ArticleScientific reports2016
Tuning of AKT-pathway by Nef and its blockade by protease inhibitors results in limited recovery in latently HIV infected T-cell line.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Meta-analysis of gene expression profiles in long-term non-progressors infected with HIV-1.BMC medical genomics · 2019Pooled it
- miR-23a-3p as a Biomarker Associated with Prediabetes in People Living with HIV: An Integrative Analysis of Inflammatory, Metabolic, and Insulin Resistance Signatures.International journal of molecular sciences · 2026Article
- CircRNA profiles of extracellular vesicle-enriched fractions from ART suppressed pregnant women living with HIV identifies interactome networks key to inflammation and viral latency.Journal of translational medicine · 2026Article
- HIV-1 Nef activates proviral DNA transcription by recruiting Src kinase to phosphorylate host protein Nef-associated factor 1 to compromise its viral restrictive function.Journal of virology · 2025Article
- SIV-specific neutralizing antibody induction following selection of a PI3K drive-attenuatedeLife · 2025Article
- Monocytes across life span in HIV infection: lights and shadows.Current opinion in HIV and AIDS · 2025Review
- Impact of HIV-1 TAT activation on retinal Müller glia: Implications for barrier properties.Journal of biosciences · 2025Article
- Viral microRNA regulation of Akt is necessary for reactivation of Human Cytomegalovirus from latency in CD34+ hematopoietic progenitor cells and humanized mice.PLoS pathogens · 2024Article
- Human cytomegalovirus attenuates AKT activity by destabilizing insulin receptor substrate proteins.bioRxiv : the preprint server for biology · 2023Article
- Article
- Oncogenic and Stemness Signatures of the High-Risk HCMV Strains in Breast Cancer Progression.Cancers · 2022Article
- Trained Immunity and HIV Infection.Frontiers in immunology · 2022Article
- HIV-1 replication and latency are balanced by mTOR-driven cell metabolism.Frontiers in cellular and infection microbiology · 2022Review
- CounterAKTing HIV: Toward a "Block and Clear" Strategy?Frontiers in cellular and infection microbiology · 2022Review
- The DNA Damage Response and HIV-Associated Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020Review
- A Matter of Life or Death: Productively Infected and Bystander CD4 T Cells in Early HIV Infection.Frontiers in immunology · 2020Article
- Control of viral infections by epigenetic-targeted therapy.Clinical epigenetics · 2019Review
- Convergent perturbation of the human domain-resolved interactome by viruses and mutations inducing similar disease phenotypes.PLoS computational biology · 2019Article
- Cell Size-Based Decision-Making of a Viral Gene Circuit.Cell reports · 2018Article
- Implications of HIV-1 Nef for "Shock and Kill" Strategies to Eliminate Latent Viral Reservoirs.Viruses · 2018Review
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Akt signaling plays a central role in many biological processes, which are key players in human immunodeficiency virus 1 (HIV-1) pathogenesis. We found that Akt interacts with HIV-1 Nef protein. In primary T cells treated with exogenous Nef or acutely infected with Nef-expressing HIV-1 in vitro, Akt became phosphorylated on serine(473) and threonine(308). In vitro, Akt activation mediated by Nef in T-cells was blocked by HIV protease inhibitors (PI), but not by reverse transcriptase inhibitors (RTI). Ex vivo, we found that the Akt pathway is hyperactivated in peripheral blood lymphocytes (PBLs) from cART naïve HIV-1-infected patients. PBLs isolated from PI-treated patients, but not from RTI-treated patients, exhibited decreased Akt activation, T-cell proliferation and IL-2 production. We found that PI but not RTI can block HIV-1 reactivation in latently infected J-Lat lymphoid cells stimulated with various stimuli. Using luciferase measurement, we further confirmed that Nef-mediated reactivation of HIV-1 from latency in 1G5 cells was blocked by PI parallel to decreased Akt activation. Our results indicate that PI-mediated blockade of Akt activation could impact the HIV-1 reservoir and support the need to further assess the therapeutic use of HIV-1 PI in order to curtail latently infected cells in HIV-1-infected patients.
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