IFN-stimulated gene expression is independent of the IFNL4 genotype in chronic HIV-1 infection.

doi:10.1007/s00705-016-3016-3

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

Community

Back to search

Article

IFN-stimulated gene expression is independent of the IFNL4 genotype in chronic HIV-1 infection.

Archives of virology - 1 Nov 2016

Monteleone Katia, Scheri Giuseppe Corano, Statzu Maura, Selvaggi Carla, Falasca Francesca, Giustini Noemi, Mezzaroma Ivano, Turriziani Ombretta, d'Ettorre Gabriella, Antonelli Guido, Scagnolari Carolina

Abstract excerpt

This study aimed to evaluate the association between the IFNL4 rs368234815 (ΔG/TT) dinucleotide polymorphism and the IFN response during chronic HIV-1 infection. We carried out genotyping analysis and measured the expression of IFN-stimulated genes (ISGs) (myxovirus resistance protein A [MxA], ISG15, ISG56, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like [APOBEC] 3F and APOBEC3G) on peripheral...

Read the complete abstract on PubMed

Topics

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

Share to Gene Expression Profiling

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genotyping Techniques

Share to HIV Infections

Share to Immunologic Factors

Share to Interleukins

Share to Leukocytes, Mononuclear

Share to Polymorphism, Genetic

Share to RNA, Messenger

Source

Open in PubMed

Identifiers

PMID: 27558125
DOI: 10.1007/s00705-016-3016-3

Genes

ISG15

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

IFN-stimulated gene expression is independent of the IFNL4 genotype in chronic HIV-1 infection.PMID 27558125Read ↗

IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection.Semantic proximity Read ↗

ISG15 expression correlates with HIV-1 viral load and with factors regulating T cell response.Semantic proximity Read ↗

Targeted next-generation sequencing approach for CCR5, CXCR4 and IFNAR1 genes in HIV+ participants: Association of single nucleotide polymorphisms with CD4+ T cell count and HIV replication in patients receiving antiretroviral therapySemantic proximity Read ↗

Evidence for a sex-dependent effect modification in the association between IFN-λ DNA polymorphisms and expression of IFN-λ and interferon-stimulated genes in human PBMCs.Semantic proximity Read ↗

Genetic Variation at IFNL4 Influences Extrahepatic Interferon-Stimulated Gene Expression in Chronic HCV Patients.Semantic proximity Read ↗

Hepatic IFNL4 expression is associated with non-response to interferon-based therapy through the regulation of basal interferon-stimulated gene expression in chronic hepatitis C patients.Semantic proximity Read ↗

Interferon lambda rs368234815 ΔG/ΔG is associated with higher CD4+:CD8+ T-cell ratio in treated HIV-1 infection.Semantic proximity Read ↗

Differential Control of HIV-1 Replication by IFN-α14 Compared to IFN-α2 Relates to Differences in the Modulation of Host Antiretroviral Restriction FactorsSemantic proximity Read ↗

Higher Expression of Several Interferon-Stimulated Genes in HIV-1-Infected Females After Adjusting for the Level of Viral ReplicationSemantic proximity Read ↗

ISG15 deficiency restricts HIV-1 infectionSemantic proximity Read ↗

The impact of the interferon-lambda family on the innate and adaptive immune response to viral infectionsSemantic proximity Read ↗

The Impact of IFNλ4 on the Adaptive Immune Response to SARS-CoV-2 Infection.Semantic proximity Read ↗

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