ArticleAntimicrobial agents and chemotherapy2014
Ruxolitinib and tofacitinib are potent and selective inhibitors of HIV-1 replication and virus reactivation in vitro.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.Retrovirology · 2015Pooled it
- Study protocol for neuroimaging using 7 T MRI in the investigation of baricitinib for reduction of HIV in the CNS: a randomized placebo-controlled trial.BMC medical imaging · 2026Trial
- Randomized Trial of Ruxolitinib in Antiretroviral-Treated Adults With Human Immunodeficiency Virus.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Trial
- Emerging CCR5-Based Therapeutic Potential of JAK/STAT Inhibitors and CCR5Δ32 Hematopoietic Stem Cell Transplantation.Viruses · 2026Review
- Multi-omics links microbial dysbiosis, systemic inflammation, and metabolomic disruptions to SNAE risk in treated HIV.JCI insight · 2026Article
- Long-term HIV-1 remission achieved through allogeneic haematopoietic stem cell transplant from a CCR5Δ32/Δ32 sibling donor.Nature microbiology · 2026Article
- Multi-omics links microbial dysbiosis, systemic inflammation and metabolomic disruptions to SNAE risk in treated HIV.bioRxiv : the preprint server for biology · 2026Article
- Article
- Mechanisms of transcriptional regulation of CCR5, which is the co-receptor for R5-tropic HIV and is also involved in other disease processes.Biochemical Society transactions · 2026Review
- Drug repositioning as a promising approach for the eradication of emerging and re-emerging viral agents.Molecular diversity · 2025Review
- Lymphoid B cells upregulate HIV-1 ex vivo and are linked to its expression in vivo.PLoS pathogens · 2025Article
- The role of chikungunya virus capsid-viral RNA interactions in programmed ribosomal frameshifting.Journal of virology · 2025Article
- Deep Thought on the HIV Cured Cases: Where Have We Been and What Lies Ahead?Biomolecules · 2025Review
- The intestinal interferon system and specialized enterocytes as putative drivers of HIV latency.Frontiers in immunology · 2025Review
- HIV and the gut: implications for HIV persistence, immune dysfunction and cure strategies.Frontiers in immunology · 2025Review
- Sustained HIV remission after allogeneic hematopoietic stem cell transplantation with wild-type CCR5 donor cells.Nature medicine · 2024Article
- Review
- JAK/STAT signaling pathway affects CCR5 expression in human CD4Science advances · 2024Article
- HIV Reservoirs and Treatment Strategies toward Curing HIV Infection.International journal of molecular sciences · 2024Review
- Sustained antiviral response againstFrontiers in pharmacology · 2024Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
The JAK-STAT pathway is activated in both macrophages and lymphocytes upon human immunodeficiency virus type 1 (HIV-1) infection and thus represents an attractive cellular target to achieve HIV suppression and reduced inflammation, which may impact virus sanctuaries. Ruxolitinib and tofacitinib are JAK1/2 inhibitors that are FDA approved for rheumatoid arthritis and myelofibrosis, respectively, but their therapeutic application for treatment of HIV infection was unexplored. Both drugs demonstrated submicromolar inhibition of infection with HIV-1, HIV-2, and a simian-human immunodeficiency virus, RT-SHIV, across primary human or rhesus macaque lymphocytes and macrophages, with no apparent significant cytotoxicity at 2 to 3 logs above the median effective antiviral concentration. Combination of tofacitinib and ruxolitinib increased the efficacy by 53- to 161-fold versus that observed for monotherapy, respectively, and each drug applied alone to primary human lymphocytes displayed similar efficacy against HIV-1 containing various polymerase substitutions. Both drugs inhibited virus replication in lymphocytes stimulated with phytohemagglutinin (PHA) plus interleukin-2 (IL-2), but not PHA alone, and inhibited reactivation of latent HIV-1 at low-micromolar concentrations across the J-Lat T cell latency model and in primary human central memory lymphocytes. Thus, targeted inhibition of JAK provided a selective, potent, and novel mechanism to inhibit HIV-1 replication in lymphocytes and macrophages, replication of drug-resistant HIV-1, and reactivation of latent HIV-1 and has the potential to reset the immunologic milieu in HIV-infected individuals.
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