Reactivation of Nedd-2, a developmentally down-regulated apoptotic gene, in apoptosis induced by a street strain of rabies virus

Ubol, Sukathida; Kasisith, Jitra

doi:10.1099/0022-1317-49-11-1043

Cited by 23 publications

(15 citation statements)

References 5 publications

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“…He et al (2001) recently showed that apoptosis induction following infection by the paramyxovirus simian virus 5 requires caspase-2. Likewise, caspase-2 needs to be expressed for apoptosis to occur in response to rabies virus infection (Ubol & Kasisith, 2000). Invasive Salmonella typhimurium was reported to activate caspase-2 in macrophages and the ensuing apoptotic response was also partially dependent on caspase-2 (Jesenberger et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Caspase-mediated cleavage of the feline calicivirus capsid protein

Al-Molawi

Beardmore

Carter

et al. 2003

Journal of General Virology

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Feline calicivirus (FCV) is responsible for an acute upper respiratory tract disease in cats. The FCV capsid protein is synthesized as a precursor (76 kDa) that is post-translationally processed into the mature 62 kDa capsid protein by removal of the N-terminal 124 amino acids. Our previous studies have also detected a 40 kDa protein, related to the FCV capsid protein, produced during infection. Here we demonstrate that cleavage of the FCV capsid protein, during infection of cells in culture, was prevented by caspase inhibitors. In addition, caspase-2, -3 and -7 were activated during FCV infection, as shown by pro-form processing, an increase in N-acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin cleavage activity and in situ poly(ADP-ribose) polymerase cleavage. Caspase activation coincided with the induction of apoptosis and capsid cleavage to the 40 kDa fragment. An in vitro cleavage assay, using recombinant human caspases and in vitroderived FCV capsid protein, revealed that caspase-2, and to a lesser extent caspase-6, cleaved the capsid protein to generate a 40 kDa fragment. Taken together, these results suggest that FCV triggers apoptosis within infected cells and that caspase-induced capsid cleavage occurs concomitantly with apoptosis. The possible role of capsid cleavage in the pathogenesis of FCV infection is discussed. INTRODUCTIONThe family Caliciviridae includes several significant pathogens of man and animals. Feline calicivirus (FCV) is a major cause of upper respiratory tract disease in cats. The genome is a single-stranded positive sense RNA of about 7?5 kb (Carter et al., 1992a). The genome is polyadenylated and covalently linked to a 15 kDa viral protein, termed VPg, at the 59 end and contains three open reading frames (ORF). ORF1 encodes the non-structural proteins, ORF2 encodes the capsid protein and ORF3 a small highly basic structural protein (reviewed in Clarke & Lambden, 1997). ORF2 and ORF3 are expressed from a single subgenomic mRNA (Herbert et al., 1996). Calicivirus particles contain a single capsid protein (58-76 kDa). The capsid of members of the vesivirus genus, such as FCV and San Miguel sea lion virus (SMSV), is formed initially as a larger precursor which is cleaved by the viral protease into the mature capsid protein (62 kDa in the case of FCV; Neill, 1992;Neill et al., 1991; Carter et al., 1992b; Sosnovstev et al., 1998). The mature FCV protein is created by removal of the N-terminal 124 amino acids from the precursor (Carter, 1989). The mature protein is incorporated into virions.A smaller form of the capsid protein (approx. 40 kDa by SDS-PAGE; called p40) has been observed during FCV infection in cell culture at late times post-infection (Carter et al., 1989). Similar truncated forms of the capsid protein have been reported in the late stages of rabbit haemorrhagic disease virus (RHDV) infection (reviewed in Carter & Cubbitt, 1998). In addition, cleaved soluble forms of the Norwalk virus (NLV) capsid protein have been associated with enteric infection in man (Hardy ...

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Section: Discussionmentioning

confidence: 99%

Caspase-mediated cleavage of the feline calicivirus capsid protein

Al-Molawi

Beardmore

Carter

et al. 2003

Journal of General Virology

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“…48,49 However, there are reports that support the notion that RABV does indeed induce apoptosis. [50][51][52] This difference may perhaps be due to the fact that induction of apoptosis is virus specific.…”

Section: Discussionmentioning

confidence: 99%

Wild-type rabies virus induces autophagy in human and mouse neuroblastoma cell lines

Peng

Sheng-He

et al. 2016

Autophagy

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Different rabies virus (RABV) strains have their own biological characteristics, but little is known about their respective impact on autophagy. Therefore, we evaluated whether attenuated RABV HEP-Flury and wildtype RABV GD-SH-01 strains triggered autophagy. We found that GD-SH-01 infection significantly increased the number of autophagy-like vesicles, the accumulation of enhanced green fluorescent protein (EGFP)-LC3 fluorescence puncta and the conversion of LC3-I to LC3-II, while HEP-Flury was not able to induce this phenomenon. When evaluating autophagic flux, we found that GD-SH-01 infection triggers a complete autophagic response in the human neuroblastoma cell line (SK), while autophagosome fusion with lysosomes was inhibited in a mouse neuroblastoma cell line (NA). In these cells, GD-SH-01 led to apoptosis and mitochondrial dysfunction while triggering autophagy, and apoptosis could be decreased by enhancing autophagy. To further identify the virus constituent causing autophagy, 5 chimeric recombinant viruses carrying single genes of HEP-Flury instead of those of GD-SH-01 were rescued. While the HEP-Flury virus carrying the wild-type matrix protein (M) gene of RABV triggered LC3-I to LC3-II conversion in SK and NA cells, replacement of genes of nucleoprotein (N), phosphoprotein (P) and glycoprotein (G) produced only minor autophagy. But no one single structural protein of GD-SH-01 induced autophagy. Moreover, the AMPK signaling pathway was activated by GD-SH-01 in SK. Therefore, our data provide strong evidence that autophagy is induced by GD-SH-01 and can decrease apoptosis in vitro. Furthermore, the M gene of GD-SH-01 may cooperatively induce autophagy.

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“…However, one must keep in mind that in a natural setting two of the most important vectors for rabies virus, particularly as a means of transmission to humans, are bats and canines. A handful of recent studies have examined a multitude of rabies virus strains isolated from these animals [58,59]. In addition, some groups have begun to use the bat as a model of rabies virus infection [60].…”

Section: Of Mice and Bats And Menmentioning

confidence: 99%

Rhabdoviruses and Apoptosis

Licata

Harty

2003

International Reviews of Immunology

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Viral-induced apoptosis is recognized as a common method utilized by viruses to overcome the host. Recent evidence indicates that infection by rhabdoviruses such as vesicular stomatitis virus (VSV), spring viremia of carp virus (SVCV), and rabies virus results in apoptotic cell death. Similar morphological changes and host cell proteins are induced in cells infected with these different viruses; however, the viral proteins responsible for these changes vary. In addition, the molecular mechanism(s) utilized by these viruses to induce apoptosis are on the brink of discovery. This article serves to summarize our current understanding of the apoptotic process during rhabdovirus infection and to illustrate forthcoming areas of study in the field

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Reactivation of Nedd-2, a developmentally down-regulated apoptotic gene, in apoptosis induced by a street strain of rabies virus

Cited by 23 publications

References 5 publications

Caspase-mediated cleavage of the feline calicivirus capsid protein

Caspase-mediated cleavage of the feline calicivirus capsid protein

Wild-type rabies virus induces autophagy in human and mouse neuroblastoma cell lines

Rhabdoviruses and Apoptosis

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