ArticleAIDS research and human retroviruses2007
Failure of TLR4-driven NF-kappa B activation to stimulate virus replication in models of HIV type 1 activation.
Article in AIDS research and human retroviruses, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Time- and Dose-Dependent PSP-Induced Modulation of Antiviral Signaling Networks in CD4+ T Cells.International journal of molecular sciences · 2026Article
- Gonadocorticoids Have Different Effects on the Expression of Toll-like Receptors When Infected with Various HIV-1 Subtypes.Viruses · 2025Article
- Female Sex Hormones Upregulate the Replication Activity of HIV-1 Sub-Subtype A6 and CRF02_AG but Not HIV-1 Subtype B.Pathogens (Basel, Switzerland) · 2023Article
- Review
- Interactions with Commensal and Pathogenic Bacteria Induce HIV-1 Latency in Macrophages through Altered Transcription Factor Recruitment to the LTR.Journal of virology · 2021Article
- Article
- Targeting Cellular and Tissue HIV Reservoirs With Toll-Like Receptor Agonists.Frontiers in immunology · 2019Review
- Immune activation and the role of TLRs and TLR agonists in the pathogenesis of HIV-1 infection in the humanized mouse model.The Journal of infectious diseases · 2013Review
- A myristoylated alanine-rich C kinase substrate-related peptide suppresses cytokine mRNA and protein expression in LPS-activated canine neutrophils.American journal of respiratory cell and molecular biology · 2013Article
- HIV type 1 infection up-regulates TLR2 and TLR4 expression and function in vivo and in vitro.AIDS research and human retroviruses · 2012Article
- Nuclear receptor signaling inhibits HIV-1 replication in macrophages through multiple trans-repression mechanisms.Journal of virology · 2011Article
- Up-regulation of TLR2 and TLR4 in dendritic cells in response to HIV type 1 and coinfection with opportunistic pathogens.AIDS research and human retroviruses · 2011Article
- Renal HIV expression is unaffected by serum LPS levels in an HIV transgenic mouse model of LPS induced kidney injury.PloS one · 2011Article
- The oral commensal, Streptococcus gordonii, synergizes with Tat protein to induce HIV-1 promoter activation in monocytes/macrophages.Cellular immunology · 2011Article
- HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis involves Toll-like receptor 2 [corrected] and 9 activation in monocytes/macrophages.Clinical and vaccine immunology : CVI · 2010Article
- Innate immune recognition and activation during HIV infection.Retrovirology · 2010Review
- Article
- Supernatants from oral epithelial cells and gingival fibroblasts modulate human immunodeficiency virus type 1 promoter activation induced by periodontopathogens in monocytes/macrophages.Molecular oral microbiology · 2010Article
- Oral infectious diseases: a potential risk factor for HIV virus recrudescence?Oral diseases · 2009Review
- Human immunodeficiency virus infection alters tumor necrosis factor alpha production via Toll-like receptor-dependent pathways in alveolar macrophages and U1 cells.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
The interaction of HIV-1 with Toll-like receptors (TLR) on host target cells is incompletely understood. Data from several in vivo and in vitro model systems suggest that TLR2, TLR4, and TLR9 remain functional and if stimulated, cause an upregulation of viral replication. In the present studies employing two different chronically HIV-1-infected cell lines and highly purified TLR agonists, we found ligation of TLR2 and TLR9, but not TLR4, resulted in significant upregulation of HIV-1 production. This result was not due to a lack of TLR4 expression or impaired NF-kappa B activation. Using HEK293 cells transfected with individual TLRs and an HIV-1 LTR reporter confirmed that TLR4 signaling does not directly activate the HIV-1 LTR. Finally, ultrapurified LPS did not enhance production of IL-1 beta or IL-6 in chronically infected U1 cells, whereas significant cytokine production was observed in uninfected U937 cells. These results confirm the biological activity of ultrapurified LPS and raise the possibility that TLR4 signaling pathways may be altered during chronic HIV-1 infection. Collectively, these studies suggest that although several TLR can upregulate NF-kappaB in HIV-1-infected cells, upregulation of NF-kappaB alone is insufficient to activate the viral LTR. Further dissection of the TLR signaling pathways is necessary to determine how TLR stimulation leads to LTR activation and whether HIV-1 infection can alter signaling through TLR4.
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