ArticleThe Journal of clinical investigation2016
Stem-loop binding protein is a multifaceted cellular regulator of HIV-1 replication.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Stem loop binding protein promotes SARS-CoV-2 replication via -1 programmed ribosomal frameshifting.Signal transduction and targeted therapy · 2025Article
- Blood leukocyte transcriptional modules and differentially expressed genes associated with disease severity and age in COVID-19 patients.Scientific reports · 2023Article
- Lactobacillus-derived extracellular vesicles enhance host immune responses against vancomycin-resistant enterococci.BMC microbiology · 2017Article
- SILAC Based Proteomic Characterization of Exosomes from HIV-1 Infected Cells.Journal of visualized experiments : JoVE · 2017Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
A rare subset of HIV-1-infected individuals is able to maintain plasma viral load (VL) at low levels without antiretroviral treatment. Identifying the mechanisms underlying this atypical response to infection may lead to therapeutic advances for treating HIV-1. Here, we developed a proteomic analysis to compare peripheral blood cell proteomes in 20 HIV-1-infected individuals who maintained either high or low VL with the aim of identifying host factors that impact HIV-1 replication. We determined that the levels of multiple histone proteins were markedly decreased in cohorts of individuals with high VL. This reduction was correlated with lower levels of stem-loop binding protein (SLBP), which is known to control histone metabolism. Depletion of cellular SLBP increased promoter engagement with the chromatin structures of the host gene high mobility group protein A1 (HMGA1) and viral long terminal repeat (LTR), which led to higher levels of HIV-1 genomic integration and proviral transcription. Further, we determined that TNF-α regulates expression of SLBP and observed that plasma TNF-α levels in HIV-1-infected individuals correlated directly with VL levels and inversely with cellular SLBP levels. Our findings identify SLBP as a potentially important cellular regulator of HIV-1, thereby establishing a link between histone metabolism, inflammation, and HIV-1 infection.
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Registered trials
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