Affiliation:
1. Université Catholique de Louvain, Christian de Duve Institute of Cellular Pathology, Microbial Pathogenesis Unit, MIPA-VIRO 74-49
2. Unit of Experimental Medicine, Ludwig Institute for Cancer Research and Université Catholique de Louvain, B-1200 Brussels, Belgium
Abstract
ABSTRACT
Mouse and human genomes carry more than a dozen genes coding for closely related alpha interferon (IFN-α) subtypes. IFN-α, as well as IFN-β, IFN-κ, IFN-ε, and limitin, are thought to bind the same receptor, raising the question of whether different IFN subtypes possess specific functions. As some confusion existed in the identity and characteristics of mouse IFN-α subtypes, the availability of data from the mouse genome sequence prompted us to characterize the murine IFN-α family. A total of 14 IFN-α genes were detected in the mouse genome, in addition to three IFN-α pseudogenes. Four IFN-α genes (IFN-α1, IFN-α7/10, IFN-α8/6, and IFN-α11) exhibited surprising allelic divergence between 129/Sv and C57BL/6 mice. All IFN-α subtypes were found to be stable at pH 2 and to exhibit antiviral activity. Interestingly, some IFN subtypes (IFN-α4, IFN-α11, IFN-α12, IFN-β, and limitin) showed higher biological activity levels than others, whereas IFN-α7/10 exhibited lower activity. Most murine IFN-α turned out to be N-glycosylated. However, no correlation was found between N-glycosylation and activity. The various IFN-α subtypes displayed a good correlation between their antiviral and antiproliferative potencies, suggesting that IFN-α subtypes did not diverge primarily to acquire specific biological activities but probably evolved to acquire specific expression patterns. In L929 cells, IFN genes activated in response to poly(I•C) transfection or to viral infection were, however, similar.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Cited by
169 articles.
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