Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Human endogenous retrovirus (HERV) expression is not induced by treatment with the histone deacetylase (HDAC) inhibitors in cellular models of HIV-1 latency

6 Feb 2016

Abstract excerpt

BACKGROUND: While antiretroviral therapies have improved life expectancy and reduced viral loads in HIV-1-positive individuals, the cessation of treatment results in a rebound of viral replication. This suggests that a reservoir of latently-infected cells remains within these patients, the identity of which is ill-defined and therefore difficult to target therapeutically. Current strategies are aimed at using...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chromosomal and Genetic Variations
Share to HIV/AIDS drug development and treatment
Share to HIV Research and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26852322
DOI: 10.1186/s12977-016-0242-4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Human endogenous retrovirus (HERV) expression is not induced by treatment with the histone deacetylase (HDAC) inhibitors in cellular models of HIV-1 latencyPMID 26852322Read ↗

Expression of latent human immunodeficiency type 1 is induced by novel and selective histone deacetylase inhibitorsSemantic proximity Read ↗

HIV latency: experimental systems and molecular modelsSemantic proximity Read ↗

Integrated Assessment of Viral Transcription, Antigen Presentation, and CD8+T Cell Function Reveals Multiple Limitations of Class I-Selective Histone Deacetylase Inhibitors during HIV-1 Latency ReversalSemantic proximity Read ↗

Entinostat is a histone deacetylase inhibitor selective for class 1 histone deacetylases and activates HIV production from latently infected primary T cellsSemantic proximity Read ↗

Therapy for Latent HIV-1 Infection: The Role of Histone Deacetylase InhibitorsSemantic proximity Read ↗

A Limited Group of Class I Histone Deacetylases Acts To Repress Human Immunodeficiency Virus Type 1 ExpressionSemantic proximity Read ↗

Molecular control of HIV-1 postintegration latency: implications for the development of new therapeutic strategiesSemantic proximity Read ↗

Dynamics of HIV Latency and Reactivation in a Primary CD4+ T Cell ModelSemantic proximity Read ↗

Expression of Latent HIV Induced by the Potent HDAC Inhibitor Suberoylanilide Hydroxamic AcidSemantic proximity Read ↗

RNA-induced epigenetic silencing inhibits HIV-1 reactivation from latencySemantic proximity Read ↗

Histone Deacetylase Inhibitor Romidepsin Inhibits<i>De Novo</i>HIV-1 InfectionsSemantic proximity Read ↗

Inhibitors of Histone DeacetylasesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.