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Updated: Apr 30, 2026

Author Spotlight: Advancements and Challenges in Hepatitis B Virus Detection
Published on: December 15, 2023
Hepatitis B virus PreS/S gene variants: pathobiology and clinical implications
Teresa Pollicino1, Irene Cacciola2, Francesca Saffioti2
1Division of Clinical and Molecular Hepatology, University Hospital of Messina, Via Consolare Valeria, 1, 98124 Messina, Italy; Department of Pediatric, Gynecologic, Microbiological and Biomedical Sciences, University Hospital of Messina, Via Consolare Valeria, 1, 98124 Messina, Italy.
Hepatitis B virus (HBV) preS/S variants can cause liver disease and cancer. These mutations lead to protein buildup, DNA damage, and immune evasion, impacting treatment outcomes.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Hepatitis B virus (HBV) preS/S variants frequently emerge spontaneously or due to treatment.
- These mutations can lead to significant pathobiological and clinical consequences.
Purpose of the Study:
- To investigate the implications of preS/S variants in HBV infection.
- To understand the mechanisms by which these variants cause disease progression.
Main Methods:
- Review of experimental data and human studies on preS/S mutations.
- Analysis of protein synthesis, endoplasmic reticulum (ER) retention, and ER stress induction.
- Assessment of oxidative DNA damage, genomic instability, and clinical outcomes.
Main Results:
- Specific preS/S mutations cause surface protein imbalance and ER retention in hepatocytes.
- Mutated protein accumulation induces ER stress, oxidative DNA damage, and genomic instability.
- Antigenically altered variants can infect immune-prophylaxed individuals, leading to occult HBV infection, fulminant hepatitis, fibrosing cholestatic hepatitis, cirrhosis, and hepatocellular carcinoma.
Conclusions:
- PreS/S variants are key drivers of HBV pathogenesis and disease progression.
- Understanding these variants is crucial for developing effective therapeutic strategies and improving patient outcomes.
- Further research into preS/S variant-associated liver disease is warranted.
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