Gene expression profiles in peripheral blood mononuclear cells of SARS patients.
OBJECTIVE
To investigate the role of inflammatory and anti-viral genes in the pathogenesis of SARS.


METHODS
cDNA microarrays were used to screen the gene expression profiles of peripheral blood mononuclear cells (PBMCs) in two SARS patients (one in the acute severe phase and the other in the convalescent phase) and a healthy donor. In addition, real-time qualitative PCR was also performed to verify the reproducibility of the microarray results. The data were further analyzed.


RESULTS
Many inflammatory and anti-viral genes were differentially expressed in SARS patients. Compared to the healthy control or the convalescent case, plenty of pro-inflammatory cytokines such as IL-1, TNF-alpha, IL-8, and MAPK signaling pathway were significantly upregulated in the acute severe case. However, anti-inflammatory agents such as IL-4 receptor, IL-13 receptor, IL-1Ra, and TNF-alpha-induced proteins 3 and 6 also increased dramatically in the acute severe case. On the contrary, a lot of IFN-stimulated genes like PKR, GBP-1 and 2, CXCL-10 and 11, and JAK/STAT signal pathway were downregulated in the acute severe case compared to the convalescent case.


CONCLUSIONS
Gene expression in SARS patients mirrors a host state of inflammation and anti-viral immunity at the transcription level, and understanding of gene expression profiles may make contribution to further studies of the SARS pathogenesis.
Yu
Shi-Yan
SY
Key Laboratory of Medical Molecular Virology, Ministry of Education and Public Health, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Hu
Yun-Wen
YW
Liu
Xiao-Ying
XY
Xiong
Wei
W
Zhou
Zhi-Tong
ZT
Yuan
Zheng-Hong
ZH
D000328:Adult; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D045169:Severe Acute Respiratory Syndrome / Q000235:genetics* / Q000276:immunology*