Detection in the serum of the “Australia antigen”, namely hepatitis B surface antigen (HBsAg), was the Nobel prize discovery that identified hepatitis B virus (HBV) about 40years ago; to this day HBsAg remains the hallmark of overt HBV infection [1,2]. HBsAg circulates in a wide array of particulate forms: competent virions (42nm, Dane particles), 20nm diameter filaments of variable length, and 20–22nm spherical defective particles, corresponding to empty viral envelopes [3]. Serum HBsAg results from the different combinations of three proteins (small, medium and large), either glycosylated or not, that are specified by a single open reading frame providing 3 carboxy-terminal colinear HBsAg proteins of different length.
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Maurizia Rossana Brunetto (2010) studied this question.
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