Children with minimal or mild bilateral hearing loss and unilateral hearing loss are at higher risk for academic, speech-language, and social-emotional difficulties than their normal hearing peers. The choice to fit infants with moderate or greater degrees of bilateral hearing loss has been standard practice for most clinicians, but for those with minimal or mild bilateral hearing loss or unilateral hearing loss, the fitting of hearing technology must be based on limited data. Evidence does not yet exist to support all the management decisions that an audiologist must make upon identifying an infant with minimal or mild bilateral hearing loss or unilateral hearing loss. It is not yet known which children are at the greatest risk for educational problems nor is it known if the provision of early amplification in this population will help a child avoid later difficulties. Some of these considerations and current hearing technology options for children with minimal or mild bilateral hearing loss or unilateral hearing loss are reviewed in this article.

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Since its first identification in Scotland, over 1000 cases of unexplained pediatric hepatitis in children have been reported worldwide, including 278 cases in the UK 1 . Here we report investigation of 38 cases, 66 age-matched immunocompetent controls and 21 immunocompromised comparator subjects, using a combination of genomic, transcriptomic, proteomic and immunohistochemical methods. We detected high levels of adeno-associated virus 2 (AAV2) DNA in liver, blood, plasma or stool from 27/28 cases. We found low levels of Adenovirus (HAdV) and Human Herpesvirus 6B (HHV-6B), in 23/31 and 16/23 respectively of the cases tested. In contrast, AAV2 was infrequently detected at low titre in blood or liver from control children with HAdV, even when profoundly immunosuppressed.AAV2, HAdV and HHV-6 phylogeny excluded emergence of novel strains in cases. Histological analyses of explanted livers showed enrichment for T-cells and B-lineage cells.Proteomic comparison of liver tissue from cases and healthy controls, identified increased expression of HLA class 2, immunoglobulin variable regions and complement proteins.HAdV and AAV2 proteins were not detected in the livers. Instead, we identified AAV2 DNA complexes reflecting both HAdV and HHV-6B-mediated replication. We hypothesize that high levels of abnormal AAV2 replication products aided by HAdV and in severe cases HHV-6B, may have triggered immune-mediated hepatic disease in genetically and immunologically predisposed children.