Viruses use a variety of cell surface molecules including carbohydrates,
lipids and proteins as receptors for attachment to cells,
efficient internalization, or uncoating (Helenius, 2007). The physiologic
functions of protein receptors utilized by viruses to enter cells
include sensing soluble molecules such as growth factors and
cytokines, binding to components of the extracellular matrix, and
facilitating interactions between cells. Engagement of these cell
surface proteins with their respective ligands often results in
activation of signaling pathways, which can alter the properties of
target cells. Because viruses often engage receptors in a manner
analogous to their native ligands, they elicit a similar signaling cascade. Viruses such as avian leukosis and sarcoma virus (ALV) and
bovine herpesvirus-1 (BHV-1) are thought to induce death signaling
by directly binding a cell surface receptor involved in death signaling.
For other viruses, such as poliovirus, virus-receptor interaction has
been implicated in initiation of prodeath signaling, although mechanisms
by which proapoptotic signaling cascades are initiated as a
consequence of receptor engagement are not known.