Sendai Virus Infection Induces Apoptosis through Activation of Caspase-8 (FLICE) and Caspase-3 (CPP32) |
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| Authors: | Michael Bitzer Florian Prinz Manuel Bauer Martin Spiegel Wolfgang J Neubert Michael Gregor Klaus Schulze-Osthoff and Ulrich Lauer |
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| Affiliation: | Abteilung Innere Medizin I, Medizinische Universitätsklinik Tübingen, 72076 Tübingen,1. and Abteilung für Virusforschung, Max-Planck-Institut für Biochemie, 82152 Martinsried,2. Germany |
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| Abstract: | Sendai virus (SV) infection and replication lead to a strong cytopathic effect with subsequent death of host cells. We now show that SV infection triggers an apoptotic program in target cells. Incubation of infected cells with the peptide inhibitor z-VAD-fmk abrogated SV-induced apoptosis, indicating that proteases of the caspase family were involved. Moreover, proteolytic activation of two distinct caspases, CPP32/caspase-3 and, as shown for the first time in virus-infected cells, FLICE/caspase-8, could be detected. So far, activation of FLICE/caspase-8 has been described in apoptosis triggered by death receptors, including CD95 and tumor necrosis factor (TNF)-R1. In contrast, we could show that SV-induced apoptosis did not require TNF or CD95 ligand. We further found that apoptosis of infected cells did not influence the maturation and budding of SV progeny. In conclusion, SV-induced cell injury is mediated by CD95- and TNF-R1-independent activation of caspases, leading to the death of host cells without impairment of the viral life cycle. |
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