Neonatal and Pediatric Infection
Deirdre A. Kelly
The Liver Unit, Birmingham Children's Hospital NHS Trust, Birmingham, UK
Search for more papers by this authorC.Y. William Tong
Department of Infectious Diseases, Guy's and St. Thomas’ NHS Foundation Trust and King's College London School of Medicine, London, UK
Search for more papers by this authorDeirdre A. Kelly
The Liver Unit, Birmingham Children's Hospital NHS Trust, Birmingham, UK
Search for more papers by this authorC.Y. William Tong
Department of Infectious Diseases, Guy's and St. Thomas’ NHS Foundation Trust and King's College London School of Medicine, London, UK
Search for more papers by this authorHoward C. Thomas BSc, PhD, FRCP, FRCPath, FMedSci
Emeritus Professor of Hepatology, Department of Medicine, Imperial College London, London, UK
Search for more papers by this authorAnna S.F. Lok MD
Alice Lohrman Andrews Research Professor in Hepatology, Director of Clinical Hepatology, Professor of Internal Medicine, Associate Chair for Clinical Research, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI, USA
Search for more papers by this authorStephen A. Locarnini MBBS, BSc(Hons), PhD, FRCPath
Head, Research & Molecular Development, Victorian Infectious Diseases Reference Laboratory, Melbourne, VIC, Australia
Search for more papers by this authorArie J. Zuckerman MD, DSc, FRCP, FRCPath, FMedSci
Emeritus Professor of Medical Microbiology, Formerly Principal and Dean, Royal Free Hospital School of Medicine
Search for more papers by this authorSummary
Viral infections in neonates and children range from asymptomatic carrier status to end-stage acute or chronic liver failure. Neonates are usually infected in utero or perinatally with the TORCH infections and could develop acute liver failure due to herpes simplex viruses, enteroviruses, or rarely adenoviruses. Acute hepatitis in older children is due to hepatitis A virus (HAV), hepatitis E virus (HEV), or Epstein–Barr virus (EBV) in adolescents. Hepatitis B may present with fulminant hepatitis in neonates of HBe antigen–negative mothers as well as in older children. Acute hepatitis from any source may progress to fulminant hepatitis requiring liver transplantation. Chronic hepatitis in childhood is due to either HBV or HCV. The main route of infection is perinatal, and children have a low natural seroconversion rate and a lifetime risk of chronic liver disease and liver cancer. Treatment for HBV is unsatisfactory, with only a 30% success rate with either interferon or nucleotides, while combination therapy with pegylated interferon and ribavirin clears between 70–90% of HCV infections dependent on the genotype.
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