Hbs-ag

In 1967, B. S. Blumberg discovered the so-called "Australian antigen", which was later referred to as hepatitis B surface antigen (HBs- Ag). He was awarded the Nobel Prize for this discovery (Leung 2008).

The hepatitis B virus was first described in 1970 by D. S. Dane et al. (Puchta 2006) and named after him as the so-called "Dane particle" (Mueller-Eckhardt 1996).

In the 1970s, radioimmunoassays and enzyme immunoassays for the detection of HBs- Ag were developed for the first time (Lee 2011).

The first vaccine for active immunization against hepatitis B was introduced in 1982 and consisted of purified, non-infectious HBs- Ag particles (Kasper 2015).

HBs- Ag is a protein that is used clinically as a diagnostic marker for hepatitis B virus infection (Lee 2011).

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).

Humans and great apes are the only natural carriers of HBs- Ag (Gressner 2019).

HBs- Ag is found in approx. 93.3 % of people suffering from acute hepatitis B (Madalinkski 1979). It remains positive for longer than 6 months in approx. 10 %. Of these, HBs- Ag can no longer be detected in 50 % over the next few years. The remaining 50 %, however, remain persistently chronically HBs- Ag positive.

However, recent studies have shown that the rate of chronic infections after acute hepatitis B in immunocompetent young adults is only 1 % (Kasper 2015), Cornberg (2021) puts it at 0.4 - 0.8 %.

Among pregnant women - even in low-endemic areas - up to 1.5% are HBs Ag carriers who can transmit an HBV infection to their child (Cornberg 2021).

HBs- Ag is produced and secreted by a complex mechanism that has not yet been fully elucidated (Lee 2011).

The main function of HBs- Ag is to encapsulate the viral components. The antigen also plays a role in cell membrane attachment to initiate the infection process. It also has the most important antigenic components such as the a-determinant (Lee 2011).

HBs- Ag can be determined qualitatively and quantitatively. Quantitative detection plays a role as a progression parameter during treatment (Gressner 2019).

In an acute infection with hepatitis B, HBs- Ag is already detectable before the onset of clinical symptoms (approx. 2 - 6 weeks before [Kasper 2015]). At the onset of the disease, it is found in approx. 90 % of patients (Herold 2022).

As a rule, HBs- Ag is no longer detectable 1 - 2 months after the onset of the disease. As soon as this is the case, antibodies against HBs- Ag appear for the first time. Occasionally, however, there may be a diagnostic gap of several weeks. Once anti-HBs appear, they persist for life (Kasper 2022).

The detection of HBs- Ag always means virus persistence (Cornberg 2021) and thus infectivity, as virus replication continues to take place in this case (Herold 2022). If HBe-Ag is also detectable, this additionally increases infectivity (Kasper 2015).

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). In > 90 % of cases, HBs- Ag-positive mothers transmit the virus to their newborn, compared to only 10 - 15 % of HBs- Ag-positive mothers (Kasper 2015).

Hepatitis D

HBs- Ag is also always detectable in the context of hepatitis D (Kasper 2015), as the hepatitis D virus is only able to form infectious virus particles through an HBs- Ag-containing envelope (RKI 2016).

Extrahepatic manifestation

HBs- Ag can occasionally be deposited in the blood vessels in acute hepatitis B and prodromally cause symptoms similar to serum sickness(Kasper 2015).

In patients with chronic hepatitis B, immune complex diseases such as glomerulonephritis with nephrotic syndrome occasionally occur. In this case, deposits of HBs- Ag are found in the glomerular basement membrane. HBs- Ag can also be detected in the small and medium-sized arterioles in polyarteritis nodosa (Kasper 2015).

HBs- Ag is detectable in the cytoplasm of hepatocytes (Herolds 2022).

Chronic hepatitis B

HBs- Ag remains positive for more than 6 months in around 10 % of patients. Recent studies have shown that the rate of chronic infections after acute hepatitis B in immunocompetent young adults is only 1 % (Kasper 2015), Cornberg (2021) puts it at 0.4 - 0.8 %.

Certain risk groups such as immunocompromised people, dialysis patients, homosexuals, newborns and drug addicts often develop persistent HBs- Ag with the development of chronic hepatitis B (Höfler 2019).

Cirrhosis of the liver

In Asian countries, hepatitis B with persistent HBs- Ag is the most common cause of liver cirrhosis. In Western countries, it is among the top 3 causes (Heintges 2006).

Hepatocellular carcinoma

HBs- Ag positive carriers have an up to 98 times higher risk of developing hepatocellular carcinoma (HCC) than HBs negative carriers (Kasper 2015).

s. Hepatitis B

Prophylaxis:

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).

Vaccination should be recommended for corresponding risk groups such as medical professionals who are HBs- Ag and anti- HBc negative and do not have adequate vaccination protection (Cornberg 2021).

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