Expression profile of immune response genes in patients with Severe Acute Respiratory Syndrome

The number of differentially expressed genes was found to be 186 under stringent filtering criteria of microarray data analysis. Several genes were highly up-regulated in patients with SARS, such as, the genes coding for Lactoferrin, S100A9 and Lipocalin 2. The real-time PCR method verified the results of the gene array analysis and showed that those genes that were up-regulated as determined by microarray analysis were also found to be comparatively up-regulated by real-time PCR analysis.This differential gene expression profiling of PBMCs from patients with SARS strongly suggests that the response of SARS affected patients seems to be mainly an innate inflammatory response, rather than a specific immune response against a viral infection, as we observed a complete lack of cytokine genes usually triggered during a viral infection. Our study shows for the first time how the immune system responds to the SARS infection, and opens new possibilities for designing new diagnostics and treatments for this new life-threatening disease.Severe acute respiratory syndrome (SARS) emerged in 2003, as a new epidemic form of life-threatening infection [1]. As of September 2003, there were 8098 cases of SARS from 29 countries with 774 deaths (WHO). SARS is characterized by high fever, malaise, rigors, headache, dry cough, and progression to interstitial infiltration in lungs with eventual mortality of greater than 10% in many countries [2]. SARS has been shown to be caused by a novel coronavirus; SARS-CoV, with genome sequences recently published [3-7]. However, the pathogenesis of SARS is poorly understood. Major hematological features of this disease are lymphopenia, transient thrombocytopenia, and normal neutrophil and monocyte counts [8]. It has been shown that SARS coronavirus infects and replicates in a wide variety of host cells, including PBMCs, in susceptible animals and human beings [9,10]. Hence, to understand the host response to this pathogen, we profiled the gene expr