Evidence map›Paper›PMID 29140109›Full record

ReviewAIDS research and human retroviruses2017

Host Methyltransferases and Demethylases: Potential New Epigenetic Targets for HIV Cure Strategies and Beyond.

Daniela Boehm, Melanie Ott

Open access · bronzeAbstract readReview
In one paragraph

Review in AIDS research and human retroviruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Daniela Boehm1 Gladstone Institute of Virology and Immunology , San Francisco, California.
Melanie Ott1 Gladstone Institute of Virology and Immunology , San Francisco, California.
University of California, San Francisco · US

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MALLORY O JOHNSON · 1988 to 2026
$93.6M
Targeting lysine methylation for latency reversal in HIV-infected drug usersR01DA043142 · NIDA · J. DAVID GLADSTONE INSTITUTES · PI OTT, MELANIE MARIA · 2016 to 2020
$3.0M
NIAID NIH HHS P30 AI027763NIDA NIH HHS R01 DA043142
6 · The paper itself

Abstract

A successful HIV cure strategy may require reversing HIV latency to purge hidden viral reservoirs or enhancing HIV latency to permanently silence HIV transcription. Epigenetic modifying agents show promise as antilatency therapeutics in vitro and ex vivo, but also affect other steps in the viral life cycle. In this review, we summarize what we know about cellular DNA and protein methyltransferases (PMTs) as well as demethylases involved in HIV infection. We describe the biology and function of DNA methyltransferases, and their controversial role in HIV infection. We further explain the biology of PMTs and their effects on lysine and arginine methylation of histone and nonhistone proteins. We end with a focus on protein demethylases, their unique modes of action and their emerging influence on HIV infection. An outlook on the use of methylation-modifying agents in investigational HIV cure strategies is provided.

Indexed as

Anti-HIV AgentsDNADNA Modification MethylasesEpigenesis, GeneticHistone DemethylasesHIV-1HIV InfectionsHumansProtein MethyltransferasesVirus ActivationVirus LatencyAnti-HIV AgentsDNADNA Modification MethylasesHistone DemethylasesProtein Methyltransferasesdemethylase inhibitorshistone demethylaseHIV curelatency reactivationmethyltransferasemethyltransferase inhibitors

Identifiers

PMID29140109
PMCPMC5684665
OpenAlexW2768222557

What OpenQuestion holds

Textmetadata
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.