The feline calicivirus leader of the capsid protein causes survivin and XIAP downregulation and apoptosis

Barrera-Vázquez, Oscar Salvador; Cancio-Lonches, Clotilde; Hernández-González, Olivia; Chávez‐Munguía, Bibiana; Villegas‐Sepúlveda, Nicolás; Gutiérrez-Escolano, Ana Lorena

doi:10.1016/j.virol.2018.11.017

Cited by 24 publications

(37 citation statements)

References 59 publications

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“…MNV contain a fourth ORF that encodes the virulence factor (VF) 1, involved in evasion of innate immunity (41). In FCV, VP1 is encoded as a precursor that is cleaved by the viral protease-polymerase NS6/7 to produce the mature VP1 and a small protein of 124 amino acids known as the leader of the capsid protein (LC) (42) which has recently been shown to be involved in triggering apoptosis (43). The NS proteins, enhance translation rounds of the viral genome and lead the cell to the establishment of a pathogenic phenotype, inducing membrane proliferation that will induce the formation of the replication complexes (RCs), or viral factories and alter the vesicular secretory pathway to evade both the innate and acquired antiviral immune response and trigger apoptosis.…”

Section: Calicivirus Genome Translation and Replicationmentioning

confidence: 99%

“…Intrinsic apoptosis in FCV infection has been well-characterized and several reports have evidenced both morphological (chromatin condensation, DNA fragmentation, plasma membrane blebbing, and cell shrinkage) as well as molecular changes (Bax translocation to the mitochondria, cytochrome C and the Second Mitochondria-derived Activator of Caspases, and Direct IAP-Binding protein with Low PI, Smac/DIABLO release to the cytosol, and caspase−9 and−3 activation) (43, 58, 61–63). The FCV protein LC, which is unique among the Caliciviridae members, is responsible for the cytopathic effect characterized in infected CrFK cells by cell rounding and caspases activation and induction of the intrinsic apoptotic pathway (43, 69).…”

Section: Apoptosis In Calicivirus Infected Cellsmentioning

confidence: 99%

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Immune Response Modulation by Caliciviruses

et al. 2019

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Noroviruses and Sapoviruses, classified in the Caliciviridae family, are small positive-stranded RNA viruses, considered nowadays the leading cause of acute gastroenteritis globally in both children and adults. Although most noroviruses have been associated with gastrointestinal disease in humans, almost 50 years after its discovery, there is still a lack of comprehensive evidence regarding its biology and pathogenesis mainly because they can be neither conveniently grown in cultured cells nor propagated in animal models. However, other members of this family such as Feline calicivirus (FCV), Murine norovirus (MNV), Rabbit hemorrhagic disease virus (RHDV), and Porcine sapovirus (PS), from which there are accessible propagation systems, have been useful to study the calicivirus replication strategies. Using cell cultures and animal models, many of the functions of the viral proteins in the viral replication cycles have been well-characterized. Moreover, evidence of the role of viral proteins from different members of the family in the establishment of infection has been generated and the mechanism of their immunopathogenesis begins to be understood. In this review, we discuss different aspects of how caliciviruses are implicated in membrane rearrangements, apoptosis, and evasion of the immune responses, highlighting some of the pathogenic mechanisms triggered by different members of the Caliciviridae family.

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Section: Calicivirus Genome Translation and Replicationmentioning

confidence: 99%

Section: Apoptosis In Calicivirus Infected Cellsmentioning

confidence: 99%

Immune Response Modulation by Caliciviruses

et al. 2019

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“…FCV viral capsid is composed of 90 dimers of VP1 and a few copies of VP2. Both structural proteins are assembled concomitantly with the gRNA to form the viral progeny, which exits the infected cells by apoptosis (Stanislav V. Sosnovtsev, Prikhod'ko, Belliot, Cohen and Green, 2003 ) ( Barrera-Vázquez et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Host cell p53 associates with the feline calicivirus major viral capsid protein VP1, the protease-polymerase NS6/7, and the double-stranded RNA playing a role in virus replication

Trujillo-Uscanga

Gutiérrez-Escolano

2020

Virology

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p53 is implicated in several cellular pathways such as induction of cell-cycle arrest, differentiation, senescence, and apoptosis. p53 is activated by a broad range of stress signals, including viral infections. While some viruses activate p53, others induce its inactivation, and occasionally p53 is differentially modulated during the replicative cycle. During calicivirus infections, apoptosis is required for virus exit and spread into the host; yet, the role of p53 during infection is unknown. By confocal microscopy, we found that p53 associates with FCV VP1, the protease-polymerase NS6/7, and the dsRNA. This interaction was further confirmed by proximity ligation assays, suggesting that p53 participates in the FCV replication. Knocked-down of p53 expression in CrFK cells before infection, resulted in a strong reduction of the non-structural protein levels and a decrease of the viral progeny production. These results indicate that p53 is associated with the viral replication complex and is required for an efficient FCV replication.

