In:
The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 124.9-124.9
Abstract:
Different influenza A virus subtypes display different pathogenicity during host infection. It is our hypothesis that the host innate immune defense inversely correlates with the viral pathogenicity, i.e., the higher the viral pathogenicity the lower is the host innate immune defense and vice versa. In order to test our hypothesis, we monitored infection of normal human bronchial epithelial cells due to high pathogenicity H1N1 and low pathogenicity H3N2 subtypes during the early stages (0 to 24 hours) of infection. Specifically, we performed whole genome microarray analysis of the infected cells, identified the genes significantly altered in their expression, and validated the expression patterns of these genes by real-time qPCR. Of particular importance were the inducer and effector genes in the IFN-α/β pathway, a prominent innate immune response against viral infection. The prominent inducers include: (i) the OAS genes involved in the production of small viral RNA, (ii) the viral RNA sensors RIG-I, MDA-5, and TLR3, and (iii) the IRF transcription factors involved in the expression of IFN-α/β. The prominent effectors include: (i) ISG15, which activates RIG-I by ubiquitination, (ii) RSAD2 which inhibit the budding of influenza A virus, and (iii) GBPs, which inhibit viral replication. We validate our hypothesis by demonstrating that the release and expression of inducers and effectors of IFN-α/β are lower in high pathogenicity H1N1 than those in low pathogenicity H3N2. .
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.192.Supp.124.9
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2014
detail.hit.zdb_id:
1475085-5
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