The β-catenin signaling pathway stimulates bovine herpesvirus 1 productive infection

Liqian Zhu, Prasanth Thunuguntla, Yilin Liu, Morgan Hancock, Clinton Jones

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)91-95
Number of pages5
StatePublished - Jan 1 2017


  • Bovine herpesvirus 1 (BoHV-1)
  • Productive infection
  • β-catenin
  • β-catenin inhibitor (iCRT14)

ASJC Scopus subject areas

  • Virology


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