Hepatitis B is a potentially life threatening liver infection caused by the hepatitis B virus (HBV). It is transmitted through contact with the blood or other body fluids of an infected person.1
The disease is not always self limiting: In adults approx. 5 % of acute infections will follow a chronic course of varying degrees of severity; infants will develop chronic hepatitis B in up to 90 % of the cases.1 An estimated 257 million people are living with HBV infection. In 2015, hepatitis B resulted in 887,000 deaths, mostly from complications (including cirrhosis and hepatocellular carcinoma).1 Hepatitis B surface antigen (HBsAg) is a polypeptide component of the external envelope of HBV, presenting various immunogenic determinants.2
After infection, HBsAg is the first immunologic marker detectable in serum and is usually present weeks before the onset of clinical symptoms and the appearance of other biochemical markers.3 HBsAg assays are used within the scope of diagnostic procedures to identify persons infected with HBV and prevent the transmission of the virus by blood and blood products.1
Under selective pressure HBV may mutate, potentially leading to escape from a host’s protection after vaccination and undetectability with certain commercially available HBsAg assays.4 The Elecsys® HBsAg II assay was specifically designed to detect a multitude of such mutants.
Most relevant HBsAg mutations - need to be detected by state-of-the-art HBsAg assays5,6
- Most relevant mutations in the a-determinant of the HBsAg
- substitutions G145R, K141E, T131I
- insertions between amino acids 122/123
- substitutions G145R, K141E, T131I
- In addition, mutations near the a-determinant or in regulatory elements of the surface gene may also affect the antigenic structure