Activation of JNK pathway during Coronavirus infection
Human Coronavirus 229E (HCoV-229E or 229E) is one of the six human coronaviruses associated with multiple respiratory illnesses. Despite its global prevalence, the viral-host interactions of 229E have not been well studied. Here, we demonstrate that 229E replicated efficiently and induced apoptosis...
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| Format: | Theses and Dissertations |
| Language: | English |
| Published: |
2016
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| Online Access: | http://hdl.handle.net/10356/69041 |
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| Institution: | Nanyang Technological University |
| Language: | English |
| Summary: | Human Coronavirus 229E (HCoV-229E or 229E) is one of the six human coronaviruses associated with multiple respiratory illnesses. Despite its global prevalence, the viral-host interactions of 229E have not been well studied. Here, we demonstrate that 229E replicated efficiently and induced apoptosis in lung adenocarcinoma H1299 cells. The c-Jun N-terminal kinase (JNK) pathway was activated in 229E-infected H1299 cells. Of the two known upstream protein kinases, MKK7, but not MKK4, is responsible for JNK activation during 229E infection. Although JNK did not significantly affect the overall 229E-induced apoptosis, it served an anti-apoptotic function by modulating B-cell lymphoma 2 (Bcl2) and Bcl2 homologous antagonist killer (Bak) in a mechanism not mediated by c-Jun. Moreover, JNK also mediated the induction of interferon β (IFNβ) and interleukin-8 (IL8) at transcriptional levels during 229E infection. Collectively, our findings show that JNK activation regulates expression of Bcl2 family proteins and innate immunity during 229E infection. |
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