Key result
Hepatitis A virus strains from 18 children with fulminant hepatic failure differed at the nucleotide level from self-limited acute infection strains.
Observational (n=41)
Viral genetic factors may contribute to the severity of hepatitis A infection and the development of fulminant hepatic failure in children.
Strain variation may flag high-risk pediatric HAV; leaves open causal role and should not yet change practice.
BACKGROUND: Hepatitis A infection, a vaccine-preventable disease, is an important cause of fulminant hepatic failure (FHF) in children in Argentina. Universal vaccination in 1-year-old children was implemented in June 2005. The limited studies about the correlation between the characteristics of the hepatitis A virus (HAV) and FHF have been carried out in adults. METHODS: Samples from 41 children with FHF were studied from September 2003 to January 2006 and HAV RNA was detected, sequenced and analysed in the 5' non-coding region and VP1/2A region. RESULTS: Eighteen HAV strains were characterized and found to be different at the nucleotide level from the self-limited acute infection strains that have been circulating in Argentina with no temporal or geographical pattern. They did not form a genetic cluster, but some of them were identical in the largest fragment characterized and some of them seemed to be more closely related in time and/or geographically. CONCLUSION: Our results suggest that viral factors could be involved in the severity of the clinical presentation of HAV infection in children in Argentina.
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Munné et al. (2007) conducted an observational in Fulminant hepatic failure (n=41). Hepatitis A virus strains vs. Self-limited acute infection strains was evaluated on Molecular characterization of HAV strains. Hepatitis A virus strains from 18 children with fulminant hepatic failure differed at the nucleotide level from self-limited acute infection strains.
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