Bovine Herpesvirus type 4 (BoHV-4), like other herpesviruses, induces a series of alterations in the host cell that modify the intracellular environment in favour of viral replication, survival and spread. This research examined the impact of BoHV-4 infection on autophagy in BoHV-4 infected Madin Darby Bovine Kidney (MDBK) cells. Protein extracts of BoHV-4 infected and control MDBK cells were subjected to western blot. The concentrations of the autophagy and apoptosis-related proteins Beclin 1, p21, PI3 Kinase, Akt1/2, mTOR, phospho mTOR, p62 and the light chain three (LC3) were normalised to the actin level and expressed as the densitometric ratio. Western blot analysis of virus-infected cells revealed that autophagic degradation pathway was induced in the late phase of BoHV-4 infection. After 48 hours post infection the protein LC3II, which is essential for autophagy, was found to be markedly increased, while infection of MDBK cells with BoHV-4 resulted in a depletion of p62 levels. Becline 1, PI3 Kinase, Akt1/2 and p21 expression increased between 24 and 48 h post infection. Surprisingly, mTOR and its phosphorylated form, which are negative regulators of autophagy, also increased after 24 hours post infection. In conclusion, our findings suggest that BoHV-4 has developed mechanisms for modulation of autophagy that are probably part of a strategy designed to enhance viral replication and to evade the immune system. Additional studies on the relationship between autophagy and BoHV-4 replication and survival, in both lytic and latent replication phases, are needed to understand the role of autophagy in BoHV-4 pathogenesis. J. Cell. Biochem. © 2013 Wiley Periodicals, Inc.

Serena, M., Roberto, C., Francesco, P., Luisa De, M., Maria Valeria, P., Giovanna Elvira, G., et al. (2013). Bovine herpesvirus type 4 infection modulates autophagy in a permissive cell line. JOURNAL OF CELLULAR BIOCHEMISTRY, 114(17), 1529-1535 [10.1002/jcb.24494].

Bovine herpesvirus type 4 infection modulates autophagy in a permissive cell line

GIORDANO, ANTONIO
2013-01-01

Abstract

Bovine Herpesvirus type 4 (BoHV-4), like other herpesviruses, induces a series of alterations in the host cell that modify the intracellular environment in favour of viral replication, survival and spread. This research examined the impact of BoHV-4 infection on autophagy in BoHV-4 infected Madin Darby Bovine Kidney (MDBK) cells. Protein extracts of BoHV-4 infected and control MDBK cells were subjected to western blot. The concentrations of the autophagy and apoptosis-related proteins Beclin 1, p21, PI3 Kinase, Akt1/2, mTOR, phospho mTOR, p62 and the light chain three (LC3) were normalised to the actin level and expressed as the densitometric ratio. Western blot analysis of virus-infected cells revealed that autophagic degradation pathway was induced in the late phase of BoHV-4 infection. After 48 hours post infection the protein LC3II, which is essential for autophagy, was found to be markedly increased, while infection of MDBK cells with BoHV-4 resulted in a depletion of p62 levels. Becline 1, PI3 Kinase, Akt1/2 and p21 expression increased between 24 and 48 h post infection. Surprisingly, mTOR and its phosphorylated form, which are negative regulators of autophagy, also increased after 24 hours post infection. In conclusion, our findings suggest that BoHV-4 has developed mechanisms for modulation of autophagy that are probably part of a strategy designed to enhance viral replication and to evade the immune system. Additional studies on the relationship between autophagy and BoHV-4 replication and survival, in both lytic and latent replication phases, are needed to understand the role of autophagy in BoHV-4 pathogenesis. J. Cell. Biochem. © 2013 Wiley Periodicals, Inc.
2013
Serena, M., Roberto, C., Francesco, P., Luisa De, M., Maria Valeria, P., Giovanna Elvira, G., et al. (2013). Bovine herpesvirus type 4 infection modulates autophagy in a permissive cell line. JOURNAL OF CELLULAR BIOCHEMISTRY, 114(17), 1529-1535 [10.1002/jcb.24494].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/44069
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