ArticleFrontiers in immunology2025
HIV subtype-specific gp140-CD4 binding, Temsavir efficacy, and identification of novel adhesion inhibitors against Chinese HIV strains.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The HIV epidemic in China is characterized by significant genetic diversity with multiple circulating recombinant forms (CRFs). The gp120-CD4 interaction, essential for viral cellular entry, exhibits subtype-dependent structural variations that compromise therapeutic efficacy. Although temsavir remains the only FDA-approved adhesion inhibitor, its activity against predominant HIV subtypes in China has not been systematically evaluated. Methods: HIV subtyping of 472 clinical samples identified five major strains (B, CRF01_AE, CRF07_BC, CRF08_BC, and CRF55_01B). Recombinant gp140 proteins from these subtypes were expressed, purified, and analyzed via bio-layer interferometry (BLI) to characterize CD4 binding properties. Structural analyses compared hydrogen bonding and interface buried surface areas. Temsavir's inhibitory efficacy was assessed, and virtual screening of 13,819 compounds combined with BLI validation was performed to identify novel inhibitors. Results: Subtype B demonstrated the strongest CD4 binding affinity (KD=79 pM), while CRF55_01Bshowed the weakest binding (KD=8.76 nM). CRF variants exhibited reduced hydrogen bonding and smaller interface buried surface areas, correlating with diminished binding affinity. Temsavir inhibition was subtype-dependent, achieving 35.7% inhibition for subtype B versus <1.3% for CRF01_AE and CRF55_01B, primarily due to steric hindrance induced by the S375H mutation. Five novel inhibitors targeting CRF55_01B were identified with inhibition rates 19%. Discussion: This study elucidates the molecular mechanisms of HIV-1 adhesion variation and provides specific candidate HIV adhesion inhibitors for prevalent CRF subtypes in China. Subsequent efforts will focus on preclinical validation and structure-activity relationship optimization of these candidates, laying the groundwork for developing personalized therapeutic strategies against region-specific strains.
Indexed as
Identifiers
What OpenQuestion holds
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.