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Publication : MAIDS resistance-associated gene expression patterns in secondary lymphoid organs.

First Author  Tepsuporn S Year  2008
Journal  Immunogenetics Volume  60
Issue  9 Pages  485-94
PubMed ID  18612634 Mgi Jnum  J:137843
Mgi Id  MGI:3803050 Doi  10.1007/s00251-008-0312-4
Citation  Tepsuporn S, et al. (2008) MAIDS resistance-associated gene expression patterns in secondary lymphoid organs. Immunogenetics 60(9):485-94
abstractText  Murine acquired immunodeficiency syndrome (MAIDS) is caused by exposure to murine leukemia virus and serves as a model to study human AIDS. In MAIDS-susceptible C57BL/6 mice, virus exposure leads to progressive immune deficiency, while resistant strains such as BALB/c recover from infection and develop protective immunity. The goal of this study was to identify early gene expression patterns that may be important in establishing this strain-specific differential response. Total RNA was isolated from spleens and pooled lymph nodes of both mouse strains at 3 and 7 days post virus infection. The complementary DNA generated from this RNA was hybridized to mouse oligonucleotide DNA microarrays using a strategy that controlled for inherent variability and highlighted only virus-induced changes. Fluorescent intensities were normalized and analyzed for statistically significant differential expression between strains across both time points and lymphoid organs. The majority of the resistance-associated genes was identified at day 3 post-infection and demonstrated the highest fold differences between strains, while more susceptibility-associated sequences were seen at 7 days post-infection. Among the most highly differentially expressed sequences seen at the earlier time point were genes related to protein metabolism, especially serine proteases. Differential patterns of chemokine-related genes were observed at the later time point. The overall pattern of expression suggests strain-specific differences in proteases and chemokines within secondary lymphoid organs shortly after infection influence the likelihood of disease progression.
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