22 October 2017
Int J Med Sci 2010; 7(3):110-119. doi:10.7150/ijms.7.110
Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture
1. Pennsylvania State College of Medicine/ Milton S. Hershey Medical Center, Hershey, PA, U.S.A.;
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
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How to cite this article:
Kivovich V, Gilbert L, Vuento M, Naides SJ. Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture. Int J Med Sci 2010; 7(3):110-119. doi:10.7150/ijms.7.110. Available from http://www.medsci.org/v07p0110.htm