ArticleAntimicrobial agents and chemotherapy2010
Persistent interactions between biguanide-based compound NB325 and CXCR4 result in prolonged inhibition of human immunodeficiency virus type 1 infection.
Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 18 citations in OpenAlex.
- Inhaled biguanides and mTOR inhibition for influenza and coronavirus (Review).World Academy of Sciences journal · 2020Article
- Application and removal of polyanionic microbicide compounds enhances subsequent infection by HIV-1.Virology journal · 2012Article
- Infection by CXCR4-Tropic Human Immunodeficiency Virus Type 1 Is Inhibited by the Cationic Cell-Penetrating Peptide Derived from HIV-1 Tat.International journal of peptides · 2012Article
- Cervicovaginal safety of the formulated, biguanide-based human immunodeficiency virus type 1 (HIV-1) inhibitor NB325 in a murine model.Journal of biomedicine & biotechnology · 2011Article
- Novel compounds containing multiple guanide groups that bind the HIV coreceptor CXCR4.Antimicrobial agents and chemotherapy · 2011Article
- Structure-activity relationships of polybiguanides with activity against human immunodeficiency virus type 1.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2010Article
- Metformin and other biguanides in oncology: advancing the research agenda.Cancer prevention research (Philadelphia, Pa.) · 2010Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
We previously demonstrated that the biguanide-based compound NB325 inhibits human immunodeficiency virus type 1 (HIV-1) infection by interacting with the CXCR4 viral coreceptor. This interaction also appeared to be persistent, since HIV-1 infection was inhibited even when the virus was introduced subsequent to the removal of NB325 from the cell culture medium. The present studies were conducted to determine the extent and mechanism of this prolonged antiviral activity. Persistent inhibition of HIV-1 infection by NB325 was concentration dependent and was apparent up to 8 h after removal of the compound. Flow cytometric analyses of stimulated CD4(+) T lymphocytes exposed to NB325 demonstrated concentration-dependent reductions in CXCR4 extracellular loop 2 epitope recognition that were maintained up to 24 h after removal of the compound. CXCL12-induced chemotaxis was also persistently inhibited following pre-exposure to NB325. These results demonstrate that persistent inhibition of X4 HIV-1 infection by NB325 involves extended perturbation of the viral coreceptor CXCR4.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.