Covalently closed circular DNA: The ultimate therapeutic target for curing HBV infections

Current antiviral therapies, such as pegylated interferon-α and nucleos(t)ide analogues, effectively improve the quality of life of patients with chronic hepatitis B. However, they can only control the infection rather than curing infected hepatocytes. Complete HBV cure is hampered by the lack of th...

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Veröffentlicht in:Journal of hepatology Jg. 75; H. 3; S. 706 - 717
Hauptverfasser: Martinez, Maria Guadalupe, Boyd, Anders, Combe, Emmanuel, Testoni, Barbara, Zoulim, Fabien
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Netherlands Elsevier B.V 01.09.2021
Elsevier Science Ltd
Elsevier
Schlagworte:
Antiviral agents
Antiviral Agents - pharmacology
Antiviral Agents - therapeutic use
cccDNA
chronic hepatitis B
Chronic infection
Circular DNA
Clinical trials
direct-acting antivirals
DNA, Circular - pharmacology
DNA, Circular - therapeutic use
HBV cure
Hepatitis B
Hepatitis B - drug therapy
Hepatitis B surface antigen
Hepatitis B virus - genetics
Hepatocytes
Human health and pathology
Humans
Hépatology and Gastroenterology
Interferon
Life Sciences
Metal-Organic Frameworks - pharmacology
Metal-Organic Frameworks - therapeutic use
Quality of life
Therapeutic targets
α-Interferon
chronic hepatitis B
HBV cure
cccDNA
direct-acting antivirals
ISSN:0168-8278, 1600-0641, 1600-0641
Online-Zugang:Volltext
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Zusammenfassung:Current antiviral therapies, such as pegylated interferon-α and nucleos(t)ide analogues, effectively improve the quality of life of patients with chronic hepatitis B. However, they can only control the infection rather than curing infected hepatocytes. Complete HBV cure is hampered by the lack of therapies that can directly affect the viral minichromosome (in the form of covalently closed circular DNA [cccDNA]). Approaches currently under investigation in early clinical trials are aimed at achieving a functional cure, defined as the loss of HBsAg and undetectable HBV DNA levels in serum. However, achieving a complete HBV cure requires therapies that can directly target the cccDNA pool, either via degradation, lethal mutations or functional silencing. In this review, we discuss cutting-edge technologies that could lead to non-cytolytic direct cccDNA targeting and cure of infected hepatocytes.
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ISSN:0168-8278
1600-0641
1600-0641
DOI:10.1016/j.jhep.2021.05.013