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).

Rôle(s) de la protéine cellulaire gC1qR dans les cycles viraux.

The cellular protein gC1qR (also named HABP1, p32, p33 or TAP) has been identified as a partner of several viral proteins belonging to different virus families. gC1qR is a mitochondrial protein also present at the cell surface and in the nucleus. In normal cells, gC1qR seems involved in diverse biological processes related to its cellular localization. gC1qR could be involved in apoptosis in mitochondria, in RNA splicing in the nucleus or in immune and inflammatory responses at the cell surface. The multiple functions of gC1qR, as the variety of its viral partners, raise the question of its possible function(s) in the viral cycle. The goal of this review is to: (i) summarize what is known about gC1qR, (ii) focus on the demonstrated or hypothetical functions of the gC1qR-viral proteins complexes reported in the literature and (iii) propose a model on the possible roles of gC1qR in the viral life cycles.