Gene expression profiles comparison between 2009 pandemic and seasonal H1N1 influenza viruses in A549 cells.
- Author:
Xiao-Xing YANG
1
;
Ning DU
;
Jian-Fang ZHOU
;
Zi LI
;
Min WANG
;
Jun-Feng GUO
;
Da-Yan WANG
;
Yue-Long SHU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; genetics; Cell Line, Tumor; Cytopathogenic Effect, Viral; Disease Outbreaks; Down-Regulation; Epithelial Cells; metabolism; virology; Gene Expression; Gene Expression Profiling; Humans; Immunity, Innate; genetics; Influenza A Virus, H1N1 Subtype; classification; pathogenicity; Influenza, Human; epidemiology; genetics; immunology; virology; Oligonucleotide Array Sequence Analysis; Pandemics; Seasons; Up-Regulation; Virulence
- From: Biomedical and Environmental Sciences 2010;23(4):259-266
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo perform gene expression profiles comparison so that to identify and understand the potential differences in pathogenesis between the pandemic and seasonal A (H1N1) influenza viruses.
METHODSA549 cells were infected with A/California/07/09 (H1N1) and A/GuangdongBaoan/51/08 (H1N1) respectively at the same MOI of 2 and collected at 2, 4, 8, and 24 h post infection (p.i.). Gene expression profiles of A549 cells were obtained using the 22 K Human Genome Oligo Array, and differentially expressed genes were analyzed at selected time points.
RESULTSMicroarrays results indicated that both of the viruses suppressed host immune response related pathways including cytokine production while pandemic H1N1 virus displayed weaker suppression of host immune response than seasonal H1N1 virus. Observation on similar anti-apoptotic events such as activation of apoptosis inhibitor and down-regulation of key genes of apoptosis pathways in both infections showed that activities of promoting apoptosis were different in later stage of infection.
CONCLUSIONSThe immuno-suppression and anti-apoptosis events of pandemic H1N1 virus were similar to those seen by seasonal H1N1 virus. The pandemic H1N1 virus had an ability to inhibit biological pathways associated with cytokine responses, NK activation and macrophage recognition.