Poliovirus infection induces apoptosis in CaCo-2 cells

Ammendolia, Maria Grazia; Tinari, Antonella; Calcabrini, Annarica; Superti, Fabiana

doi:10.1002/(sici)1096-9071(199909)59:1<122::aid-jmv20>3.0.co;2-9

Cited by 38 publications

(17 citation statements)

References 38 publications

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“…In our study of coxsackievirus B and poliovirus infected cell cultures, apoptosis of supernatant cells was complete at 4 h. This is consonant with the findings by other authors of apoptosis early in the viral replication of poliovirus [15] and coxsackievirus B infected cells [16]. We observed that virus replication in infected cell cultures took place in both the nuclei and cytoplasm.…”

Section: Discussionsupporting

confidence: 92%

Evidence for an enterovirus as the cause of encephalitis lethargica

et al. 2012

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BackgroundThe epidemic of encephalitis lethargica (EL), called classical EL, was rampant throughout the world during 1917–1926, affecting half a million persons. The acute phase was lethal for many victims. Post-encephalitic parkinsonism (PEP) affected patients for decades. Our purpose was to investigate the cause of classical EL by studying the few available brain specimens. Cases of PEP and modern EL were also studied. Transmission electron microscopy (TEM) and immunohistochemistry were employed to examine brain from four classical EL cases, two modern EL cases and one PEP case.MethodsStandard methods for TEM, immunohistochemistry and RTPCR were applied.Results27 nm virus-like particles (VLP) were observed in the cytoplasm and nuclei of midbrain neurons in all classical EL cases studied. Large (50 nm) VLP and 27 nm intranuclear VLP were observed in the modern EL cases and the PEP case. Influenza virus particles were not found. VLP were not observed in the control cases. TEM of cell cultures inoculated with coxsackievirus B4 and poliovirus revealed both small and large intranuclear virus particles and small cytoplasmic particles, similar to the VLP in EL neurons. In the EL brains, nascent VLP were embedded in putative virus factories and on endoplasmic reticulum (ER). The VLP in the cases of classical EL survived, whereas ribosomes underwent autolysis due to the lack of refrigeration and slow formaldehyde fixation of whole brain. The VLP were larger than ribosomes from well preserved brain. Immunohistochemistry of classical EL cases using anti-poliovirus and anti-coxsackievirus B polyclonal antibodies showed significant staining of cytoplasm and nuclei of neurons as well as microglia and neuropil. Purkinje cells were strongly stained.A 97-bp RNA fragment of a unique virus was isolated from brain tissue from acute EL case #91558. Sequence analysis revealed up to 95% identity to multiple human Enteroviruses. Additional cases had Enterovirus positive reactions by real time PCR.ConclusionsThe data presented here support the hypothesis that the VLP observed in EL tissue is an Enterovirus.

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Section: Discussionsupporting

confidence: 92%

Evidence for an enterovirus as the cause of encephalitis lethargica

et al. 2012

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“…Results from these experiments demonstrated that, as reported for some other non-enveloped viruses [18][19][20][21][22][23][24][25], bLf prevents viral cytopathic effect. Enteroviruses are highly cytopathic and it has been reported that viral infection can induce two distinct pathways of cell death: necrosis and apoptosis [29][30][31]. Although some viruses have developed different ways to suppress apoptosis, several viruses trigger apoptosis in host cells at the late stage of infection probably to spread viral progeny [32].…”

Section: Discussionsupporting

confidence: 92%

“…In our experimental conditions, we demonstrated that echovirus infection mainly induces apoptosis. These results are in agreement with those reported for poliovirus and coxsackievirus B [31,33]. Moreover, exploring the possibility of an antiapoptotic activity of bLf in virus-infected cells, we demonstrated that this protein prevents both cell death and viral replication.…”

Section: Discussionmentioning

confidence: 97%

Inhibitory activity of bovine lactoferrin against echovirus induced programmed cell death in vitro

Tinari¹,

Pietrantoni²,

Ammendolia³

et al. 2005

International Journal of Antimicrobial Agents

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“…PV-induced motor neuron death was recently found to be mediated through an apoptotic process 32–34 . PV was also reported to induce apoptosis in vitro in other cell types, including CaCo-2 colon cancer cell line 35 , U937 promonocytic cell line 36 , dendritic cells and macrophages 37 , and HeLa cells 38, 39 . However, the mechanisms by which PV induces apoptosis are not totally clear.…”

Section: Discussionmentioning

confidence: 97%

Different Mechanisms Preserve Translation of Programmed Cell Death 8 and JunB in Virus-Infected Endothelial Cells

Jiang

Schwertz

Schmid

et al. 2012

ATVB

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Objective Translation initiation of eukaryotic mRNAs typically occurs by cap-dependent ribosome scanning mechanism. However, certain mRNAs are translated by ribosome assembly at internal ribosome entry sites (IRES). Whether IRES-mediated translation occurs in stressed primary human endothelial cells (EC) is unknown. Methods and Results We performed microarray analysis of polyribosomal mRNA from EC to identify IRES-containing mRNAs. Cap-dependent translation was disabled by poliovirus (PV) infection and confirmed by loss of polysome peaks, detection of eIF4G cleavage, and decreased protein synthesis. 87.4% of mRNAs were dissociated from polysomes in virus-infected EC. 12% of mRNAs remained associated with polysomes and 0.6% were enriched ≥2-fold in polysome fractions from infected EC. Quantitative RT-PCR confirmed the microarray findings for 31 selected mRNAs. We found that enriched polysome associations of PDCD8 and JunB mRNA resulted in increased protein expression in PV-infected EC. The presence of IRES in the 5’UTR of PDCD8 mRNA, but not of JunB mRNA, was confirmed by dicistronic analysis. Conclusions We show that microarray profiling of polyribosomal mRNA transcripts from PV-infected EC successfully identifies mRNAs whose translation is preserved in the face of stress-induced, near complete cessation of cap-dependent initiation. Nevertheless, internal ribosome entry is not the only mechanism responsible for this privileged translation.

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Poliovirus infection induces apoptosis in CaCo-2 cells

Cited by 38 publications

References 38 publications

Evidence for an enterovirus as the cause of encephalitis lethargica

Evidence for an enterovirus as the cause of encephalitis lethargica

Inhibitory activity of bovine lactoferrin against echovirus induced programmed cell death in vitro

Different Mechanisms Preserve Translation of Programmed Cell Death 8 and JunB in Virus-Infected Endothelial Cells

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