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REVIEW ARTICLE Table of Contents   
Year : 2008  |  Volume : 5  |  Issue : 1  |  Page : 81-94
Chronic delta hepatitis: An overview

Department of Gastroenterology, University of Ankara Medical School, Cebeci Tip Fakultesi Hastanesi, Dikimevi, 06100 Ankara, Turkey

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Date of Web Publication9-Jan-2010


Delta hepatitis or hepatitis D leads to acute and chronic liver disease in humans. The causative agent, the hepatitis delta virus (HDV), is a defective virus which leads to hepatitis in humans in the presence of the hepatitis B virus. This helper function of HBV is required for transmission and propagation of HDV infection but not for replication. HDV RNA replication occurs through the double-rolling circle model and does not possess a reverse transcription step. Hepatitis D-induced liver disease is immune-mediated and occurs either as co-infection of both viruses or as superinfection of a hepatitis B carrier with hepatitis D. Based on a sequence variation of 19-38%, to date seven genotypes of HDV have been described. HDV infection has declined significantly in many endemic areas in the last decades, however, due to migration to industrialized countries, this decline appears to have reached a plateau in western countries. The clinical course of delta hepatitis in general is associated with rapid progression. Delta hepatitis may be an additional risk factor for the development of hepatocellular carcinoma. The only established management for delta hepatitis consists of treatment with interferon for a period of at least one year. For those unresponsive to interferon treatment and patients with advanced disease new therapies are an urgent need. Such therapies may be on the horizon but translation of bench work to clinical practice is required.

Keywords: Delta hepatitis, epidemiology, hepatitis D virus, natural history, treatment, virology.

How to cite this article:
Yurdaydin C. Chronic delta hepatitis: An overview. Hep B Annual 2008;5:81-94

How to cite this URL:
Yurdaydin C. Chronic delta hepatitis: An overview. Hep B Annual [serial online] 2008 [cited 2023 Dec 5];5:81-94. Available from: https://www.hepatitisbannual.org/text.asp?2008/5/1/81/58807

Delta hepatitis leads to acute and chronic liver disease in humans. The causative agent, the hepatitis delta virus (HDV), discovered by Rizetto et al., [1] is a defective virus which leads to hepatitis in humans in the presence of the hepatitis B virus (HBV). The association of both viruses in the human condition either occurs as co-infection of hepatitis B and D viruses or as superinfection with HDV of patients who are carriers of the hepatitis B virus. [2] Co-infection causes acute hepatitis. Superinfection with HDV leads to chronic hepatitis in the vast majority of cases. [2],[3] Chronic delta hepatitis represents the most severe form of chronic viral hepatitis and is associated with the most rapid progression of disease among hepatotrop virus infections.

The hepatitis delta virus

The hepatitis delta virus is an approximately 36 nm large particle containing HDV RNA and delta antigen. [2]-[4] HDV RNA is single stranded, highly base-paired, circular and is the smallest genome of any animal virus containing close to 1700 nucleotides. It is coated with envelope protein derived from the pre-S and S antigens of the hepatitis B virus. The production of HBsAg is the only HBV function on which the HDV depends. This helper function of HBV is required for transmission and propagation of HDV infection but not for replication. The HDV RNA has six open reading frames (ORFs) of which only one appears to be actively transcribed. [2],[4] This ORF codes for the hepatitis delta antigen (HDAg). Two HDAgs exist: the small HDAg (24 kd) is 195 amino acids long and the large HDAg (27kd) is 214 amino acids long. The large delta antigen is identical in sequence to the small delta antigen except that it contains an extra 19 amino acids at its carboxyl terminus which is a result of a specific RNA editing event occurring during replication of the HDV genome. The small HDAg is required for HDV RNA replication whereas the large HDAg inhibits HDV RNA synthesis but is necessary for virion morphogenesis. [2],[3],[4]

Replication of HDV RNA occurs through a 'double rolling circle model' in which the genomic strand is replicated by a host RNA polymerase to yield a multimeric linear structure which is then autocatalytically cleaved to linear monomers and ligated into the circular HDV RNA viral progeny [Figure 1].

