmentation were also detected at 48 and 72 hours. Cell cycle analysis by flow cytometry showed that infected HepG2 cells were arrested at G 0 /G 1 phase. Furthermore, virus titer increased with apoptosis progression, suggesting that viral replication is necessary for the apoptotic process. These results indicate that PTV infection alone, without a secondary inflammatory cellular reaction, induces hepatocytic apoptosis and suggest that future therapeutics for RVFV hemorrhagic disease might target inhibition of cellular apoptotic pathways during the acute infection. Punta Toro virus (PTV) is a member of the genus Phlebovirus, family Bunyaviridae. Viruses in this genus contain a negative-sense, single-strand RNA genome that consists of three segments, large (L), medium (M), and small (S), and are associated with a variety of diseases, including a brief self-limited febrile illness, retinitis, encephalitis, meningoencephalitis, and a severe hemorrhagic fever.

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“…Therefore, the apparent lack of influence of VP5-absence or presence-to block apoptosis could be due to the fact that such actions might be perfectly covered by other viral proteins. It could even be that the apparent limited capacity of IPNV induction of apoptosis [57,111] was due to the fact that not one but several of its viral proteins are involved in limiting apoptosis.…”

Section: Is Vp5 Expression a Determinant Of Virulence?mentioning

confidence: 99%

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

Dopazo

2020

Pathogens

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Infectious pancreatic necrosis (IPN) is a disease of great concern in aquaculture, mainly among salmonid farmers, since losses in salmonid fish—mostly very young rainbow trout (Salmo gairdnery) fry and Atlantic salmon (Salmo salar) post-smolt—frequently reach 80–90% of stocks. The virus causing the typical signs of the IPN disease in salmonids, named infectious pancreatic necrosis virus (IPNV), has also been isolated from other fish species either suffering related diseases (then named IPNV-like virus) or asymptomatic; the general term aquabirnavirus is used to encompass all these viruses. Aquabirnaviruses are non-enveloped, icosahedral bisegmented dsRNA viruses, whose genome codifies five viral proteins, three of which are structural, and one of them is an RNA-dependent RNA polymerase. Due to the great importance of the disease, there have been great efforts to find a way to predict the level of virulence of IPNV isolates. The viral genome and proteins have been the main focus of research. However, to date such a reliable magic marker has not been discovered. This review describes the processes followed for decades in the attempts to discover the viral determinants of virulence, and to help the reader understand how viral components can be involved in virulence modulation in vitro and in vivo. There is also a brief description of the disease, of host defenses, and of the molecular structure and function of the virus and its viral components.

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Necrosis of infectious pancreatic necrosis virus (IPNV) infected cells rarely is preceded by apoptosis

Cited by 15 publications

References 15 publications

Over-expression of severe acute respiratory syndrome coronavirus 3b protein induces both apoptosis and necrosis in Vero E6 cells

Over-expression of severe acute respiratory syndrome coronavirus 3b protein induces both apoptosis and necrosis in Vero E6 cells

Apoptosis of Hepatocytes Caused by Punta Toro Virus (Bunyaviridae: Phlebovirus) and Its Implication for Phlebovirus Pathogenesis

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

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