Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/94163
Title: Determination of encephalomyocarditis viral diabetogenicity by a putative binding site of the viral capsid protein
Authors: Notkins, Abner L.
Yoon, Ho Sup
Jun, Hee-Sook
Kang, Yup
Kim, Ki Hwan
Yoon, Ji-Won
Keywords: DRNTU::Science::Biological sciences::Microbiology::Virology
Issue Date: 1998
Source: Jun, H. S., Kang, Y., Yoon, H. S., Kim, K. H., Notkins, A. L. & Yoon, J. W. (1998). Determination of Encephalomyocarditis Viral Diabetogenicity by a Putative Binding Site of the Viral Capsid Protein. Diabetes, 47(4), 576-582.
Series/Report no.: Diabetes
Abstract: The molecular mechanism by which some, but not all, variants of encephalomyocarditis (EMC) virus selectively infect pancreatic beta-cells in mice and induce IDDM has been an enigma for more than a decade. We report here that the binding site of the EMC viral capsid protein VP1 determines viral diabetogenicity. Recombinant chimeric EMC viruses containing threonine, serine, proline, aspartic acid, or valine at position 152 of the major capsid protein VP1 bind poorly to beta-cells. In contrast, recombinant chimeric EMC viruses containing alanine or glycine at position 152 of the VP1 bind efficiently to and infect beta-cells, resulting in the development of diabetes. Three-dimensional molecular modeling reveals that the van der Waals interactions are greater and the residues surrounding position 152 of the VP1 are more closely packed in recombinant chimeric viruses containing threonine, serine, proline, aspartic acid, or valine at position 152 than in recombinant chimeric viruses containing alanine or glycine at the same position. Our studies reveal that the surface areas surrounding alanine or glycine at position 152 of the VP1 are more accessible, thus increasing the availability of the binding sites for attachment to beta-cell receptors and resulting in viral infection and the development of diabetes.
URI: https://hdl.handle.net/10356/94163
http://hdl.handle.net/10220/7489
DOI: 10.2337/diabetes.47.4.576
Rights: © 1998 American Diabetes Association. This is the author created version of a work that has been peer reviewed and accepted for publication by Diabetes, American Diabetes Association. It incorporates referee’s comments but changes resulting from the publishing process, such as copyediting, structural formatting, may not be reflected in this document. The published version is available at: http://dx.doi.org/10.2337/diabetes.47.4.576
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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