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Review
. 2010 Sep;5(9):1349-65.
doi: 10.2217/fmb.10.105.

Immune evasion by Kaposi's sarcoma-associated herpesvirus

Hye-Ra Lee  1 , Stacy Lee, Preet M Chaudhary, Parkash Gill, Jae U Jung
Affiliations
Review

Immune evasion by Kaposi's sarcoma-associated herpesvirus

Hye-Ra Lee et al. Future Microbiol. 2010 Sep.

Abstract

Persistent viral infections are often associated with serious diseases, primarily by altering functions of the host immune system. The hallmark of Kaposi's sarcoma-associated herpesvirus (KSHV) infection is the establishment of a life-long persistent infection, which leads to several clinical, epidemiological and infectious diseases, such as Kaposi's sarcoma, a plasmablastic variant of multicentric Castleman's disease, and primary effusion lymphoma. To sustain an efficient life-long persistency, KSHV dedicates a large portion of its genome to encoding immunomodulatory proteins that antagonize the immune system of its host. In this article, we highlight the strategies KSHV uses to evade, escape and survive its battle against the host's immune system.

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Figures

Figure 1
Figure 1. Kaposi’s sarcoma-associated herpesvirus immune evasion strategies
CCR: CC-chemokine receptor; GPCR: G-protein-coupled chemokine receptor; LANA: Latency-associated nuclear antigen; NK: Natural killer; RTA: Replication and transcription activator; TLR: Toll-like receptor.
See this image and copyright information in PMC

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