Inhibition of programmed cell death by cytomegaloviruses

被引:47
作者
Brune, Wolfram [1 ]
机构
[1] Leibniz Inst Expt Virol, Heinrich Pette Inst, D-20251 Hamburg, Germany
关键词
Cytomegalovirus; Herpesvirus; Innate immunity; Apoptosis; Programmed necrosis; Necroptosis; MITOCHONDRIA-LOCALIZED INHIBITOR; RIBONUCLEOTIDE REDUCTASE HOMOLOG; IMMEDIATE-EARLY PROTEINS; MURINE CYTOMEGALOVIRUS; FAMILY-MEMBERS; MEDIATED APOPTOSIS; PROAPOPTOTIC BAX; GENE-PRODUCT; REPLICATION; BCL-2;
D O I
10.1016/j.virusres.2010.10.012
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The elimination of infected cells by programmed cell death (PCD) is one of the most ancestral defense mechanisms against infectious agents. This mechanism should be most effective against intracellular parasites, such as viruses, which depend on the host cell for their replication. However, even large and slowly replicating viruses like the cytomegaloviruses (CMVs) can prevail and persist in face of cellular suicide programs and other innate defense mechanisms. During evolution, these viruses have developed an impressive set of counter measures against premature demise of the host cell. In the last decade, several genes encoding suppressors of apoptosis and necrosis have been identified in the genomes of human and murine CMV (HCMV and MCMV). Curiously, most of the gene products are not homologous to cellular antiapoptotic proteins, suggesting that the CMVs did not capture the genes from the host cell genome. This review summarizes our current understanding of how the CMVs suppress PCD and which signaling pathways they target. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:144 / 150
页数:7
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