This is fortunate because:

• Most viruses infect cells other than APCs.
• While viral antigens displayed on the surface of infected cells can serve as targets for cytotoxic T cells (CTLs),
• the lack of any costimulatory molecules on the cell surface makes them poor stimulants for the development of clones of CTLs in the first place.

1. When an infected cell dies, it can be engulfed by a professional APC and the viral antigens within it can enter the class I pathway.
   • The dead cell is engulfed by phagocytosis as described above.
   • The endosome that forms fuses with a lysosome and degradation of the dead cell begins.
   • Viral antigens pass into the cytosol and are degraded in proteasomes.
   • The viral peptides formed are then are picked up by TAP and, as described above,
   • inserted into class I MHC molecules and
   • displayed at the cell surface — along with the costimulatory molecules needed to start a vigorous clonal expansion of CD8+ cytotoxic T cells.
2. Cells infected with viruses can also transfer viral peptides directly from their cytosol to an adjacent cell like
   • a professional APC able to present the peptide — with the needed costimulatory molecules — to CTLs;
   • or simply a cell of the same type that can then present it in a class I molecule and be killed by a CTL before the infection can spread to it. This mechanism provides a way of walling off the infection.
   • In both cases, the transfer occurs through gap junctions linking the adjacent cells.