A Kaposi's sarcoma-associated herpesviral protein inhibits virus-mediated induction of type I interferon by blocking IRF-7 phosphorylation and nuclear accumulation. Export

@article{citeulike:3733150, abstract = {Interferons constitute the earliest immune response against viral infection. They elicit antiviral effects as well as multiple biological responses involved in cell growth regulation and immune activation. Because the interferon-induced cellular antiviral response is the primary defense mechanism against viral infection, many viruses have evolved strategies to antagonize the inhibitory effects of interferon. Here, we demonstrate a strategy that Kaposi's sarcoma-associated herpesvirus uses to block virus-mediated induction of type I interferon. We found that a viral immediate-early protein, namely ORF45, interacts with cellular interferon-regulatory factor 7 (IRF-7). In consequence, IRF-7 phosphorylation is inhibited and the accumulation of IRF-7 in the nucleus in response to viral infection is blocked. IRF-7 is a transcription regulator that is responsible for virus-mediated activation of type I interferon genes. By blocking the phosphorylation and nuclear translocation of IRF-7, ORF45 efficiently inhibits the activation of interferon alpha and beta genes during viral infection. Inhibition of interferon gene expression through a viral protein blocking the activation and nuclear translocation of a crucial transcription factor is a novel mechanism for viral immune evasion.}, author = {Zhu, F. X. and King, S. M. and Smith, E. J. and Levy, D. E. and Yuan, Y.}, citeulike-article-id = {3733150}, citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.082420599}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/11943871}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=11943871}, day = {16}, doi = {10.1073/pnas.082420599}, issn = {0027-8424}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, keywords = {irf7, kshv, orf45}, month = {April}, number = {8}, pages = {5573--5578}, posted-at = {2008-12-01 17:17:13}, priority = {3}, title = {A Kaposi's sarcoma-associated herpesviral protein inhibits virus-mediated induction of type I interferon by blocking IRF-7 phosphorylation and nuclear accumulation.}, url = {http://dx.doi.org/10.1073/pnas.082420599}, volume = {99}, year = {2002} }

TY - JOUR ID - citeulike:3733150 L3 - citeulike-article-id:3733150 N2 - Interferons constitute the earliest immune response against viral infection. They elicit antiviral effects as well as multiple biological responses involved in cell growth regulation and immune activation. Because the interferon-induced cellular antiviral response is the primary defense mechanism against viral infection, many viruses have evolved strategies to antagonize the inhibitory effects of interferon. Here, we demonstrate a strategy that Kaposi's sarcoma-associated herpesvirus uses to block virus-mediated induction of type I interferon. We found that a viral immediate-early protein, namely ORF45, interacts with cellular interferon-regulatory factor 7 (IRF-7). In consequence, IRF-7 phosphorylation is inhibited and the accumulation of IRF-7 in the nucleus in response to viral infection is blocked. IRF-7 is a transcription regulator that is responsible for virus-mediated activation of type I interferon genes. By blocking the phosphorylation and nuclear translocation of IRF-7, ORF45 efficiently inhibits the activation of interferon alpha and beta genes during viral infection. Inhibition of interferon gene expression through a viral protein blocking the activation and nuclear translocation of a crucial transcription factor is a novel mechanism for viral immune evasion. IS - 8 JF - Proceedings of the National Academy of Sciences of the United States of America SN - 0027-8424 EP - 5578 TI - A Kaposi's sarcoma-associated herpesviral protein inhibits virus-mediated induction of type I interferon by blocking IRF-7 phosphorylation and nuclear accumulation. VL - 99 SP - 5573 KW - irf7 KW - kshv KW - orf45 AU - Zhu, FX AU - King, SM AU - Smith, EJ AU - Levy, DE AU - Yuan, Y PY - 2002/04/16/ UR - http://dx.doi.org/10.1073/pnas.082420599 ER -