Bovine herpesvirus-1 infection affects the peptide transport activity in bovine cells.

Infection of cattle with bovine herpesvirus-1 (BHV-1) impairs the cell-mediated immune response (CMI) of the affected host. We investigated the location of interference of BHV-1 with the major histocompatibility complex (MHC) class I antigen presentation pathway by employing an assay that allows assessment of the peptide transport activity of the Transporter associated with Antigen Presentation (TAP) from the cytoplasm into the endoplasmic reticulum (ER). We found a considerable down-regulation of the peptide transport activity in bovine epithelial cells, taking place as early as 2 h after virus infection. This down-regulation was also dose-dependent, and, at high multiplicities of infection (moi), led to an almost complete shutdown of TAP. By inhibiting peptide transport into the ER, the virus impairs loading of MHC class I molecules and their subsequent egress from the ER to the cell surface. This may lead to defective priming of cytotoxic T lymphocytes. Thus, BHV-1 is yet another member of its family Herpesviridae that selectively interferes with the host's antigen presentation machinery to evade the host's immune response in vivo.