Chronic hepatitis B: back to the future with HBsAg

Moucari, Rami; Lada, Olivier; Marcellin, Patrick

doi:10.1586/eri.09.57

Cited by 20 publications

(14 citation statements)

References 27 publications

(20 reference statements)

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“…NUC reduce serum level of HBV DNA rapidly by inhibiting the reverse transcription, but this inhibition does not reduce the cccDNA level . On the other hand, serum levels of HBsAg and hepatitis B core‐related antigen (HBcrAg) have been reported as markers reflecting cccDNA levels in hepatocytes even under NUC treatment . HBcrAg assay measures all antigens coded by precore/core genome simultaneously which include HBcAg, HBeAg and p22crAg, and has been reported to be useful for predicting clinical outcomes of patients who were treated with NUC .…”

Section: Serum Markers Reflecting Amount Of Hbv Cccdna In Hepatocytesmentioning

confidence: 99%

“…HBcrAg assay measures all antigens coded by precore/core genome simultaneously which include HBcAg, HBeAg and p22crAg, and has been reported to be useful for predicting clinical outcomes of patients who were treated with NUC . HBsAg level has received attention recently as a new marker and has been reported to be efficient in prediction of treatment effects by interferon and others …”

Section: Serum Markers Reflecting Amount Of Hbv Cccdna In Hepatocytesmentioning

confidence: 99%

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Guidelines for avoiding risks resulting from discontinuation of nucleoside/nucleotide analogs in patients with chronic hepatitis B

Tanaka

Matsumoto

2013

Hepatology Research

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Section: Serum Markers Reflecting Amount Of Hbv Cccdna In Hepatocytesmentioning

confidence: 99%

Section: Serum Markers Reflecting Amount Of Hbv Cccdna In Hepatocytesmentioning

confidence: 99%

Guidelines for avoiding risks resulting from discontinuation of nucleoside/nucleotide analogs in patients with chronic hepatitis B

Tanaka

Matsumoto

2013

Hepatology Research

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“…Over the years, HBsAg has proven to be a steady, reliable but unspectacular marker of active HBV infection. HBsAg is still the hallmark of overt HBV infection today, and the detection of HBsAg in serum is still the fundamental diagnostic marker of HBV infection (2,3). HBsAg seroconversion is the ultimate laboratory marker of successful therapy in patients with chronic hepatitis B (CHB).…”

Section: Introductionmentioning

confidence: 99%

Quantification of hepatitis B surface antigen: a new concept for the management of chronic hepatitis B

Moucari

Marcellin

2011

Liver International

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HBsAg is a very important clinical test that might not only indicate active hepatitis B virus (HBV) infection but might also be used to predict clinical and treatment outcome. Clearance of HBsAg in patients with chronic HBV infection is associated with a much better clinical outcome, although surveillance for early detection of hepatocellular carcinoma (HCC) should continue. HBV DNA quantification is currently used for selecting candidates for therapy, monitoring response to therapy and detecting the emergence of drug resistance. Assays for HBsAg quantification are less expensive than HBV DNA and fully automated with a high throughput capacity. HBsAg titering may be a useful tool to manage patients with chronic HBV, to more clearly define which patients may, and more importantly, may not, benefit from treatment. Baseline and on-treatment HBsAg quantification may help to refine future treatment algorithms for both immune-modulator therapy and nucleos(t)ide analogues. Both HBV markers provide complementary information on the status of HBV infection. However, the relevance of serum HBsAg levels and its use as a reliable replacement for both covalently closed circular DNA and HBV DNA remain unclear.

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“…The hepatitis B virus (HBV) causes chronic liver infection in more than 248 million persons worldwide, which leads to liver fibrosis, cirrhosis, and development of hepatocellular carcinoma . The disappearance of the hepatitis B surface antigen (HBsAg) from the blood (HBsAg loss) is considered the best indicator of the establishment of functional control over HBV infection which endures in the absence of therapy . Currently approved treatments include nucleos(t)ide analogs (NUCs) that block the maturation of HBV by inhibiting the viral polymerase and interferon (IFN)‐based therapy to improve host immune control of HBV infection .…”

mentioning

confidence: 99%

“…considered the best indicator of the establishment of functional control over HBV infection which endures in the absence of therapy. (3)(4)(5) Currently approved treatments include nucleos(t)ide analogs (NUCs) that block the maturation of HBV by inhibiting the viral polymerase and interferon (IFN)-based therapy to improve host immune control of HBV infection. (6,7) However, although NUCs suppress HBV DNA and control the progression to fibrosis, they rarely result in HBsAg loss, and IFN-based therapy can only achieve HBsAg loss in a small fraction of treated patients, (8,9) indicating the need for new therapies capable of directly targeting HBsAg clearance from the blood.…”

mentioning

confidence: 99%

Nucleic acid polymer REP 2139 and nucleos(T)ide analogues act synergistically against chronic hepadnaviral infection in vivo in Pekin ducks

et al. 2018

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Nucleic acid polymer (NAP) REP 2139 treatment was shown to block the release of viral surface antigen in duck HBV (DHBV)‐infected ducks and in patients with chronic HBV or HBV/hepatitis D virus infection. In this preclinical study, a combination therapy consisting of REP 2139 with tenofovir disoproxil fumarate (TDF) and entecavir (ETV) was evaluated in vivo in the chronic DHBV infection model. DHBV‐infected duck groups were treated as follows: normal saline (control); REP 2139 TDF; REP 2139 + TDF; and REP 2139 + TDF + ETV. After 4 weeks of treatment, all animals were followed for 8 weeks. Serum DHBsAg and anti‐DHBsAg antibodies were monitored by enzyme‐linked immunosorbent assay and viremia by qPCR. Total viral DNA and covalently closed circular DNA (cccDNA) were quantified in autopsy liver samples by qPCR. Intrahepatic DHBsAg was assessed at the end of follow‐up by immunohistochemistry. On‐treatment reduction of serum DHBsAg and viremia was more rapid when REP 2139 was combined with TDF or TDF and ETV, and, in contrast to TDF monotherapy, no viral rebound was observed after treatment cessation. Importantly, combination therapy resulted in a significant decrease in intrahepatic viral DNA (>3 log) and cccDNA (>2 log), which were tightly correlated with the clearance of DHBsAg in the liver. Conclusion: Synergistic antiviral effects were observed when REP 2139 was combined with TDF or TDF + ETV leading to control of infection in blood and liver, associated with intrahepatic viral surface antigen elimination that persisted after treatment withdrawal. Our findings suggest the potential of developing such combination therapy for treatment of chronically infected patients in the absence of pegylated interferon. (Hepatology 2018;67:2127‐2140).

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Chronic hepatitis B: back to the future with HBsAg

Cited by 20 publications

References 27 publications

Guidelines for avoiding risks resulting from discontinuation of nucleoside/nucleotide analogs in patients with chronic hepatitis B

Guidelines for avoiding risks resulting from discontinuation of nucleoside/nucleotide analogs in patients with chronic hepatitis B

Quantification of hepatitis B surface antigen: a new concept for the management of chronic hepatitis B

Nucleic acid polymer REP 2139 and nucleos(T)ide analogues act synergistically against chronic hepadnaviral infection in vivo in Pekin ducks

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