Evidence map›Paper›PMID 25776761›Full record

ArticleVirology2015

IFI44 suppresses HIV-1 LTR promoter activity and facilitates its latency.

Derek Power, Netty Santoso, Michael Dieringer, Jack Yu, Huachao Huang, Sydney Simpson, Ishir Seth, Hongyu Miao, Jian Zhu

Abstract read
In one paragraph

Article in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  3. Impact of sex chromosomes and gonad type in stress susceptibility in corticostriatal brain regions.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 2 institutions in 1 country.

Derek PowerDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Netty SantosoDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA; Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Michael DieringerSchool of Arts and Sciences, University of Rochester, Rochester, NY 14627, USA.
Jack YuSchool of Arts and Sciences, University of Rochester, Rochester, NY 14627, USA.
Huachao HuangDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Sydney SimpsonDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Ishir SethDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Hongyu MiaoDepartment of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Jian ZhuDepartment of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA. Electronic address: Jian_Zhu@urmc.rochester.edu.
University of Rochester Medical Center · USUniversity of Rochester · US

Funding

Virology/Immunology CoreP30AI078498 · NIAID · UNIVERSITY OF ROCHESTER · PI DEWHURST, STEPHEN · 2008 to 2018
$14.6M
Investigation of Latency Promoting Genes (LPGs) in HIV Oral Reservoir CellsR01DE025447 · NIDCR · UNIVERSITY OF ROCHESTER · PI ZHU, JIAN · 2015 to 2019
$1.9M
Cooperation of BRD4 and TAT Associated Proteins in HIV Transcription and LatencyR33AI116180 · NIAID · UNIVERSITY OF ROCHESTER · PI ZHU, JIAN · 2016 to 2018
$1.2M
Cooperation of BRD4 and TAT Associated Proteins in HIV Transcription and LatencyR21AI116180 · NIAID · UNIVERSITY OF ROCHESTER · PI ZHU, JIAN · 2014 to 2015
$421k
NIAID NIH HHS P30 AI078498NIAID NIH HHS P30AI078498NIAID NIH HHS R21 AI116180NIAID NIH HHS R21AI116180NIAID NIH HHS R33 AI116180NIDCR NIH HHS R01 DE025447
6 · The paper itself

Abstract

IFI44 is an interferon-alfa inducible protein, and is associated with infection of several viruses. However, IFI44 elicits minimal antiviral effects on these viruses, and its exact role is still unknown. Here we show that IFI44 inhibits HIV-1 replication in vitro. Through depletion of endogenous IFI44 or overexpression of IFI44 we confirm that IFI44 suppresses HIV-1 LTR promoter activity and affects viral transcription. Furthermore, we find that IFI44 localizes to nuclei and binds to the HIV-1 LTR promoter in HIV-1 infected cells. Removing suppression of HIV-1 transcription benefits reactivation of HIV-1 proviruses for purging latent reservoirs. We demonstrate that depletion of endogenous IFI44 in J-LAT cells induces reactivation of latent HIV-1. Based on these results, we propose a model in which IFI44 is recruited to the HIV-1 LTR, which may suppress viral transcription and prevent reactivation of latent HIV-1. Our study suggests a previously unrecognized anti-HIV phenomenon for interferon-stimulated proteins.

Indexed as

Down-RegulationHIV Long Terminal RepeatVirus LatencyAntigensCell LineCell NucleusCytoskeletal ProteinsGene Expression Regulation, ViralHIV-1HIV InfectionsHumansProtein TransportVirus ReplicationAntigensCytoskeletal ProteinsIFI44 protein, humanHIV-1IFI44InterferonISGLatencyLTRReactivationTranscription

Identifiers

PMID25776761
PMCPMC4437885
OpenAlexW2018998191

What OpenQuestion holds

Textmetadata
LicenceTDM
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.