Feeling manipulated: cytomegalovirus immune manipulation

被引:87
作者
Miller-Kittrell, Mindy [1 ]
Sparer, Tim E. [1 ]
机构
[1] Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA
来源
VIROLOGY JOURNAL | 2009年 / 6卷
关键词
MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I MOLECULES; OPEN READING FRAME; NATURAL-KILLER-CELLS; CHEMOKINE RECEPTOR US28; MITOCHONDRIA-LOCALIZED INHIBITOR; GUINEA-PIG CYTOMEGALOVIRUS; HERPESVIRUS ENTRY MEDIATOR; INFECTED HUMAN-FIBROBLASTS; ENVELOPED VIRUS-PARTICLES;
D O I
10.1186/1743-422X-6-4
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
No one likes to feel like they have been manipulated, but in the case of cytomegalovirus (CMV) immune manipulation, we do not really have much choice. Whether you call it CMV immune modulation, manipulation, or evasion, the bottom line is that CMV alters the immune response in such a way to allow the establishment of latency with lifelong shedding. With millions of years of coevolution within their hosts, CMVs, like other herpesviruses, encode numerous proteins that can broadly influence the magnitude and quality of both innate and adaptive immune responses. These viral proteins include both homologues of host proteins, such as MHC class I or chemokine homologues, and proteins with little similarity to any other known proteins, such as the chemokine binding protein. Although a strong immune response is launched against CMV, these virally encoded proteins can interfere with the host's ability to efficiently recognize and clear virus, while others induce or alter specific immune responses to benefit viral replication or spread within the host. Modulation of host immunity allows survival of both the virus and the host. One way of describing it would be a kind of "mutually assured survival" (as opposed to MAD, Mutually Assured Destruction). Evaluation of this relationship provides important insights into the life cycle of CMV as well as a greater understanding of the complexity of the immune response to pathogens in general.
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页数:20
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