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10.1186/s12985-015-0284-6

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suck abstract from ncbi


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pmid26021751
      Virol+J 2015 ; 12 (ä): 61
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  • The effects of H3N2 swine influenza virus infection on TLRs and RLRs signaling pathways in porcine alveolar macrophages #MMPMID26021751
  • Zhang J ; Miao J ; Hou J ; Lu C
  • Virol J 2015[Apr]; 12 (ä): 61 PMID26021751 show ga
  • BACKGROUND: Swine influenza is an economically important respiratory disease of swine resulting from infection with influenza A virus. Swine influenza virus (SIV) becomes the focus as pigs have been hypothesized to serve as an intermediate host for the adaptation of avian influenza viruses to humans or as mixing vessels for the generation of genetically reassortant viruses. The ability of the innate immune system to detect and respond to pathogens is important for survival. Therefore, there is a critical need to evaluate the immediate response to viral infection, especially the role of the toll-like receptors (TLRs) and RNA helicase RIG-I-like receptors (RLRs) innate immunity signaling pathways in H3N2 swine influenza virus infection. METHOD: In this study, porcine alveolar macrophages (PAMs) were obtained from porcine lungs and were infected with SIV at a multiplicity of infection (MOI) of 5 in vitro. The changes of the related receptors, signaling proteins and effector molecules of TLRs and RLRs signaling pathways post H3N2 virus infection of PAMs were quantified by Real-time quantitative RT-PCR and western blotting. RESULTS: The results showed that H3N2 SIV infection significantly increased mRNA expression of TLR-3, TLR-7, RIG- I and MDA5 after 4 hpi (P?
  • |*Signal Transduction [MESH]
  • |Animals [MESH]
  • |Cell Line [MESH]
  • |Cytokines/metabolism [MESH]
  • |Gene Expression [MESH]
  • |Influenza A Virus, H3N2 Subtype/*physiology [MESH]
  • |Macrophages, Alveolar/immunology/*virology [MESH]
  • |Myeloid Differentiation Factor 88/genetics/metabolism [MESH]
  • |Orthomyxoviridae Infections/*veterinary [MESH]
  • |RNA, Messenger/genetics/metabolism [MESH]
  • |Swine [MESH]
  • |Swine Diseases/genetics/immunology/*metabolism/*virology [MESH]
  • |Toll-Like Receptors/genetics/*metabolism [MESH]


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