Newcastle Disease Virus Infection Promotes Bax Redistribution to Mitochondria and Cell Death in HeLa Cells

Molouki, Aidin; Hsu, Yi‐Te; Jahanshiri, Fatemeh; Rosli, Rozita; Yusoff, Khatijah

doi:10.1159/000264198

Cited by 36 publications

(39 citation statements)

References 95 publications

(61 reference statements)

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“…To investigate whether their infectivity on another colorectal cancer cell line was also retained, we performed infections in HT29 cells. HT29 cells were previously shown to be susceptible to NDV oncolytic activities [19]. Spent culture media collected from the mock-infected SW480P cells were used to infect HT29 as described in the Materials and methods section.…”

Section: Resultsmentioning

confidence: 99%

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Viral persistence in colorectal cancer cells infected by Newcastle disease virus

Chia

Yusoff

Shafee

2014

Virol J

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BackgroundNewcastle disease virus (NDV), a single-stranded RNA virus of the family Paramyxoviridae, is a candidate virotherapy agent in cancer treatment. Promising responses were observed in clinical studies. Despite its high potential, the possibility of the virus to develop a persistent form of infection in cancer cells has not been investigated. Occurrence of persistent infection by NDV in cancer cells may cause the cells to be less susceptible to the virus killing. This would give rise to a population of cancer cells that remains viable and resistant to treatment.ResultsDuring infection experiment in a series of colorectal cancer cell lines, we adventitiously observed a development of persistent infection by NDV in SW480 cells, but not in other cell lines tested. This cell population, designated as SW480P, showed resistancy towards NDV killing in a re-infection experiment. The SW480P cells retained NDV genome and produced virus progeny with reduced plaque forming ability.ConclusionThese observations showed that NDV could develop persistent infection in cancer cells and this factor needs to be taken into consideration when using NDV in clinical settings.

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Section: Resultsmentioning

confidence: 99%

“…The DIPs are characterized by their inability to infect cells on their own due to large genetic mutations [27]. This mNDV virus was also able to infect another colorectal cancer cell line, HT29 [19] albeit at lower cytotoxicity. This suggested that the mNDV maintained its infectivity in other cancer cells besides the parental cells.…”

Section: Discussionmentioning

confidence: 99%

Viral persistence in colorectal cancer cells infected by Newcastle disease virus

Chia

Yusoff

Shafee

2014

Virol J

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“…On the other hand, NDV has also gained a lot of interest in cancer virotherapy since it can selectively kill human cancer cells [5]. It has been shown that NDV induces apoptosis in cancer cells by activating the mitochondrial pathway [8,9]. The proteins of the Bcl-2 family are known central regulators of this pathway [10].…”

Section: Resultsmentioning

confidence: 99%

NDV-induced apoptosis in absence of Bax; evidence of involvement of apoptotic proteins upstream of mitochondria

Molouki

Yusoff

2012

Virol J

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BackgroundRecently it was shown that following infection of HeLa cells with Newcastle disease virus (NDV), the matrix (M) protein binds to Bax and subsequently the intrinsic pathway of apoptosis is activated. Moreover, there was very little alteration on mRNA and protein levels of Bax and Bcl-2 after infection with NDV.FindingIn order to further investigate the role of members of the Bcl-2 family, Bax-knockout and wild-type HCT116 cells were infected with NDV strain AF2240. Although both cells underwent apoptosis through the activation of the intrinsic pathway and the release of cytochrome c from mitochondria, the percentage of dead Bax-knockout cells was significantly lower than wt cells (more than 10% at 48 h post-infection). In a parallel experiment, the effect of NDV on HT29 cells, that are originally Bcl-2-free, was studied. Apoptosis in HT29 cells was associated with Bax redistribution from cytoplasm to mitochondria, similar to that of HeLa and wt HCT116 cells.ConclusionAlthough the presence of Bax during NDV-induced apoptosis contributes to a faster cell death, it was concluded that other apoptotic protein(s) upstream of mitochondria are also involved since cancer cells die whether in the presence or absence of Bax. Therefore, the classic Bax/Bcl-2 ratio may not be a major determinant in NDV-induced apoptosis.

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“…Many viruses have recently been found to activate Bax, including influenza A virus (49), respiratory syncytial virus (24), hepatitis B virus (44), hepatitis C virus (5), Theiler's murine encephalomyelitis virus (67), West Nile virus (55), rabies virus (36,74), poliovirus (2), rotavirus (48), and Newcastle disease virus (51). A common link for the ability of many different viruses to activate Bax may be induction of apoptosis via antiviral innate immunity pathways.…”

Section: Fig 9 Apoptosis Is Decreased At 9 Dpi In Baxmentioning

confidence: 99%

The Proapoptotic Bcl-2 Protein Bax Plays an Important Role in the Pathogenesis of Reovirus Encephalitis

Berens

Tyler

2011

J Virol

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Encephalitis induced by reovirus serotype 3 (T3) strains results from the apoptotic death of infected neurons. Extrinsic apoptotic signaling is activated in reovirus-infected neurons in vitro and in vivo, but the role of intrinsic apoptosis signaling during encephalitis is largely unknown. Bax plays a key role in intrinsic apoptotic signaling in neurons by allowing the release of mitochondrial cytochrome c. We found Bax activation and cytochrome c release in neurons following infection of neonatal mice with T3 reoviruses. Bax ؊/؊ mice infected with T3 Abney (T3A) have reduced central nervous system (CNS) tissue injury and decreased apoptosis, despite viral replication that is similar to that in wild-type (WT) Bax ؉/؉ mice. In contrast, in the heart, T3A-infected Bax ؊/؊ mice have viral growth, caspase activation, and injury comparable to those in WT mice, indicating that the role of Bax in pathogenesis is organ specific. Nonmyocarditic T3 Dearing (T3D)-infected Bax ؊/؊ mice had delayed disease and enhanced survival compared to WT mice. T3D-infected Bax ؊/؊ mice had significantly lower viral titers and levels of activated caspase 3 in the brain despite unaffected transneuronal spread of virus. Cytochrome c and Smac release occurred in some reovirus-infected neurons in the absence of Bax; however, this was clearly reduced compared to levels seen in Bax ؉/؉ wild-type mice, indicating that Bax is necessary for efficient activation of proapoptotic mitochondrial signaling in infected neurons. Our studies suggest that Bax is important for reovirus growth and pathogenesis in neurons and that the intrinsic pathway of apoptosis, mediated by Bax, is important for full expression of disease, CNS tissue injury, apoptosis, and viral growth in the CNS of reovirus-infected mice.

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Newcastle Disease Virus Infection Promotes Bax Redistribution to Mitochondria and Cell Death in HeLa Cells

Cited by 36 publications

References 95 publications

Viral persistence in colorectal cancer cells infected by Newcastle disease virus

Viral persistence in colorectal cancer cells infected by Newcastle disease virus

NDV-induced apoptosis in absence of Bax; evidence of involvement of apoptotic proteins upstream of mitochondria

The Proapoptotic Bcl-2 Protein Bax Plays an Important Role in the Pathogenesis of Reovirus Encephalitis

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