Activation of the intrinsic mitochondrial apoptotic pathway in swine influenza virus-mediated cell death

Ki Choi Young, Tae Kyung Kim, Chul Joong Kim, Joong Seob Lee, Se Young Oh, Han S Joo, Douglas N. Foster, Ki Chang Hong, Seungkwon You, Hyunggee Kim

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24 Scopus citations


The mitochondrial pathway of swine influenza virus (SIV)-induced apoptosis was investigated using porcine kidney (PK-15) cells, swine testicle (ST) cells, and HeLa cervical carcinoma cells which are known not to support viral replication. As judged by cell morphology, annexin V staining, and DNA fragmentation, PK-15 and ST cells infected with three different subtypes of SIV (H1N1, H3N2, and H1N2) were obviously killed by apoptosis, not necrosis. SIV infection in PK-15 and HeLa cells was shown to decrease the cellular levels of Bcl-2 protein compared to that of mock-infected control cells at 24 h post-infection, whereas expression levels of Bax protein increased in the PK-15 cells, but did not increase in HeLa cells by SIV infection. Cytochrome c upregulation was also observed in cytosolic fractions of the PK-15 and HeLa cells infected with SIV. Apoptosome (a multi-protein complex consisting of cytochrome c, Apaf-1, caspase-9, and ATP) formation was confirmed by immunoprecipitation using cytochrome c antibody. Furthermore, SIV infection increased the cellular levels of TAJ, an activator of the JNK- stressing pathway, and the c-Jun protein in the PK-15 and HeLa cells. Taken together, these results suggest that the mitochondrial pathway should be implicated in the apoptosis of PK-15 cells induced by SIV infection.

Original languageEnglish (US)
Pages (from-to)11-17
Number of pages7
JournalExperimental and Molecular Medicine
Issue number1
StatePublished - Feb 28 2006


  • Apoptosis
  • Cytochrome c
  • Influenza virus
  • Mitochondria
  • Proto-oncogene proteins c-Bcl-2
  • Proto-oncogene proteins c-jun


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