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“…It is known that FCV as all caliciviruses undergoes the mitochondrial pathway of apoptosis for successful infection, particularly to facilitate the release and spread of the viral progeny into the host. Evidence of the translocation and activation of pro- and anti-apoptotic molecules has been extensively documented, including translocation of Bax protein into the mitochondria, the release of cytochrome C to the cytosol, activation of caspase-9 and -3 during FCV and murine norovirus 1 (MNV-1), and the downregulation of survivin during MNV [8,9,10,11,12]. Recently, our group has reported the translocation of the pro-apoptotic factor Smac/DIABLO (second mitochondria-derived activator of caspases and direct IAP-binding protein with low PI) from the mitochondria to the cytoplasm, with the concomitant downregulation of the anti-apoptotic proteins survivin and XIAP during FCV infection.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, our group has reported the translocation of the pro-apoptotic factor Smac/DIABLO (second mitochondria-derived activator of caspases and direct IAP-binding protein with low PI) from the mitochondria to the cytoplasm, with the concomitant downregulation of the anti-apoptotic proteins survivin and XIAP during FCV infection. Moreover, we found that the leader of the capsid protein (LC)—a 124 aa protein produced by processing of the VP1 precursor protein—is responsible for these changes and for induction of apoptosis [12]. We also found that the inhibition of endogenous survivin degradation induced by FCV infection with lactacystin treatment caused a delay in apoptosis progression, reducing the amount of FCV particles released into the supernatant and without affecting virus production, indicating the association between apoptosis and virus release [12,13].…”

Section: Introductionmentioning

confidence: 99%

Survivin Overexpression Has a Negative Effect on Feline Calicivirus Infection

Barrera-Vázquez

Cancio-Lonches

Miguel-Rodríguez

et al. 2019

Viruses

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It is known that levels of the anti-apoptotic protein survivin are reduced during Murine norovirus MNV-1 and Feline calicivirus (FCV) infection as part of the apoptosis establishment required for virus release and propagation in the host. Recently, our group has reported that overexpression of survivin causes a reduction of FCV protein synthesis and viral progeny production, suggesting that survivin may affect early steps of the replicative cycle. Using immunofluorescence assays, we observed that overexpression of survivin, resulted in the reduction of FCV infection not only in transfected but also in the neighboring nontransfected CrFK cells, thus suggesting autocrine and paracrine protective effects. Cells treated with the supernatants collected from CrFK cells overexpressing survivin showed a reduction in FCV but not MNV-1 protein production and viral yield, suggesting that FCV binding and/or entry were specifically altered. The reduced ability of FCV to bind to the surface of the cells overexpressing survivin, or treated with the supernatants collected from these cells, correlate with the reduction in the cell surface of the FCV receptor, the feline junctional adhesion molecule (fJAM) 1, while no effect was observed in the cells transfected with the pAm-Cyan vector or in cells treated with the corresponding supernatants. Moreover, the overexpression of survivin affects neither Vaccinia virus (VACV) production in CrFK cells nor MNV-1 virus production in RAW 267.4 cells, indicating that the effect is specific for FCV. All of these results taken together indicate that cells that overexpress survivin, or cell treatment with the conditioned medium from these cells, results in the reduction of the fJAM-1 molecule and, therefore, a specific reduction in FCV entry and infection.

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The feline calicivirus leader of the capsid protein causes survivin and XIAP downregulation and apoptosis

Cited by 24 publications

References 59 publications

Immune Response Modulation by Caliciviruses

Immune Response Modulation by Caliciviruses

Host cell p53 associates with the feline calicivirus major viral capsid protein VP1, the protease-polymerase NS6/7, and the double-stranded RNA playing a role in virus replication

Survivin Overexpression Has a Negative Effect on Feline Calicivirus Infection

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