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. 2018 Jul 16;9:1561. doi: 10.3389/fimmu.2018.01561

Figure 3.

Figure 3

Hepatitis B virus (HBV) evasion of the host CD8+ T cell-mediated immune response. Viral peptides are processed into 7–12 mers by proteasomal degradation and are transported via the Transporter associated with Antigen Processing (TAP) into the endoplasmic reticulum. Peptides containing an appropriate motif are bound by human leukocyte antigen (HLA) class I molecules and transported to the cell surface for expression (92). Each T cell receptor (TCR) binds a range of specific HLA-peptide combinations. TCRs are concentrated on the cell surface over time at an “immunological synapse” triggering intracellular signaling (93). HBV can potentially escape the host CD8+ response at a number of points. 1. Evading antigen processing, 2. Downregulating presentation (37–40), 3. Altering HLA binding residues (54–56, 94), 4. Masking HLA epitope with N-linked glycosylation (NLG) sites (32, 95), 5. Altering TCR binding residues of the epitope (10, 96–99). Examples of polymorphic sites in HBV core antigen HLA-A*02 restricted FV10 epitope (residues 18–27) are highlighted (54).