期刊
NATURE REVIEWS IMMUNOLOGY
卷 8, 期 11, 页码 861-873出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nri2434
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- NCI NIH HHS [P01 CA069381-130001, P01 CA069381] Funding Source: Medline
- NIAID NIH HHS [R01 AI067890-01A2, R01 AI048073-08, R37 AI033068-16, R01 AI057840, R37 AI033068, R01 AI057840-04, R01 AI048073, R01 AI067890-02, R01 AI067890] Funding Source: Medline
Herpesviruses have evolved numerous strategies to subvert host immune responses so they can coexist with their host species. These viruses 'co-opt' host genes for entry into host cells and then express immunomodulatory genes, including mimics of members of the tumour-necrosis factor (TNF) superfamily, that initiate and alter host-cell signalling pathways. TNF superfamily members have crucial roles in controlling herpesvirus infection by mediating the direct killing of infected cells and by enhancing immune responses. Despite these strong immune responses, herpesviruses persist in a latent form, which suggests a dynamic relationship between the host immune system and the virus that results in a balance between host survival and viral control.
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