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New insights about host response to smallpox using microarray data

DOI: 10.1186/1752-0509-1-38

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Abstract:

We used KEGG pathways annotations to define groups of genes (or modules), and subsequently compared them to macaque survival times. This technique provided additional insights about the host response to this disease, such as increased expression of the cytokines and ECM receptors in the individuals with higher survival times. These results could indicate that these gene groups could influence an effective response from the host to smallpox.Macaques with higher survival times clearly express some specific pathways previously unidentified using regular gene-by-gene approaches. Our work also shows how third party analysis of public datasets can be important to support new hypotheses to relevant biological problems.Large scale gene expression analysis with microarray technology is expanding and generating a large amount of high quality, publicly available data. In the present work we analyzed a dataset derived from monkeys infected by smallpox, published by Rubins et al [1]. Smallpox is a lethal disease that was endemic in many parts of the world until eradicated by a massive immunization program developed by the World Health Organization. Its fatality rate was estimated to be 30%, and the survivors often had disfiguring scars [2].There are serious concerns about the use of smallpox as a bioweapon [3,4]. Recently, some health care workers were vaccinated by the UK government for the analysis of antibody responses [5]. Pox viruses display unique abilities to interfere with the host immune system, producing immune modulators [6] and there are at least 16 viral genes involved in combating the host immune response [7]. The original study's goal was to analyze the evolution of the gene expression of the peripheral blood cells of variola-infected monkeys, so as to clarify the biological processes associated with host-pathogen interactions [1].Among the important results was the absence of a TNF-α/NF-κB-activated transcriptional mechanism during systemic infection, which could

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