Negative effect of heat shock on feline calicivirus release from infected cells is associated with the control of apoptosis

Alvarez-Sanchez, Cristal; Cancio-Lonches, Clotilde; Mora-Heredia, José Eduardo; Santos-Valencia, Juan Carlos; Barrera-Vázquez, Oscar Salvador; Yocupicio-Monroy, Martha; Gutiérrez-Escolano, Ana Lorena

doi:10.1016/j.virusres.2015.01.003

Cited by 5 publications

(2 citation statements)

References 46 publications

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“…Meanwhile, we measured candidate host protein levels after RNAi by western blot analysis, and the results revealed significant interference effects and confirmed the specificity of RNAi silencing. Bioinformatic analysis by GeneMANIA indicated that these candidate host proteins belong to the following families: (1) HSPs that participate in a wide variety of cellular processes, including activation of proteolysis, protecting the proteome against stress, infection, and transport of newly synthesized polypeptides ( Alvarez-Sanchez et al, 2015 ; Chaudhary et al, 2016 ; Heck et al, 2017 ); (2) 14-3-3 protein families that bind a number of signaling proteins including kinases, phosphatases and transmembrane receptors ( Radhakrishnan et al, 2012 ; Obsilova et al, 2014 ; Aghazadeh and Papadopoulos, 2016 ); (3) Annexin families that are involved in trafficking and organization of endocytosis, vesicles, exocytosis, and calcium ion channel formation ( Grieve et al, 2012 ; Kuehnl et al, 2016 ); (4) MAP kinase families, which play critical roles in signal transduction, phosphorylation and activation of MAPK1/ERK2 and MAPK3/ERK1 pathways ( Vomastek et al, 2008 ; Robinson and Pitcher, 2013 ; Cook et al, 2017 ). Further functional analysis confirmed that the candidate host proteins were strongly associated with cytoplasmic vesicle membranes, mitochondrial membranes, mitochondria, the COP9 signalosome, and phospholipid binding, and connected with antigen binding, viral endocytosis, transportation, anti-virus responses, and viral budding ( Bech-Otschir et al, 2001 ; Horner et al, 2011 ; van Zuylen et al, 2012 ; Richard et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Chaperones, Membrane Trafficking and Signal Transduction Proteins Regulate Zaire Ebola Virus trVLPs and Interact With trVLP Elements

Weng

et al. 2018

Front. Microbiol.

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Ebolavirus (EBOV) life cycle involves interactions with numerous host factors, but it remains poorly understood, as does pathogenesis. Herein, we synthesized 65 siRNAs targeting host genes mostly connected with aspects of the negative-sense RNA virus life cycle (including viral entry, uncoating, fusion, replication, assembly, and budding). We produced EBOV transcription- and replication-competent virus-like particles (trVLPs) to mimic the EBOV life cycle. After screening host factors associated with the trVLP life cycle, we assessed interactions of host proteins with trVLP glycoprotein (GP), VP40, and RNA by co-immunoprecipitation (Co-IP) and chromatin immunoprecipitation (ChIP). The results demonstrate that RNAi silencing with 11 siRNAs (ANXA5, ARFGAP1, FLT4, GRP78, HSPA1A, HSP90AB1, HSPA8, MAPK11, MEK2, NTRK1, and YWHAZ) decreased the replication efficiency of trVLPs. Co-IP revealed nine candidate host proteins (FLT4, GRP78, HSPA1A, HSP90AB1, HSPA8, MAPK11, MEK2, NTRK1, and YWHAZ) potentially interacting with trVLP GP, and four (ANXA5, GRP78, HSPA1A, and HSP90AB1) potentially interacting with trVLP VP40. Ch-IP identified nine candidate host proteins (ANXA5, ARFGAP1, FLT4, GRP78, HSPA1A, HSP90AB1, MAPK11, MEK2, and NTRK1) interacting with trVLP RNA. This study was based on trVLP and could not replace live ebolavirus entirely; in particular, the interaction between trVLP RNA and host proteins cannot be assumed to be identical in live virus. However, the results provide valuable information for further studies and deepen our understanding of essential host factors involved in the EBOV life cycle.

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Section: Discussionmentioning

confidence: 99%

Chaperones, Membrane Trafficking and Signal Transduction Proteins Regulate Zaire Ebola Virus trVLPs and Interact With trVLP Elements

Weng

et al. 2018

Front. Microbiol.

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“…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]. Moreover, FCV infection of cells that overexpress survivin resulted in a reduction of both viral protein levels and viral yield production [12], suggesting that survivin overexpression affects early stages of the FCV replicative cycle, such as binding and/or entry to permissive cells.…”

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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Calicivirus Biology

Gutiérrez-Escolano¹

2017

Human Virology in Latin America

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Negative effect of heat shock on feline calicivirus release from infected cells is associated with the control of apoptosis

Cited by 5 publications

References 46 publications

Chaperones, Membrane Trafficking and Signal Transduction Proteins Regulate Zaire Ebola Virus trVLPs and Interact With trVLP Elements

Chaperones, Membrane Trafficking and Signal Transduction Proteins Regulate Zaire Ebola Virus trVLPs and Interact With trVLP Elements

Survivin Overexpression Has a Negative Effect on Feline Calicivirus Infection

Calicivirus Biology

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