Based on a sequence variation of 19-38%, to date seven genotypes of HDV have been described [Figure 2]. [5] Since genotypes IIa and IIb in the old nomenclature have only 77% of nucleotide homology, they were assigned to genotypes II and IV in the new nomenclature. Genotypes V, VI and VII have been recently described and these genotypes are based on newly found isolates from Africa. [5] Genotype I is the most prevalent one and distributed throughout the world. [6] It is most common in Mediterranean countries, Africa, Europe and North America. Genotypes II and IV are mostly reported from the Far East and some parts of Russia and are in general associated with a milder disease compared to genotype I. [7],[8] However, a genotype IV (former genotype IIb) variant may be associated with severe liver disease. [9] Genotype III causes the most severe disease and is particularly responsible for outbreaks of fulminant and severe hepatitis in northern South American countries, such as Columbia, Venezuela, Peru and Ecuador. [10]


HDV is distributed worldwide. The distribution of the disease varies widely and does not exactly reflect the prevalence of HBV infection worldwide. [11] For example, although HBV infection is common in the Far East, HDV infection in the same region is infrequent. Up to 5% of the world's population is known to be infected with HBV and it is considered that at least 5% of all hepatitis B carriers are infected with HDV. With increased control of HBV infection achieved by universal HBV vaccination programs, use of disposable needles, screening blood donors for HBsAg and socioeconomic improvements, HDV infection has declined significantly in many endemic areas like some parts of Southern Europe [12],[13],[14] and Southeast Asia. [15] However, migration from East Europe to West Europe [16] or from poorer countries in general appears to have brought the decline in prevalence to a plateau. [17],[18] On the other hand, in other parts of the Mediterranean basin, such as Turkey, the disease is still endemic [19] and continues to be an important health problem. [20]


The pathogenesis of HDV infection remains poorly understood and under-investigated. Liver disease in delta hepatitis is most likely immune mediated. Observation of mononuclear cell infiltration in liver tissue specimens of patients with delta hepatitis and the lack of liver disease in mice made transgenic for both small and large HDAg [21] support this view. One study analyzed proliferative responses of CD4+ T cells to HDV antigen. [22] Overall, 27% of the patients responded to HDV antigen and this response was targeted against different parts of the HDV genome. Only patients with inactive HDV-disease displayed HDV-specific proliferation of CD4+ T cells suggesting that cellular immune responses are able to control HDV. [22] Recently, the contribution of perforin-positive (cytotoxic) CD4 + T cells to the more aggressive course of delta hepatitis has been suggested. [23]

Disease characteristics

Hepatitis D infection develops either as co-infection with hepatitis B or as superinfection of HBsAg carriers with delta viruses. In co-infection, most cases resemble a typical self-limited hepatitis that is clinically and histologically indistinguishable from hepatitis B or other types of viral hepatitis. [3] However, acute HDV infection tends to aggravate the course of the acute HBV infection and is more likely to lead to fulminant hepatitis. [3],[4] But most often it resolves with complete recovery, as typically observed in acute hepatitis B. The rate of chronicity following co-infection is very low (<5%) and similar to that of HBV infection alone.

Superinfection of chronically HBV-infected patients with HDV leads to chronic delta hepatitis in 90% of patients. Only rarely does HDV superinfection result in the clearance of both HDV and HBV. Although there are chronic delta hepatitis cases with a benign course and inactive disease, chronic delta hepatitis, in general, leads to more serious disease compared to chronic hepatitis B and chronic hepatitis C, with an accelerated course and early decompensation. [3] Severe forms are more often seen in patients with a history of intravenous drug use. Furthermore, chronic delta hepatitis may be an additional risk factor for the development of hepatocellular carcinoma (HCC). [24] However, it is also noteworthy that control of HDV in developed countries has resulted not only in dramatic reduction of new HDV cases but also in significant changes in the clinical features of the patients; fresh and severe forms of the disease are less commonly seen, and a majority of the patients have long-standing infections either due to indolent, non-progressive, mild disease or advanced cirrhosis. [25]

In liver transplant recipients, patients with cirrhosis due to HDV have a better prognosis than patients transplanted for HBV-induced cirrhosis. [26] In those patients where HDV infection recurs after transplantation this appears to follow the typical HDV infection pattern through the helper function of HBV. [27]


