Bovine herpesvirus type 5 infection regulates Bax/BCL-2 ratio

Af, Garcia; Jb, Novais; Tf, Antello; Silva-Frade, Camila; Mc, Ferrarezi; Ef, Flores; Tc, Cardoso

doi:10.4238/2013.september.23.8

Cited by 5 publications

(2 citation statements)

References 12 publications

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“…Although different apoptotic forms have been described induced by BHV1 and 5 infection (Brenner et al 2012;Cardoso et al 2012Cardoso et al , 2015Delhon et al 2002;Garcia et al 2013;Geiser et al 2008;Ladelfa et al 2013;Silva-Frade et al 2010Zhu et al 2016), this particular mechanism remains unknown. Likewise, only few reports describe the susceptibility of human tumor cells to BHV1 (Cuddington and Mossman 2014).…”

Section: Discussionmentioning

confidence: 95%

“…Rabies virus, a neurotropic virus that infects human and animals, has been incriminated to induce neuronal death by ROS formation (Alandijany et al 2013). Previous studies revealed that mitochondrial membrane potential can be altered without affecting non-transformed cellular cycle after infected by BHV5 (Brenner et al 2012;Garcia et al 2013). The expression of anti-oxidant protein-like 1 (AOP-1), a protective pathway, has been detected in bovine embryos and brain histological sections, both infected by BHV5 (Brenner et al 2012;Cardoso et al 2010).…”

Section: Discussionmentioning

confidence: 98%

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Bovine herpesviruses induce different cell death forms in neuronal and glial-derived tumor cell cultures

et al. 2016

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Oncolytic viruses have the ability to infect tumor cells and leave healthy cells intact. In this study, bovine herpesvirus 1 (BHV1; Los Angeles, Cooper, and SV56/90 strains) and bovine herpesvirus 5 (BHV5; SV507/99 and GU9457818 strains) were used to infect two neuronal tumor cell lineages: neuro2a (mouse neuroblastoma cells) and C6 (rat glial cells). BHV1 and BHV5 strains infected both cell lines and positively correlated with viral antigen detection (p < 0.005). When neuro2a cells were infected by Los Angeles, SV507/99, and GU9457818 strains, 40 % of infected cells were under early apoptosis and necroptosis pathways. Infected C6 cells were >40 % in necroptosis phase when infected by BHV5 (GU9457818 strain). Blocking caspase activation did not interfere with cell death. However, when necroptosis was blocked, 60-80 % of both infected cells with either virus switched to early apoptosis pathway with no interference with virus replication. Moreover, reactive oxygen species production and mitochondrial membrane dysfunction were detected at high levels in both infected cell lines. In spite of apoptosis and necroptosis blockage, tumor necrosis factor alpha (TNFA) and virus transcription were positively correlated for all viral strains studied. Thus, these results contribute to the characterization of BHV1 and BHV5 as potential oncolytic viruses for non-human cells. Nonetheless, the mechanisms underlying their oncolytic activity in human cells are still to be determined.

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