Modulation of the immune system by Kaposi's sarcoma-associated herpesvirus

被引:67
作者
Areste, Cristina [1 ]
Blackbourn, David J. [1 ]
机构
[1] Univ Birmingham, Canc Res UK Inst Canc Studies, Birmingham B15 2TT, W Midlands, England
基金
英国医学研究理事会;
关键词
HOST GENE-EXPRESSION; E3 UBIQUITIN LIGASES; T-CELL RESPONSES; ENDOTHELIAL-CELLS; VIRUS COUNTERMEASURES; COMPLEMENT REGULATION; ANTIVIRAL RESPONSES; SIGNAL-TRANSDUCTION; INNATE IMMUNITY; DOWN-REGULATION;
D O I
10.1016/j.tim.2008.12.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The most recently identified human herpesvirus is Kaposi's sarcoma-associated herpesvirus (KSHV). It causes Kaposi's sarcoma, a tumour occurring most commonly in untreated AIDS patients and the leading cancer of men in certain parts of Africa. KSHV might also contribute to the pathogenesis of primary effusion lymphoma and multicentric Castleman's disease. The genome of KSHV contains 86 genes, almost a quarter of which encode proteins with either demonstrated or potential immunoregulatory activity. They include homologues of cellular proteins and unique KSHV proteins that can deregulate many aspects of the immune response, including T- and B-cell functions, complement activation, the innate antiviral interferon response and natural killer cell activity. The functions of these proteins and the ways in which they perturb the normal immune response are the subjects of the present review.
引用
收藏
页码:119 / 129
页数:11
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