ArticleThe Journal of biological chemistry2013
TLR-TRIF pathway enhances the expression of KSHV replication and transcription activator.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Modulation of Lymphotoxin β Surface Expression by Kaposi's Sarcoma-Associated Herpesvirus K3 Through Glycosylation Interference.Journal of medical virology · 2025Article
- Review
- Review
- Review
- Molecular Mechanisms of Kaposi Sarcoma Development.Cancers · 2022Article
- The regulation of KSHV lytic reactivation by viral and cellular factors.Current opinion in virology · 2022Review
- Anti-viral and pro-inflammatory functions of Toll-like receptors during gamma-herpesvirus infections.Virology journal · 2021Review
- Review
- The Activated Macrophage - A Tough Fortress for Virus Invasion: How Viruses Strike Back.Frontiers in microbiology · 2021Review
- Toll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways.Virology journal · 2020Review
- KSHV: Immune Modulation and Immunotherapy.Frontiers in immunology · 2019Review
- Expression of TLR4 gene is downregulated in acquired immune deficiency syndrome-associated Kaposi's sarcoma.Experimental and therapeutic medicine · 2019Article
- Activation and counteraction of antiviral innate immunity by KSHV: an Update.Science bulletin · 2018Article
- Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression.PLoS pathogens · 2018Article
- Caspase-Dependent Suppression of Type I Interferon Signaling Promotes Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2018Article
- Viral Inhibition of PRR-Mediated Innate Immune Response: Learning from KSHV Evasion Strategies.Molecules and cells · 2016Review
- Multi-step regulation of innate immune signaling by Kaposi's sarcoma-associated herpesvirus.Virus research · 2015Review
- Interplay between Kaposi's sarcoma-associated herpesvirus and the innate immune system.Cytokine & growth factor reviews · 2014Review
- Recognition of human oncogenic viruses by host pattern-recognition receptors.Frontiers in immunology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is a human γ-herpesvirus. KSHV replication and transcription activator (RTA) is necessary and sufficient for KSHV reactivation from latency. Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns, act through adaptors, and initiate innate and adaptive immune responses against pathogens. Toll/interleukin-1-receptor domain containing adaptor protein inducing interferon-β (TRIF) is an adaptor associated with TLR3 and TLR4 signaling, and is closely related to antiviral signaling to activate type I interferon (IFN) production. We previously found that KSHV RTA degrades TRIF indirectly and blocks TLR3 pathways. In this report, we find that TRIF, as well as TLR3 activation, enhances KSHV RTA protein expression. The C-terminal region of the RTA is involved in the responding TRIF-mediated enhancement. The degradation of TRIF and the enhancement of RTA expression are using two different pathways. The enhancement by TLR-TRIF is at least partially via promoting translational efficiency of RTA mRNA. Finally, the receptor-interacting protein 1 (RIP1) may be involved in TRIF-mediated enhancement of RTA expression, but not in the RTA-mediated degradation of TRIF. Therefore, the activation of TLR-TRIF pathway enhances KSHV RTA protein expression, and KSHV RTA in turn degrades TRIF to block innate immunity. The putative KSHV-TLR-adaptor-interacting loop may be a critical element to evade and usurp host innate immunity in KSHV life-cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.