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Modulation of Innate Immune Signaling Pathways by Herpesviruses

Section of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, 925 W 34th Street, Los Angeles, CA 90089, USA
Author to whom correspondence should be addressed.
Viruses 2019, 11(6), 572;
Received: 11 May 2019 / Revised: 16 June 2019 / Accepted: 18 June 2019 / Published: 21 June 2019
PDF [850 KB, uploaded 21 June 2019]


Herpesviruses can be detected by pattern recognition receptors (PRRs), which then activate downstream adaptors, kinases and transcription factors (TFs) to induce the expression of interferons (IFNs) and inflammatory cytokines. IFNs further activate the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, inducing the expression of interferon-stimulated genes (ISGs). These signaling events constitute host innate immunity to defeat herpesvirus infection and replication. A hallmark of all herpesviruses is their ability to establish persistent infection in the presence of active immune response. To achieve this, herpesviruses have evolved multiple strategies to suppress or exploit host innate immune signaling pathways to facilitate their infection. This review summarizes the key host innate immune components and their regulation by herpesviruses during infection. Also we highlight unanswered questions and research gaps for future perspectives. View Full-Text
Keywords: innate immunity; IFN-independent ISGs; herpesvrial modulation innate immunity; IFN-independent ISGs; herpesvrial modulation

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Liu, Q.; Rao, Y.; Tian, M.; Zhang, S.; Feng, P. Modulation of Innate Immune Signaling Pathways by Herpesviruses. Viruses 2019, 11, 572.

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