Clinical stage drugs targeting inhibitor of apoptosis proteins purge episomal Hepatitis B viral genome in preclinical models.
Michelle P ClarkThao HuynhShringar RaoLiana MackiewiczHugh MasonShahla RomalMichael D StutzSang H AhnLinda EarnestVitina SozziMargaret LittlejohnBang M TranNorbert WiedemannElizabeth VincanJoseph TorresiHans J NetterTokameh MahmoudiPeter RevillMarc PellegriniGregor EbertPublished in: Cell death & disease (2021)
A major unmet clinical need is a therapeutic capable of removing hepatitis B virus (HBV) genome from the liver of infected individuals to reduce their risk of developing liver cancer. A strategy to deliver such a therapy could utilize the ability to target and promote apoptosis of infected hepatocytes. Presently there is no clinically relevant strategy that has been shown to effectively remove persistent episomal covalently closed circular HBV DNA (cccDNA) from the nucleus of hepatocytes. We used linearized single genome length HBV DNA of various genotypes to establish a cccDNA-like reservoir in immunocompetent mice and showed that clinical-stage orally administered drugs that antagonize the function of cellular inhibitor of apoptosis proteins can eliminate HBV replication and episomal HBV genome in the liver. Primary human liver organoid models were used to confirm the clinical relevance of these results. This study underscores a clinically tenable strategy for the potential elimination of chronic HBV reservoirs in patients.
Keyphrases
- hepatitis b virus
- liver failure
- oxidative stress
- endoplasmic reticulum stress
- cell cycle arrest
- genome wide
- cell death
- circulating tumor
- end stage renal disease
- liver injury
- single molecule
- cell free
- drug induced
- newly diagnosed
- stem cells
- type diabetes
- gene expression
- dna methylation
- mesenchymal stem cells
- peritoneal dialysis
- prognostic factors
- risk assessment
- bone marrow
- climate change
- adipose tissue
- cell proliferation
- cell therapy