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Related Concept Videos

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...
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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...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Polymorphic APOBEC3 modulates chronic hepatitis B in Moroccan population.

S Ezzikouri1, B Kitab, K Rebbani

  • 1Viral Hepatitis Laboratory, Pasteur Institute of Morocco, Casablanca, Morocco.

Journal of Viral Hepatitis
|September 10, 2013
PubMed
Summary
This summary is machine-generated.

Genetic variations in apolipoprotein B mRNA editing catalytic subunit-3 (APOBEC3) deaminases do not predispose to chronic hepatitis B virus (HBV) infection but can influence its progression. APOBEC3B deletion carriers showed lower HBV viral loads, suggesting a role in modulating persistent infection.

Keywords:
3D-PCRAPOBEC3HBVcytidine deaminaseshypermutationpolymorphisms

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Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • The apolipoprotein B mRNA editing catalytic subunit-3 (APOBEC3) family are key components of innate immunity against viruses, including hepatitis B virus (HBV).
  • APOBEC3 enzymes induce G-to-A hypermutation in viral genomes, acting as a defense mechanism.
  • Understanding the role of APOBEC3 genetic variants in HBV infection is crucial for comprehending disease pathogenesis and progression.

Purpose of the Study:

  • To investigate the association between APOBEC3 genetic variants and HBV carriage in a Moroccan population.
  • To assess the impact of APOBEC3 deaminases on circulating HBV genomes and viral load.
  • To explore the relationship between APOBEC3 genotypes and the progression of chronic hepatitis B.

Main Methods:

  • A case-control study involving 179 chronic HBV carriers and 216 healthy controls.
  • Genotyping of a polymorphic deletion in APOBEC3B and the H186R variant in APOBEC3G.
  • Detection of hyperedited HBV genomes using 3D-PCR to analyze editing context.
  • Statistical analysis of allele and genotype frequencies, and correlation with disease progression and viral load.

Main Results:

  • No significant difference in APOBEC3B deletion or APOBEC3G H186R genotype frequencies between HBV carriers and controls.
  • Subjects with the APOBEC3B deletion genotype showed a trend towards faster liver disease progression (adjusted OR, 3.72).
  • APOBEC3B deletion carriers exhibited significantly lower HBV viral loads compared to wild-type individuals (median 539 vs. 2213 IU/mL, P = 0.0023).
  • 3D-PCR detected G-to-A hypermutations in 14% of samples, indicative of APOBEC3 activity.

Conclusions:

  • Genetic variations in APOBEC3 deaminases do not appear to predispose individuals to chronic HBV infection.
  • APOBEC3 genetic variants, particularly APOBEC3B deletion, may modulate the course and viral load of persistent HBV infection.
  • APOBEC3 enzymes play a role in controlling HBV replication during chronic infection.