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Omics · study · 2026

Type I Interferon Reprograms Intestinal Epithelial Cells for Sustained HIV-1 Latency in CD4+ T Cells of People with HIV-1 Receiving Antiretroviral Therapy

Listed in NCBI GEO

The intestinal environment sustains a state of HIV latency via yet unclear mechanisms.

Description

We recently demonstrated that specific cytokines act on intestinal epithelial cells (IEC) to promote viral reservoir (VR) latency or reactivation, with TNF-activated IEC limiting HIV outgrowth in CD4+ T cells of people with HIV (PWH) on antiretroviral therapy (ART). The pro-latency effect of TNF coincided with the induction of IL-32, a pro-inflammatory cytokine overexpressed in ART-treated PWH.

Since type I IFNs are strong modulators of IL-32, we investigated IFN-β ability to modulate the crosstalk between IEC and CD4+ T cells via IL-32-dependent mechanisms.

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Life Sciences
Provenance · 1 source records, 7 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE32006715 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[organism].NCBITaxon:9606source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title