Human respiratory syncytial virus (RSV) is a highly pathogenic lung-tropic virus that causes severe respiratory diseases. Enzymatic activity of inducible nitric oxide (iNOS) is required for NO generation. Although NO contributes to exaggerated lung disease during RSV infection, the role of NO in apoptosis during infection is not known. In addition, host trans-activator(s) required for iNOS gene expression during RSV infection is unknown. In the current study we have uncovered the mechanism of iNOS gene induction by identifying kruppel-like factor 6 (KLF6) as a critical transcription factor required for iNOS gene expression during RSV infection. Furthermore, we have also uncovered the role of iNOS as a critical host factor regulating apoptosis during RSV infection.
Keywords: Apoptosis; BMDMs; ChIP; Inducible nitric oxide synthase; KLF6; KO; Kruppel-like factor 6; L-NIL; N(6)-(1-iminoethyl)-l-lysine dihydrochloride; NO; Nitric oxide; RSV; Respiratory syncytial virus; Transcription factor; WT; bone marrow-derived macrophages; chromatin immuno-precipitation; iNOS; inducible nitric oxide synthase; knock-out; kruppel-like factor 6; nitric oxide; respiratory syncytial virus; wild type.
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