Full-length genome characterization and genetic relatedness analysis of hepatitis A virus outbreak strains associated with acute liver failure among children

Clinical infection by hepatitis A virus (HAV) is generally self‐limited but in some cases can progress to liver failure. Here, an HAV outbreak investigation among children with acute liver failure in a highly endemic country is presented. In addition, a sensitive method for HAV whole genome amplific...

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Bibliographic Details
Published in:Journal of medical virology 2014-02, Vol.86 (2), p.202-208
Main Authors: Vaughan, Gilberto, Forbi, Joseph C., Xia, Guo-Liang, Fonseca-Ford, Maureen, Vazquez, Roberto, Khudyakov, Yury E., Montiel, Sonia, Waterman, Steve, Alpuche, Celia, Gonçalves Rossi, Livia Maria, Luna, Norma
Format: Article
Language:English
Subjects:
acute liver failure
Adolescent
Child
Children & youth
Cluster Analysis
Disease Outbreaks
Female
Genome, Viral
Genomics
Hepatitis
Hepatitis A - complications
Hepatitis A - epidemiology
Hepatitis A - pathology
Hepatitis A - virology
Hepatitis A virus
Hepatitis A virus - genetics
Hepatitis A virus - isolation & purification
Humans
Liver diseases
Liver Failure, Acute - epidemiology
Liver Failure, Acute - pathology
Liver Failure, Acute - virology
Male
Mexico
Molecular Sequence Data
Phylogeny
RNA, Viral - genetics
Sequence Analysis, DNA
United States
Virology
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Description
Summary:Clinical infection by hepatitis A virus (HAV) is generally self‐limited but in some cases can progress to liver failure. Here, an HAV outbreak investigation among children with acute liver failure in a highly endemic country is presented. In addition, a sensitive method for HAV whole genome amplification and sequencing suitable for analysis of clinical samples is described. In this setting, two fatal cases attributed to acute liver failure and two asymptomatic cases living in the same household were identified. In a second household, one HAV case was observed with jaundice which resolved spontaneously. Partial molecular characterization showed that both households were infected by HAV subtype IA; however, the infecting strains in the two households were different. The HAV outbreak strains recovered from all cases grouped together within cluster IA1, which contains closely related HAV strains from the United States commonly associated with international travelers. Full‐genome HAV sequences obtained from the household with the acute liver failure cases were related (genetic distances ranging from 0.01% to 0.04%), indicating a common‐source infection. Interestingly, the strain recovered from the asymptomatic household contact was nearly identical to the strain causing acute liver failure. The whole genome sequence from the case in the second household was distinctly different from the strains associated with acute liver failure. Thus, infection with almost identical HAV strains resulted in drastically different clinical outcomes. J. Med. Virol. 86:202–208, 2014. © 2013 Wiley Periodicals, Inc.
ISSN:0146-6615
1096-9071
DOI:10.1002/jmv.23843