Evaluation of viral replication in children with chronic hepatitis B with and without interferon treatment

Călin Lazăr1, Paula Grigorescu-Sido, Rodica Manasia

  • 1Axente Iancu, 1st Pediatric Clinic, Iuliu Moldovan Institute of Hygine, Cluj-Napoca, Romania. calinlazar2004@yahoo.com

Insights

Hepatitis B virus (HBV) DNA testing is crucial for monitoring viral replication in chronic hepatitis B patients, even when HBeAg is negative. Long-term follow-up is essential for effective management.

Area of Science:

  • Hepatology
  • Virology
  • Infectious Diseases

Background:

  • Chronic hepatitis B infection can persist even when HBeAg is negative.
  • HBeAg negativity does not always indicate suppressed hepatitis B virus (HBV) replication.

Purpose of the Study:

  • To assess HBV replication in patients with chronic hepatitis B or cirrhosis.
  • To compare the efficacy of interferon therapy versus no therapy in managing HBV.
  • To evaluate the utility of HBV DNA testing versus HBeAg testing for monitoring viral activity.

Main Methods:

  • 74 patients with chronic hepatitis B or cirrhosis were divided into two groups: interferon therapy (n=36) and control (n=38).
  • Patients were monitored for 6 years with clinical, biochemical, and serological tests.
  • HBV DNA was detected using hybridization on solid medium.

Main Results:

  • HBV DNA testing revealed higher viral replication levels than HBeAg testing in both groups (69.4% vs. 25% in the interferon group; 55.2% vs. 7.9% in the control group).
  • Absence of viral replication (HBV DNA negative) occurred in similar rates in both groups (30.6% vs. 44.8%).
  • HBV DNA titers were significantly higher in HBeAg-positive patients, and concordance between HBeAg and HBV DNA was 100%.

Conclusions:

  • Long-term follow-up and monitoring, including HBV DNA testing, are necessary for patients with chronic hepatitis B.
  • This is particularly important for inactive HBsAg carriers to detect potential viral replication.
  • HBeAg status alone is insufficient for assessing viral suppression in chronic hepatitis B.
Abstract

Related Concept Videos

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...