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.: Home > International Journal of Medical Sciences > 2010 > Volume 7 Number 3 > Violetta Kivovich 1,2 , Leona Gilbert 2, Matti Vuento 2 and Stanley J. Naides 3

Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein’s Cytotoxicity in Culture

Violetta Kivovich 1,2 , Leona Gilbert 2, Matti Vuento 2 and Stanley J. Naides 3
1. Pennsylvania State College of Medicine/ Milton S. Hershey Medical Center, Hershey, PA, U.S.A.; 2. Department of Biological and Environmental Science and Nanoscience Center, University of Jyvنskylن, Jyvنskylن, Finland; 3. Quest Diagnostics Nichols Institute, San Juan Capistrano, CA, U.S.A.
Abstract :

A clinical association between idiopathic liver disease and parvovirus B19 infection has been observed. Fulminant liver failure, not associated with other liver-tropic viruses, has been attributed to B19 in  numerous reports, suggesting a possible role for B19 components in the extensive hepatocyte cytotoxicity observed in this condition. A recent report by Abe and colleagues (Int J Med Sci. 2007;4:105-9) demonstrated a link between persistent parvovirus B19 genotype I and III infection and fulminant liver failure. The genetic analysis of isolates obtained from these patients demonstrated a conservation of key amino acids in the nonstructural protein 1 (NS1) of the disease-associated genotypes. In this report we examine a conserved residue identified by Abe and colleagues and show that substitution of isoleucine
181 for methionine, as occurs in B19 genotype II, results in the reduction of B19 NS1-induced cytotoxicity of liver cells. Our results support the hypothesis that in the setting of persistent B19 infection, direct B19 NS1-induced cytotoxicity may play a role in idiopathic fulminant liver failure.

Keywords :
Parvovirus, B19, Fulminant Liver Failure, Cytotoxicity, Apoptosis

Date Deposited : 27 Jul 2011 12:35

Last Modified : 27 Jul 2011 12:35

Official URL: http://www.medsci.org/archive

Volume 7, Number 3, - 2010 , ISSN 1449-1907

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