Hepatitis D future or investigational therapies
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Jolanta Marszalek, M.D. [3]
Overview
Potential targets for antiviral therapy of HDV include drugs that interfere with postranslational modification and viral assembly. New drugs, such as prenylation inhibitors, HBV entry inhibitors, and new forms of interferons are currently being studied and tested for the treatment of hepatitis D, with better efficacy and tolerability.[1][2][3][4]
Future or Investigational Therapies
Although the lack of viral enzymes represents a challenge for the development of antiviral drugs, the life cycle of HDV relies deeply on postranslational modification of proteins and viral assembly. Therefore, these two stages are potential targets for antiviral drugs.[1]
Prenylation inhibitors are one example of antiviral drugs that target HDV replication cycle. These drugs have been used in cancer treatments, and are now being studied in therapies for hepatitis D.[2]
The dependence of HDV on previous, or simultaneous infection of hepatocytes by HBV, makes this another potential target for antiviral treatments. Myrcludex B (entry inhibitor of HBV) was shown to inhibit infection of the host cell by HBV in in vitro models and in vivo mice, consequently preventing infection by HDV. The drug is currently in the trial phase.[3][4]
Other potential antiviral target is the optimization of current treatments, such as interferons, or TLR agonists. A commonly used interferon is the type I interferon, which has receptors in different cells across the body, leading to its many side-effects. Other potential interferon, with less side effects, is the interferon-lambda. Because its receptors are less expressed in other cells, interferon-lambda, already being tested for hepatitis C, represents an alternative treatment for patients with hepatitis B and delta.[5]
References
- ↑ 1.0 1.1 Heidrich B, Manns MP, Wedemeyer H (2013). "Treatment options for hepatitis delta virus infection". Curr Infect Dis Rep. 15 (1): 31–8. doi:10.1007/s11908-012-0307-z. PMID 23242761.
- ↑ 2.0 2.1 Bordier BB, Ohkanda J, Liu P, Lee SY, Salazar FH, Marion PL; et al. (2003). "In vivo antiviral efficacy of prenylation inhibitors against hepatitis delta virus". J Clin Invest. 112 (3): 407–14. doi:10.1172/JCI17704. PMC 166292. PMID 12897208.
- ↑ 3.0 3.1 Petersen J, Dandri M, Mier W, Lütgehetmann M, Volz T, von Weizsäcker F; et al. (2008). "Prevention of hepatitis B virus infection in vivo by entry inhibitors derived from the large envelope protein". Nat Biotechnol. 26 (3): 335–41. doi:10.1038/nbt1389. PMID 18297057.
- ↑ 4.0 4.1 Lütgehetmann M, Mancke LV, Volz T, Helbig M, Allweiss L, Bornscheuer T; et al. (2012). "Humanized chimeric uPA mouse model for the study of hepatitis B and D virus interactions and preclinical drug evaluation". Hepatology. 55 (3): 685–94. doi:10.1002/hep.24758. PMID 22031488.
- ↑ Muir AJ, Shiffman ML, Zaman A, Yoffe B, de la Torre A, Flamm S; et al. (2010). "Phase 1b study of pegylated interferon lambda 1 with or without ribavirin in patients with chronic genotype 1 hepatitis C virus infection". Hepatology. 52 (3): 822–32. doi:10.1002/hep.23743. PMID 20564352.