Therapy for chronic delta hepatitis with proven efficacy consists of interferon (IFN) and peginterferon (peg-IFN). In the early 1990s, controlled clinical trials showed that IFN-alpha is effective in chronic hepatitis D but relapse is high and its efficacy is related to the dose and the duration of the therapy. [28],[29],[30] High doses (9-10 million units (MU) thrice weekly or 5 MU daily) for at least one year are required for achieving a better outcome, determined by a biochemical and virologic response (ALT normalization and loss of HDV viremia measured by PCR) both of which correlate with improvement in liver histology. [28],[30] Long-term follow-up (median 13.0 years) of patients in the original study by Farci et al. [28] indicates that high dose interferon may favorably affect the natural history of the disease. [31]

Some patients may need treatment beyond one year. Common sense would suggest that patients with a partial biochemical and virologic response and those who relapse after treatment discontinuation would be the typical candidates for prolonged treatment. Successful eradication of both HBV and HDV in a patient treated daily with interferon for 12 years supports this view. [32] Pilot studies of the use of INF-alpha for 2 years do not appear to show superiority over one year of therapy. [33],[34],[35] However, all of these studies were small cohort studies and did not have a comparator arm of standard one-year treatment. Side effects decreasing compliance to treatment appears to be a problem in prolonged courses of treatment.

Experience with PEG-IFN-alpha has been reported recently by 4 groups. [36],[37],[38],[39] A sustained virologic response, defined as negative HDV RNA 6 months after treatment cessation was reported in 17 to 47% of patients. Differences in dropout rates, in the sensitivities of HDV RNA PCR assays used, in the proportion of patients who had used interferon in the past and who were cirrhotic at baseline may account for the divergent results. Several studies emphasize the importance of measuring HDV RNA at month 6 of treatment, [36],[38],[40] which may predict those who will respond to 1 year of treatment and those who may need extended duration of treatment [Figure 3]. In an analysis of baseline factors predicting response to treatment, patients who were treatment naοve at baseline or who had a low baseline GGT tended to respond better compared to patients who had used IFN in the past or whose baseline GGT was high. [40] In concert with these data, disease of short duration had been previously reported to be predictive of response to treatment. [33] Combination of nucleos(t)ide analogs with interferons with the expectation of better treatment outcomes has failed to show superiority to interferon monotherapy. [35],[36],[39],[40]

Although the HDV has an obligatory dependence on HBV to cause disease, drugs that specifically inhibit HBV replication have shown no effect in CDH. Famciclovir, lamivudine and adefovir have so far been assessed in this context for the treatment of CDH. [39],[40],[41],[42],[43] The most likely reason for this is that none of the current HBV therapies can inhibit the production of HBsAg, the only part of HBV that HDV depends on.

A new nucleoside analog may have therapeutic potential. Clevudine, in the woodchuck hepatitis model, significantly inhibited the production of the surface antigen in a dose-dependent manner. [44] Indeed, in a preliminary study, clevudine was able to significantly decrease HDV RNA in woodchucks infected with HDV. [45]

Another new approach would be the use of prenylation inhibitors. The large, but not the small, delta antigen contains at its carboxyl terminal a cystein containing four amino acid motif? serving as substrate for prenyl transferases which add a prenyl group to the large delta antigen. [46] It has been shown that prenylation of the large delta antigen is necessary for virion morphogenesis. Prenylation inhibitors have been shown to specifically abolish HDV-like particle production in vitro. [47],[48] Recently, antiviral efficacy of prenylation inhibitors has also been reported in the in vivo setting in a mouse-based model of HDV infection [49] which suggests its use in human delta infection. Some prenylation inhibitors have been tested in humans as potential treatment for some malignant tumors and they appear to be without major side effects in humans. [50]

In conclusion, successful treatment of delta hepatitis continues to be confined to the rational use of interferons. However, there are many patients who do not respond to interferons or cannot use them. Development of new treatment strategies is therefore an urgent need.

   References Top

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Correspondence Address:
Cihan Yurdaydin
Department of Gastroenterology, University of Ankara Medical School, Cebeci Tip Fakultesi Hastanesi, Dikimevi, 06100 Ankara
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-9747.58807

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