Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture
<p>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 hep...
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doaj-5725772ac7b244668dd67568dc67584e2020-11-25T02:25:21ZengIvyspring International PublisherInternational Journal of Medical Sciences1449-19072010-01-0173110119Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in CultureVioletta Kivovich, Leona Gilbert, Matti Vuento, Stanley J. Naides<p>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 (<i>Int J Med S</i>ci. 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.</p>http://www.medsci.org/v07p0110.htm |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Violetta Kivovich, Leona Gilbert, Matti Vuento, Stanley J. Naides |
spellingShingle |
Violetta Kivovich, Leona Gilbert, Matti Vuento, Stanley J. Naides Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture International Journal of Medical Sciences |
author_facet |
Violetta Kivovich, Leona Gilbert, Matti Vuento, Stanley J. Naides |
author_sort |
Violetta Kivovich, Leona Gilbert, Matti Vuento, Stanley J. Naides |
title |
Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture |
title_short |
Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture |
title_full |
Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture |
title_fullStr |
Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture |
title_full_unstemmed |
Parvovirus B19 Genotype Specific Amino Acid Substitution in NS1 Reduces the Protein's Cytotoxicity in Culture |
title_sort |
parvovirus b19 genotype specific amino acid substitution in ns1 reduces the protein's cytotoxicity in culture |
publisher |
Ivyspring International Publisher |
series |
International Journal of Medical Sciences |
issn |
1449-1907 |
publishDate |
2010-01-01 |
description |
<p>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 (<i>Int J Med S</i>ci. 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.</p> |
url |
http://www.medsci.org/v07p0110.htm |
work_keys_str_mv |
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