Abstract
Bovine herpesvirus 1 (BoHV-1) can provoke conjunctivitis, abortions and shipping fever. BoHV-1 infection can also cause immunosuppression and increased susceptibility to secondary bacterial infections, leading to pneumonia and occasionally to death. Herein, we investigated the influence of MG-132, a proteasome inhibitor, on BoHV-1 infection in bovine kidney (MDBK) cells. Infection of MDBK cells with BoHV-1 induces apoptotic cell death that enhances virus release. Whereas, MG-132 inhibited virus-induced apoptosis and stimulated autophagy. Protein expression of viral infected cell protein 0 (bICP0), which is constitutively expressed during infection and is able to stimulate Nuclear factor kappa B (NF-κB), was completely inhibited by MG-132. These results were accompanied by a significant delay in the NF-κB activation. Interestingly, the efficient virus release provoked by BoHV-1-induced apoptosis was significantly reduced by MG-132. Overall, this study suggests that MG-132, through the activation of autophagy, may limit BoHV-1 replication during productive infection, by providing an antiviral defense mechanism.
Highlights
Bovine herpesvirus 1 (BoHV-1), a double-stranded DNA virus, is an important pathogen that in cattle can provoke infectious bovine rhinotracheitis (IBR), conjunctivitis, abortions and shipping fever, which is a complicated infection of the upper respiratory tract
MDBK cells, epithelial-like bovine cells commonly used for growing and assaying BoHV-1, were infected with BoHV-1 virus (Cooper strain), in the presence or absence of MG-132, and we examined the pathway of BoHV1-induced apoptosis, viral and cellular proteins, and analyzed virus replication in infected cells
The effect of MG-132 on MDBK cell growth was determined by trypan blue exclusion test
Summary
Bovine herpesvirus 1 (BoHV-1), a double-stranded DNA virus, is an important pathogen that in cattle can provoke infectious bovine rhinotracheitis (IBR), conjunctivitis, abortions and shipping fever, which is a complicated infection of the upper respiratory tract. Several viruses use cellular signaling pathways, like NF-κB, to stimulate viral gene expression[16]. Immediate early protein bICP0, could stimulate NF-κB responsive reporter gene expression in different cell lines and induce NF-κB to translocate from cytoplasm into the nucleus where it promotes NF-κB DNA binding affinity[17]. Proteasome inhibitors decreased immediate early and late proteins expression in HSV-118, have a role in post-entry stages of HSV-1 infection[19,20,21,22,23,24], and facilitate the entry of HSV-1 at a post-penetration step[25]. MDBK cells, epithelial-like bovine cells commonly used for growing and assaying BoHV-1, were infected with BoHV-1 virus (Cooper strain), in the presence or absence of MG-132, and we examined the pathway of BoHV1-induced apoptosis, viral and cellular proteins, and analyzed virus replication in infected cells
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