Novel pandemic influenza A (H1N1) virus infection modulates apoptotic pathways that impact its replication in A549 cells |
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| Institution: | 1. Lab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Bethesda, MD 20892, USA;2. Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA;1. Telethon Institute for Child Health Research, University of Western Australia, Perth, Australia;2. School of Paediatrics and Child Health, University of Western Australia, Perth, Australia;3. School of Public Health, Curtin University, Perth, Australia;1. Chinese National Influenza Center, National Institute for Viral Disease Control and Prevention, China CDC, 155 Changbai Road, Beijing, 102206, PR China;2. Public Health School (Shenzhen), Sun Yat-sen University, No.135, Xingang Xi Road, Guangzhou, 510275, PR China;1. Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, United States;2. Department of Immunology and Microbial Pathogenesis, Weill Cornell Medical College, New York, NY 10065, United States;1. Unidade de Investigação e Desenvolvimento, Departamento de Doenças Infecciosas, Instituto Nacional de Saúde Doutor Ricardo Jorge, Av. Padre Cruz, 1649-016 Lisboa, Portugal;2. Centro de Patogénese Molecular, Unidade dos Retrovírus e Infecções Associadas, Instituto de Medicina Molecular e Instituto de Investigação do Medicamento (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal;3. Instituto de Investigação do Medicamento (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal;1. Department of Medical Laboratory Sciences, Faculty of Health Sciences, Beirut Arab University, Lebanon;2. Faculty of Medicine, Department of Experimental Pathology, Immunology & Microbiology, American University of Beirut, Beirut, Lebanon;3. Faculty of Medicine, Center for Infectious Diseases Research, American University of Beirut, Beirut, Lebanon;4. Doctoral School of Sciences and Technology, Research Platform for Environmental Science (PRASE), Faculty of Sciences, Lebanese University, Lebanon;1. Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Republic of Korea;2. The Airway Mucus Institute, Yonsei University College of Medicine, Seoul, Republic of Korea;3. BK 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea;4. Research Center for Natural Human Defense System, Yonsei University College of Medicine, Seoul, Republic of Korea;5. Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, Republic of Korea |
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| Abstract: | It is not well-known whether apoptosis signaling affects influenza virus infection and reproduction in human lung epithelial cells. Using A549 cell line, we studied the relationship of some apoptosis-associated molecules with novel pandemic influenza A (H1N1) virus, A/California/04/2009. Infected cells displayed upregulated Fas ligand, activated FADD and caspase-8, and downregulated FLIP in the extrinsic apoptotic pathway. p53 expression increased and Bcl-XL expression decreased in the intrinsic pathway. Expression of pre-apoptotic molecules (FasL, FADD, and p53) increased virus replication, while inhibition of activity of FADD, caspase-8 and caspase-3, and expression of anti-apoptotic proteins (FLIP and Bcl-XL) decreased virus replication. p38, ERK and JNK from MAPK pathways were activated in infected cells, and inhibition with their inhibitors diminished virus replication. In the p38 superfamily, p38α expression increased viral RNA production, while expression of p38β and p38γ decreased. These data indicated that influenza virus induces apoptotic signaling pathways, which benefit virus replication. |
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| Keywords: | Pandemic influenza A (H1N1) virus Apoptosis Bax Fas MAPK Viral replication |
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