The SAT protein of porcine parvovirus accelerates viral spreading through induction of irreversible endoplasmic reticulum stress

István Mészáros, Renáta Tóth, Ferenc Olasz, Peter Tijssen, Zoltán Zádori

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The SAT protein (SATp) of porcine parvovirus (PPV) accumulates in the endoplasmic reticulum (ER), and SAT deletion induces the slow-spreading phenotype. The in vitro comparison of the wild-type Kresse strain and its SAT knockout (SAT-) mutant revealed that prolonged cell integrity and late viral release are responsible for the slower spreading of the SAT- virus. During PPV infection, regardless of the presence or absence of SATp, the expression of downstream ER stress response proteins (Xbp1 and CHOP) was induced. However, in the absence of SATp, significant differences in the quantity and the localization of CHOP were detected, suggesting a role of SATp in the induction of irreversible ER stress in infected cells. The involvement of the induction of irreversible ER stress in porcine testis (PT) cell necrosis and viral egress was confirmed by treatment of infected cells by ER stressinducing chemicals (MG132, dithiothreitol, and thapsigargin), which accelerated the egress and spreading of both the wild-type and the SAT- viruses. UV stress induction had no beneficial effect on PPV infection, underscoring the specificity of ER stress pathways in the process. However, induction of CHOP and its nuclear translocation cannot alone be responsible for the biological effect of SAT, since nuclear CHOP could not complement the lack of SAT in a coexpression experiment.

Original languageEnglish
Article numbere00627-17
JournalJournal of Virology
Issue number16
Publication statusPublished - Aug 1 2017



  • Alternative ORF
  • CHOP
  • ER stress
  • Parvovirus
  • Protoparvovirus
  • SAT
  • Viral egress
  • Xbp1

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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