bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.10.14.759022

Decoding Clade-Specific bNAb-HIV-1 Env Interactions Using Machine Learning

Abstract

Human immunodeficiency virus type 1 (HIV-1) exhibits extensive genetic diversity, posing a major challenge to AIDS vaccine development. Broadly neutralizing antibodies (bNAbs) isolated from HIV-1-infected individuals offer valuable templates for designing broadly protective immunogens. Here, structural and energetic descriptors extracted from experimentally resolved bNAb/HIV-1 Envelope (Env) protein-protein complexes were used to develop machine-learning (ML) models predicting binding free energies ({triangleup}G) and dissociation constants (KD) across multiple HIV-1 clades. Among the algorithms evaluated, extreme gradient boosting (XGBoost) achieved the best predictive performance, with training and test R2 values of 0.92 and 0.658, respectively. Applying the optimized model to HIV-1 datasets revealed clade-dependent binding patterns, with clade B showing the greatest variability and clade G exhibiting signatures associated with reduced neutralization potency. Predicted {triangleup}G of different bNAb classes followed the trend gp120-gp41 interface {approx} fusion domain > CD4 binding site (CD4bs) > V1V2 loop {approx} V3-glycan, consistent with experimentally reported affinity profiles of benchmark bNAbs. Clade C exhibited intermediate {triangleup}G with PGT121, VRC01, and 10-1074 maintaining high-affinity interactions, whereas PG9 and 2G12 show reduced binding affinity. These findings offer quantitative insight into clade-specific bNAb binding energetics and demonstrate the potential of machine-learning approaches to guide HIV-1 immunogen design and vaccine development.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Kumar, Y., Lin, S.-T., Dixit, N. M., Maiti, P. K.. 2026-10-16. Decoding Clade-Specific bNAb-HIV-1 Env Interactions Using Machine Learning. https://doi.org/10.64898/2026.10.14.759022

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Investigating Histone Lysine Acetylation and Acetyl-methylation in Mouse Brain using Enhanced Trimethylacetic Anhydride Derivatization Protocol

Histone post-translational modifications (PTMs) are key regulators of gene expression, and mass spectrometry (MS) provides a powerful platform for their characterization and quantification. However, conventional histone sample preparation using derivatization of non-modified lysines by propionic anhydride (PA) presents analytical limitations, including non-detection of short hydrophilic peptides, incomplete chromatographic separation of positional isomers, and masking of endogenous lysine propionylation and butyrylation. Here, we optimized a trimethylacetic anhydride (TMA)-based derivatization workflow to improve histone PTM analysis. Compared with PA derivatization, TMA enhanced the detection of acetylated peptides, particularly short and hydrophilic species, although peptide-dependent ionization biases affected relative peptidoform quantification. We further evaluated the suitability of TMA derivatization for investigating endogenous lysine propionylation and butyrylation. Unexpectedly, we identified lysine acetyl-methylation (Kacme) at seven sites on histone H3 and validated these assignments by targeted MS using synthetic reference peptides. To investigate the metabolic dynamics of Kacme, we performed in vivo isotope tracing in mice administered 13C-labeled glucose. Unlike canonical lysine acetylation, Kacme exhibited minimal incorporation of glucose-derived acetyl groups over 2h, suggesting substantially slower turnover of its acetyl moiety. Collectively, these findings highlight the analytical advantages and quantitative limitations of TMA-based histone derivatization, while revealing Kacme as a metabolically distinct histone modification and expanding the scope of MS-based histone PTM analysis.

biochemistry↗

Bivalent Inhibitor Development for a Dynamic Epigenetic Tandem Reader Protein Using a Combinatorial Histone Code

Epigenetic readers are a class of proteins that recognize specific chemical modifications on histones to differentially regulate gene expression. Aberrant expression of readers can drive the progression of many diseases and cancers, making this protein class viable therapeutic targets. Understanding the landscape of histone modifications recognized by reader domains, and the structural mechanisms that drive these molecular recognition events, is crucial for guiding the design of pharmaceutically relevant chemical probes. BPTF contains a plant homeodomain (PHD) finger and tandem bromodomain (BRD). Here, we expand upon previous studies that found the BPTF BRD can engage acetyllysine modifications on the N-terminus of histone H3. We uncover H3K4me3K14ac as the specific modifications recognized by the PHD BRD cassette, which is confirmed by crystallography. Using orthogonal methods, our work explores how these modifications can be read cooperatively, including in cis. We report the first experimental evidence proposing a ligand-induced conformational change between the two reader domains of BPTF, supporting previous computational approaches that have predicted a macromolecular rearrangement. We leverage these structural insights to rationally design a peptide-small molecule conjugate MJ-1 that inhibits both domains of BPTF and overcomes ligandability challenges associated with PHD-finger-containing proteins. The results presented here elucidate the molecular basis of the bivalent recognition of multiply modified histone H3 by BPTF and provide structural insight for developing compounds targeting the PHD finger of BPTF for therapeutic applications.

biochemistry↗

Binding of a Macrocyclic Nonapeptide Inhibitor to Histone Deacetylase 6

Histone deacetylase 6 (HDAC6) plays an essential role in the regulation of post-translational lysine acetylation. Myriad biological processes depend on the precise regulation of lysine acetylation-deacetylation cycles, and their dysregulation is linked to human pathologies such as cancer and neurodegeneration. Broad-specificity HDAC inhibitors are efficacious in treating disease, but the inhibitors currently approved for clinical use often cause deleterious side effects due to inhibition of multiple HDAC isozymes as well as other zinc enzymes. Cyclic peptides comprise novel platforms that, in principle, can be tailored for affinity and selectivity. A key advantage of cyclic peptide design is the ability to incorporate both canonical and noncanonical amino acids. As part of our program focusing on cyclic peptide HDAC inhibitors, we now report the 1.9-[A] resolution crystal structure of HDAC6 CD2 complexed with macrocyclic nonapeptide 1. The structure reveals zinc coordination by a noncanonical thiolate-containing amino acid, plus direct and water-mediated enzyme-inhibitor hydrogen bonds that contribute to nanomolar inhibitory potency. Structural comparisons with previously reported HDAC6 CD2 complexes with tetrapeptide and octapeptide macrocycles reveal similar networks of direct and water-mediated interactions. Given the surge of interest in cyclic peptide inhibitors, fueled in part by advances in computational design approaches, the crystal structure of the HDAC6 CD2-1 complex sets an important foundation for further development of macrocyclic peptide inhibitors.

biochemistry↗