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Bovine herpesvirus-1 infection affects the peptide transport activity in bovine cells
S Hinkley1, A B Hill, S Srikumaran
1Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln 68583-0905, USA.
Insights
Bovine herpesvirus-1 (BHV-1) infection significantly hinders the cell-mediated immune response in cattle. The virus disrupts peptide transport into the endoplasmic reticulum, impairing antigen presentation and immune evasion.
Area of Science:
- Veterinary Immunology
- Virology
- Molecular Biology
Background:
- Bovine herpesvirus-1 (BHV-1) infection in cattle compromises cell-mediated immunity (CMI).
- Understanding BHV-1's immune evasion mechanisms is crucial for cattle health.
- The major histocompatibility complex (MHC) class I pathway is vital for CMI.
Purpose of the Study:
- To pinpoint where BHV-1 interferes with MHC class I antigen presentation.
- To assess the impact of BHV-1 on peptide transport activity via the Transporter associated with Antigen Presentation (TAP).
Main Methods:
- Utilized an assay to measure peptide transport activity of TAP from cytoplasm to endoplasmic reticulum (ER).
- Infected bovine epithelial cells with BHV-1 at varying multiplicities of infection (moi).
- Quantified TAP activity at different time points post-infection.
Main Results:
- BHV-1 infection caused significant down-regulation of TAP peptide transport activity in bovine epithelial cells.
- This impairment occurred as early as 2 hours post-infection.
- High moi led to a near-complete shutdown of TAP activity, dose-dependently.
Conclusions:
- BHV-1 actively interferes with the host's antigen presentation machinery.
- By inhibiting TAP, BHV-1 impairs MHC class I loading and cell surface presentation.
- This mechanism likely contributes to BHV-1's immune evasion in vivo, potentially leading to defective cytotoxic T lymphocyte priming.
Abstract:
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.
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