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. 2011 Jan 5;2(1):1.
doi: 10.1186/2042-4280-2-1.

Innate Immune Modulation in EBV Infection

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Free PMC article

Innate Immune Modulation in EBV Infection

Shunbin Ning. Herpesviridae. .
Free PMC article

Abstract

Epstein-Barr Virus (EBV) belongs to the gammaherpesvirus family, members of which are oncogenic. Compared with other closely related herpesviruses, EBV has developed much more elaborate and sophisticated strategies for subverting host immune system, which may account for its high prevalence in immune competent hosts. Thus, study of EBV-specific immune dysregulation is important for understanding EBV latency and oncogenesis, and will identify potential molecular targets for immunotherapeutic interventions. Here I summarize the recent findings of individual EBV products in regulating host immune responses, with emphasis on the innate immune modulation.

Figures

Figure 1
Figure 1
Elicitation of innate immune response in EBV infection. EBV dUTPase and GP350 act as ligands for TLR2. EBV EBERs can mount innate immune responses via both TLR3 and RIG-I signaling pathways. Infection of EBV also activates TLR9 signaling leading to IFNα production in pDCs. In latency, EBV manipulates the TLR7/IRF5 signaling pathway, which promotes cell proliferation. EBV products are indicated in red fonts.
Figure 2
Figure 2
Evasion of immune responses by individual EBV products. Individual EBV products, including proteins, miRNAs, and EBERs, are shown to evade immune responses in both latent (upper) and lytic (lower) infections. For innate immune evasion, three main strategies are employed: (1) manipulating type I and II IFN Jak-STAT pathway; (2) regulating expression and activity of IRFs, and (3) repressing apoptosis signaling. EBV products are indicated in red fonts. PRD: positive regulatory domain; VRE: virus responsive element; ISRE: IFN-stimulated response element

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