TY - JOUR
T1 - The β-catenin signaling pathway stimulates bovine herpesvirus 1 productive infection
AU - Zhu, Liqian
AU - Thunuguntla, Prasanth
AU - Liu, Yilin
AU - Hancock, Morgan
AU - Jones, Clinton
N1 - Publisher Copyright:
© 2016
PY - 2017/1/1
Y1 - 2017/1/1
N2 - Bovine herpes virus 1 (BoHV-1), an important bovine pathogen, causes conjunctivitis and disorders in the upper respiratory tract. Following acute infection, BoHV1 establishes life-long latency in sensory neurons. Recent studies demonstrated that viral gene products expressed in trigeminal ganglionic neurons during latency stabilize β-catenin levels, an important signaling molecule that interacts with a family of DNA binding proteins (T-cell factors) and subsequently stimulates transcription. In this study, we provide new evidence demonstrating that BoHV-1 transiently increased β-catenin protein levels in bovine kidney (CRIB) cells, but not in rabbit skin cells. β-catenin dependent transcription was also stimulated by infection of CRIB cells. The β-catenin small molecule inhibitor (iCRT14) significantly reduced the levels of BoHV-1 virus during productive infection of CRIB cells and rabbit skin cells. In summary, these studies suggested the ability of β-catenin to stimulate cell survival and cell cycle regulatory factors enhances productive infection in non-neuronal cells.
AB - Bovine herpes virus 1 (BoHV-1), an important bovine pathogen, causes conjunctivitis and disorders in the upper respiratory tract. Following acute infection, BoHV1 establishes life-long latency in sensory neurons. Recent studies demonstrated that viral gene products expressed in trigeminal ganglionic neurons during latency stabilize β-catenin levels, an important signaling molecule that interacts with a family of DNA binding proteins (T-cell factors) and subsequently stimulates transcription. In this study, we provide new evidence demonstrating that BoHV-1 transiently increased β-catenin protein levels in bovine kidney (CRIB) cells, but not in rabbit skin cells. β-catenin dependent transcription was also stimulated by infection of CRIB cells. The β-catenin small molecule inhibitor (iCRT14) significantly reduced the levels of BoHV-1 virus during productive infection of CRIB cells and rabbit skin cells. In summary, these studies suggested the ability of β-catenin to stimulate cell survival and cell cycle regulatory factors enhances productive infection in non-neuronal cells.
KW - Bovine herpesvirus 1 (BoHV-1)
KW - Productive infection
KW - β-catenin
KW - β-catenin inhibitor (iCRT14)
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U2 - 10.1016/j.virol.2016.10.014
DO - 10.1016/j.virol.2016.10.014
M3 - Article
C2 - 27788397
AN - SCOPUS:84994048849
SN - 0042-6822
VL - 500
SP - 91
EP - 95
JO - Virology
JF - Virology
ER -