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Effects of Antiretroviral Protease Inhibitors on Live Poxvirus‐mediated Target Antigen Expression

Background: Live poxvirus‐based HIV‐1 vaccines have been tested as therapeutic vaccines and live highly attenuated strains of modified vaccinia Ankara (MVA) has been evaluated as an alternative vaccine against smallpox in HIV‐1‐infected individuals receiving antiretroviral therapy (ART). The objective of this study was to determine the affect of ART on poxvirus‐mediated target antigen expression, processing, and presentation. Methods: Using a recombinant EGFP‐expressing VV (EGFP‐VV), we studied the efficiency of virus‐mediated protein expression in primary human monocytes in the presence of HIV‐1 protease inhibitors (PIs). Results: The PI, atazanavir, significantly inhibited EGFP expression in primary human monocytes infected with EGFP‐VV. Further studies demonstrated that atazanavir could block VV‐induced activation of PI3K signaling pathway in monocytes. PI3K was the most critical pathway among four cellular signaling pathways (PI3K, p38 MAKP, JNK, and ERK) examined in antigen expression by VV‐infected cells, as blocking the PI3K pathway with the specific inhibitor LY294002 at 25 μM exhibited 90.1% decrease of EGFP expression compared to non‐inhibitor‐treated control (DMSO).