HBe- Ag is a protein that is encoded by the pre-core/core antigen in the context of hepatitis B disease. It corresponds to the secretory form of HBc- Ag (Herold 2022) and serves as a marker of infectivity (Braun 2018).
Hbe-ag
DefinitionThis section has been translated automatically.
ClassificationThis section has been translated automatically.
HBe- Ag is a protein freshly produced during acute hepatitis B that is secreted during the replication phase of the virus (Müller 2023).
HBe-Ag plays a particularly important role in the forms of chronic hepatitis B. The following forms can occur:
- HBe- Ag- negative chronic hepatitis B
Clear histological activity is detectable in this case. The risk of developing liver cirrhosis is 20% within 10 years. The risk of HCC is 60 times higher (Herold 2022).
- HBe- Ag- negative chronic HBV infection
In the past, this form was also referred to as "asymptomatic HBe-Ag carrier status" (Neumann-Haefelin 2022). The risk of infection in this group of people is low and the prognosis is relatively favorable. The risk of developing HCC is only slightly increased (Herold 2022).
- HBe- Ag- positive chronic hepatitis B
Clear histological activity is detectable here. The risk of developing liver cirrhosis is 20% within 10 years. The risk of HCC is 60 times higher (Herold 2022).
- HBe- Ag- positive chronic HBV infection
In the past, this form was also incorrectly referred to as the "immunotolerant stage" (Neumann-Haefelin 2022). After years, this can lead to a transition to chronic hepatitis. Reactivation can occur, for example, during chemotherapy (Herold 2022)
General informationThis section has been translated automatically.
The viral components of hepatitis B disease include:
- HBV DNA
- Proteins such as:
- Surface antigen (HBs- Ag)
- Envelope antigen (HBe- Ag) This corresponds to the secretory form of HBc- Ag.
- Core antigen(HBc- Ag and HBcr- antigen = HB- core- related- antigen)
The corresponding antibodies are anti- HBs, anti- HBe and anti- HBc (Herold 2022).
OccurrenceThis section has been translated automatically.
In Germany, the HBe minus mutant now occurs in over 50 % of people suffering from chronic hepatitis B (Herold 2022).
PathophysiologyThis section has been translated automatically.
HBe- Ag has a dual role as a telerogen and as an immunogen. The exact mechanisms in this regard have not yet been clarified. HBe-Ag is also able to suppress the immune response.
It can also protect hepatocytes from apoptosis and thus contributes to the survival of infected hepatocytes (Padarath 2023).
LaboratoryThis section has been translated automatically.
The main clinical benefit of HBe Ag is that it is an indicator of relative infectivity (Kasper 2015). It is also considered a prognostic marker and can be a surrogate marker for the activity of viral RNA transcription and provide prognostic information on the response to therapy (Cornberg 2021).
In an acute infection with the hepatitis B virus, HBe Ag can only be detected for a short time at the beginning of the disease. If the acute form of the disease progresses to a chronic form, HBe Ag can still be detected (in addition to HBs- Ag) (Braun 2018).
However, if seroconversion occurs, as is usually the case, the patient becomes a so-called "inactive HBs- Ag carrier" (Alexopoulou 2014)
The detection of HBV Ag and HBV DNA is evidence of an acute hepatitis B infection (Braun 2018).
If HBe Ag is also detectable in addition to HBs Ag, this significantly increases infectivity (Kasper 2015).
Complication(s)This section has been translated automatically.
Chronic hepatitis B
As HBe Ag acts as an immunomodulator, it can promote chronic courses of hepatitis B through immunological tolerance (Müller 2023).
In around 10 % of adult patients with hepatitis B, the disease progresses to a chronic form; in young children, the chronic form of the disease occurs in up to 90 % (Müller 2023).
Liver cirrhosis
Even after seroconversion of HBe-Ag and formation of anti-HBe antibodies, liver cirrhosis occurs in approx. 50 % within 10 years (Braun 2018).
Hepatocellular carcinoma
Hepatocellular carcinoma is found in up to 10 % after seroconversion of HBe-Ag (Braun 2018).
Hepatitis B virus mutants
In the HBe minus mutation, also known as the pre-core stop codon variant (Herold 2022), the virus has lost the ability to secrete HBe Ag. In this case, there is a poorer therapeutic response in chronic forms of the disease (Braun 2018).
TherapyThis section has been translated automatically.
Before and during the treatment of hepatitis B, the HBe-Ag should always be determined, as this allows predictions to be made about the possible response to therapeutic interventions and anti-HBe-Ag seroconversion can be documented (Cornberg 2021).
Therapy see Hepatitis B
Note(s)This section has been translated automatically.
Since 1994, general HBs- Ag screening for pregnant women has been mandatory in Germany, as there is a risk of infection for the child if the mother is HBs- Ag positive (Cornberg 2021). If the mother is also HBe- Ag positive, 70 - 95 % of newborns become infected, but only 20 - 25 % of HBe- Ag negative mothers. If anti-HBe-AK is detectable, transmission to the child occurs in only 10 % of cases (Müller 2023).
In HBs- Ag positive pregnant women, the newborn receives active and passive immunization against hepatitis B within the first 12 h post partum (Cornberg 2021).
LiteratureThis section has been translated automatically.
- Alexopoulou A, Karayiannis P (2014) HBeAg negative variants and their role in the natural history of chronic hepatitis B virus infection. World J Gastroenterol. 20 (24) 7644 - 7652
- Braun J, Müller- Wieland D, Renz- Polster H, Krautzig S (2018) Basic textbook of internal medicine. Elsevier Urban and Fischer Publishers 608 - 610
- Cornberg M, Sandmann L, Protzer U, Niederau C, Tacke F, Berg T, Glebe D, Jilg W, Wedemeyer H, Wirth S, Höner zu Siederdissen C, Lynen- Jansen P, van Leeuwen P, Petersoen J (2021) S3 guideline of the German Society of Gastroenterology, Digestive and Metabolic Diseases (DGVS) on the prophylaxis, diagnosis and treatment of hepatitis B virus infection (AWMF Registry No. 021-11)
- Glitscher M, Hildt E, Bender D (2022) Hepatitis B and C: Mechanisms of virus-induced liver pathogenesis and tumorigenesis. Federal Health Gazette, Health Research, Health Protection 65 (2) 228 - 237
- Herold G et al. (2022) Internal Medicine. Herold Publishing House 527 - 530
- Kasper D L, Fauci A S, Hauser S L, Longo D L, Jameson J L, Loscalzo J et al. (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 2016
- Müller M (2023) Laboratory Medicine: Microbiology - Clinical Chemistry - Infectiology - Transfusion Medicine in Question and Answer. BoD - Books on Demand Norderstedt 69, 417, 423, 424, 457
- Neumann- Haefelin C, Thimme R (2022) Chronic hepatitis B virus infection: current and future treatment strategies. Federal Health Gazette, Health Research, Health Protection. 65 (2) 238 - 245
- Padarath K, Deroubaix A, Kramvis A (2023) The Complex Role of HBeAg and Its Precursors in the Pathway to Hepatocellular Carcino. Viruses 15 (4) 857