Sherlock's Diseases of the Liver and Biliary System 2018

DOI: 10.1002/9781119237662.ch22

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Hepatitis D

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Clinical Manifestations and Diagnosis5

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“…One such factor is genotypic variability. Among the eight known genotypes, HDV-1 has the highest pathogenic potential[ 31 , 33 , 35 ], while HDV-2 and HDV-4 are associated with milder forms of the disease[ 35 ]. According to a study conducted in Taiwan, patients infected with HDV-2 develop liver failure less frequently than those with genotype 1[ 34 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…The pathogenic properties of HDV 5-8 are not well characterized[ 7 , 36 ]. Among the spectrum of host and viral factors that may underlie the different outcomes of infection with these various genotypes, we can include variability in virus replication and virion assembly efficacy, both of which contribute to the rate of HDV virion secretion, and such host factors as race or presence of single-nucleotide polymorphisms[ 35 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…The anti-HD IgG antibody reaches a detectable level after the IgM antibodies disappear, and may persist for months or even years. A failure in anti-HD IgM clearance predicts the chronicity of hepatitis[ 26 , 35 , 42 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…Conversely, in HDV super-infection, the virus infects individuals with chronic HBV infection, and it typically leads to HDV persistence with development of cirrhosis[ 35 ]. It may present either as an exacerbation of a known chronic hepatitis B status accompanied by hepatic decompensation, or as a new acute hepatitis status in asymptomatic HBsAg carriers[ 35 ]. Super-infection usually leads to a chronic infection (in > 90% of cases), with rapid progression to cirrhosis[ 23 , 38 - 40 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…Super-infection usually leads to a chronic infection (in > 90% of cases), with rapid progression to cirrhosis[ 23 , 38 - 40 ]. Diagnosis of the super-infection is based upon a positive test for anti-HD IgM and a negative test for anti-HBc IgM in HBsAg carriers[ 35 , 37 ]. The super-infection itself is characterized by early presence of HDV-RNA and HDV antigen, followed by increase in anti-HD IgM that remains persistently detectable, in parallel with development of chronicity.…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

See 4 more Smart Citations

Hepatitis delta virus: From infection to new therapeutic strategies

Niro¹,

et al. 2021

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The hepatitis delta virus (HDV) is a small RNA virus that encodes a single protein and which requires the hepatitis B virus (HBV)-encoded hepatitis B surface antigen (HBsAg) for its assembly and transmission. HBV/HDV co-infections exist worldwide and show a higher prevalence among selected groups of HBV-infected populations, specifically intravenous drug users, practitioners of high-risk sexual behaviours, and patients with cirrhosis and hepatocellular carcinoma. The chronic form of HDV-related hepatitis is usually severe and rapidly progressive. Patterns of the viral infection itself, including the status of co-infection or super-infection, virus genotypes (both for HBV and HDV), and persistence of the virus’ replication, influence the outcome of the accompanying and manifested liver disease. Unfortunately, disease severity is burdened by the lack of an effective cure for either virus type. For decades, the main treatment option has been interferon, administered as mono-therapy or in combination with nucleos(t)ide analogues. While its efficacy has been reported for different doses, durations and courses, only a minority of patients achieve a sustained response, which is the foundation of eventual improvement in related liver fibrosis. The need for an efficient therapeutic alternative remains. Research efforts towards this end have led to new treatment options that target specific steps in the HDV life cycle; the most promising among these are myrcludex B, which inhibits virus entry into hepatocytes, lonafarnib, which inhibits farnesylation of the viral-encoded L-HDAg large hepatitis D antigen, and REP-2139, which interferes with HBsAg release and assembly.

“…One such factor is genotypic variability. Among the eight known genotypes, HDV-1 has the highest pathogenic potential[ 31 , 33 , 35 ], while HDV-2 and HDV-4 are associated with milder forms of the disease[ 35 ]. According to a study conducted in Taiwan, patients infected with HDV-2 develop liver failure less frequently than those with genotype 1[ 34 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…The pathogenic properties of HDV 5-8 are not well characterized[ 7 , 36 ]. Among the spectrum of host and viral factors that may underlie the different outcomes of infection with these various genotypes, we can include variability in virus replication and virion assembly efficacy, both of which contribute to the rate of HDV virion secretion, and such host factors as race or presence of single-nucleotide polymorphisms[ 35 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…The anti-HD IgG antibody reaches a detectable level after the IgM antibodies disappear, and may persist for months or even years. A failure in anti-HD IgM clearance predicts the chronicity of hepatitis[ 26 , 35 , 42 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…Conversely, in HDV super-infection, the virus infects individuals with chronic HBV infection, and it typically leads to HDV persistence with development of cirrhosis[ 35 ]. It may present either as an exacerbation of a known chronic hepatitis B status accompanied by hepatic decompensation, or as a new acute hepatitis status in asymptomatic HBsAg carriers[ 35 ]. Super-infection usually leads to a chronic infection (in > 90% of cases), with rapid progression to cirrhosis[ 23 , 38 - 40 ].…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

“…Super-infection usually leads to a chronic infection (in > 90% of cases), with rapid progression to cirrhosis[ 23 , 38 - 40 ]. Diagnosis of the super-infection is based upon a positive test for anti-HD IgM and a negative test for anti-HBc IgM in HBsAg carriers[ 35 , 37 ]. The super-infection itself is characterized by early presence of HDV-RNA and HDV antigen, followed by increase in anti-HD IgM that remains persistently detectable, in parallel with development of chronicity.…”

Section: Clinical Manifestations and Diagnosismentioning

confidence: 99%

See 3 more Smart Citations

Hepatitis delta virus: From infection to new therapeutic strategies

Niro¹,

et al. 2021

View full text Add to dashboard Cite

The hepatitis delta virus (HDV) is a small RNA virus that encodes a single protein and which requires the hepatitis B virus (HBV)-encoded hepatitis B surface antigen (HBsAg) for its assembly and transmission. HBV/HDV co-infections exist worldwide and show a higher prevalence among selected groups of HBV-infected populations, specifically intravenous drug users, practitioners of high-risk sexual behaviours, and patients with cirrhosis and hepatocellular carcinoma. The chronic form of HDV-related hepatitis is usually severe and rapidly progressive. Patterns of the viral infection itself, including the status of co-infection or super-infection, virus genotypes (both for HBV and HDV), and persistence of the virus’ replication, influence the outcome of the accompanying and manifested liver disease. Unfortunately, disease severity is burdened by the lack of an effective cure for either virus type. For decades, the main treatment option has been interferon, administered as mono-therapy or in combination with nucleos(t)ide analogues. While its efficacy has been reported for different doses, durations and courses, only a minority of patients achieve a sustained response, which is the foundation of eventual improvement in related liver fibrosis. The need for an efficient therapeutic alternative remains. Research efforts towards this end have led to new treatment options that target specific steps in the HDV life cycle; the most promising among these are myrcludex B, which inhibits virus entry into hepatocytes, lonafarnib, which inhibits farnesylation of the viral-encoded L-HDAg large hepatitis D antigen, and REP-2139, which interferes with HBsAg release and assembly.

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