Human hepatitis B viral e antigen and its precursor P20 inhibit T lymphocyte proliferation

The hepatitis B virus (HBV) Precore protein is processed through the secretory pathway directly as HBeAg or with the generation of an intermediate (P20). Precore gene has been shown to be implicated in viral persistence, but the functions of HBeAg and its precursors have not been fully elucidated. We show that the secreted proteins HBeAg and P20 interact with T cell surface and alter Kit-225 and primary T cells proliferation, a process which may facilitate the establishment of HBV persistence. Our data indicate that the N-terminal end of Precore is important for these inhibitory effects and exclude that they are dependent on the association of HBeAg and P20 with two characterized cell surface ligands, the Interleukin-1 Receptor Accessory Protein and gC1qR (present study).

► P20, precursor of the HBeAg, interacts with the cellular protein gC1qR.
► HBeAg and P20 bind to T cell surface and inhibit mitogen-induced T cell division.
► HBeAg and P20 inhibition of T cell proliferation is gC1qR and IL-1RAcP-independent.