Evidence map›Paper›PMID 32348766›Full record

ArticleCell reports2020

ADAR1 Facilitates KSHV Lytic Reactivation by Modulating the RLR-Dependent Signaling Pathway.

Huirong Zhang, Guoxin Ni, Blossom Damania

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  3. RMzyme: regulations of RNA-modifying enzymes in humans.Signal transduction and targeted therapy · 2026
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  9. The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Huirong ZhangDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Guoxin NiDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Blossom DamaniaDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: damania@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Vironomics and Biostatistics CoreP01CA019014 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, NANCY JOAN RAAB-TRAUB · 1985 to 2026
$43.8M
Role of KSHV Viral Proteins in Signaling and PathogenesisR01CA096500 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A · 2002 to 2022
$6.0M
Targeted Therapies for HIV-Associated Kaposi Sarcoma and LymphomaR01CA163217 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, Dirk P Dittmer · 2011 to 2026
$5.5M
Mechanisms of KSHV TransmissionR01CA239583 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A, DITTMER, DIRK P · 2019 to 2023
$2.8M
Modulation of Innate Immunity by KSHVR01DE028211 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A · 2018 to 2022
$2.1M
NCI NIH HHS P01 CA019014NCI NIH HHS R01 CA096500NCI NIH HHS R01 CA163217NCI NIH HHS R01 CA239583NIDCR NIH HHS R01 DE028211
6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA virus that exhibits two alternative life cycles: latency and lytic reactivation. During lytic reactivation, host innate immune responses are activated to restrict viral replication. Here, we report that adenosine deaminase acting on RNA 1 (ADAR1) is required for optimal KSHV lytic reactivation from latency. Knockdown of ADAR1 in KSHV latently infected cells inhibits viral gene transcription and viral replication during KSHV lytic reactivation. ADAR1 deficiency also significantly increases type I interferon production during KSHV reactivation. This increased interferon response is dependent on activation of the RIG-I-like receptor (RLR) pathway. Depletion of ADAR1 together with either RIG-I, MDA5, or MAVS reverses the increased IFNβ production and rescues KSHV lytic replication. These data suggest that ADAR1 serves as a proviral factor for KSHV lytic reactivation and facilitates DNA virus reactivation by dampening the RLR pathway-mediated innate immune response.

Indexed as

Adenosine DeaminaseDEAD Box Protein 58Gene Knockout TechniquesHEK293 CellsHerpesvirus 8, HumanHumansInterferon-betaReceptors, ImmunologicRNA-Binding ProteinsSignal TransductionVirus ActivationVirus LatencyADARB1 protein, humanADAR protein, humanAdenosine DeaminaseDEAD Box Protein 58Interferon-betaReceptors, ImmunologicRIGI protein, humanRNA-Binding ProteinsADAR1KSHVMDA5RIG-IRLR

Identifiers

PMID32348766
PMCPMC7319254
OpenAlexW3020444262

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.