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Biology subjects

Chenna, A.

Publications and source records attributed to Chenna, A..

4 recordsLinked to original sources

Protein Language Model Based Structure-guided Antibody Screening for Disordered Protein Targets

A crucial step in the pathogenesis of Parkinsons disease involves cell-to-cell transmission of -Synuclein proto-fibrils via endocytosis, driven primarily by the interaction of its disordered C-terminal peptide with domain 1 of Lymphocyte Activation Gene 3 (LAG3) neuronal receptors. High-affinity antibodies have been proposed as therapeutic modalities to delay this progression and subsequent amyloid formation. In our work, we develop an end-to-end computational pipeline to enable rapid screening of antibody sequences that have a high-affinity for the disordered C-terminal peptide of -Synuclein using no information of known binders. This de novo screening was enabled by a structural bioinformatics based in silico data generation pipeline combined with a deep learning framework. Our simple feed forward network model built upon sequence embeddings from a protein language model ranked the binding affinities ({Delta}G) of antibodies to -Synuclein with a high accuracy (Spearman{rho} = 0.86) when the training and the evaluation datasets contained sequences having some overlap in the complementarity determining regions (CDRs). However, for vastly different CDR sequences, a transformer encoder model trained using the antibody sequence embeddings showed a low Spearman rank correlation of{rho} = 0.18. The models have a mean Precision@100 of 38 and 12 respectively, significantly outperforming a random process. Overall, our work demonstrates a computational protocol for generating a high quality dataset of antibody-antigen complexes spanning a very large diversity in antibody sequences followed by training of a deep learning model for prediction of high-affinity antibody sequences for a specific protein target with no known binders.

bioinformatics↗

The effect of circulating neutralizing antibodies on the replication of SARS-CoV-2 variants following post-vaccination infections.

The impact of pre-existing neutralizing antibodies (NAbs) titers on SARS-CoV-2 viral shedding dynamics in post-vaccination infection (PVI) are not well understood. We characterized viral shedding longitudinally in nasal specimens in relation to baseline (pre/peri-infection) serum neutralizing antibody titers in 125 participants infected with distinct SARS-CoV-2 variants. Among 68 participants who had received vaccinations, we quantified the effect of baseline serum NAb titers on maximum viral RNA titers and on the duration of infectivity. Baseline NAb titers were higher and efficiently targeted a broader range of variants in participants who received one or two monovalent ancestral booster vaccinations compared to those with a full primary vaccine series. In participants with Delta variant infections, baseline NAb titers targeting Delta were negatively correlated with maximum viral RNA copies. Per log10 increase in baseline NAb IC50, maximum viral load was reduced -2.43 (95% confidence interval [CI] -3.76, -1.11) log10 N copies and days of infectious viral shedding were reduced -2.79 [95% CI: -4.99, -0.60] days. By contrast, in those with Omicron infections (BA.1, BA.2, BA.4 or BA.5 lineages) baseline NAb responses against Omicron lineages did not predict viral outcomes. Our results provide robust estimates of the effect of baseline NAbs on the magnitude and duration of nasal viral replication after PVI (albeit with an unclear effect on transmission) and show how immune escape variants efficiently evade these modulating effects.

immunology↗

Markers of Fungal Translocation Are Elevated During Post-Acute Sequelae of SARS-CoV-2 Infection and Induce NF-κB Triggered Inflammation.

Long COVID, a type of Post-Acute Sequelae of SARS CoV-2 infection (PASC), has been associated with sustained elevated levels of immune activation and inflammation. However, the pathophysiological mechanisms that drive this inflammation remain unknown. Inflammation during acute Coronavirus Disease 2019 (COVID-19) could be exacerbated by microbial translocation (from the gut and/or lung) to the blood. Whether microbial translocation contributes to inflammation during PASC is unknown. We found higher levels of fungal translocation - measured as {beta}-glucan, a fungal cell wall polysaccharide - in the plasma of individuals experiencing PASC compared to those without PASC or SARS-CoV-2 negative controls. The higher {beta}-glucan correlated with higher levels of markers of inflammation and elevated levels of host metabolites involved in activating N-Methyl-D-aspartate receptors (such as metabolites within the tryptophan catabolism pathway) with established neuro-toxic properties. Mechanistically, {beta}-glucan can directly induce inflammation by binding to myeloid cells (via the Dectin-1 receptor) and activating Syk/NF-{kappa}B signaling. Using an in vitro Dectin-1/NF-{kappa}B reporter model, we found that plasma from individuals experiencing PASC induced higher NF-{kappa}B signaling compared to plasma from SARS-CoV-2 negative controls. This higher NF-{kappa}B signaling was abrogated by the Syk inhibitor Piceatannol. These data suggest a potential targetable mechanism linking fungal translocation and inflammation during PASC.

microbiology↗

Template-based design of peptides to inhibit SARS-CoV-2 RNA-dependent RNA polymerase complexation.

The RNA-dependent RNA polymerase (RdRp) complex of SARS-CoV-2 lies at the core of its replication and transcription processes. The interfaces between the subunits of the RdRp complex are highly conserved, facilitating the design of inhibitors with high affinity for the interaction hotspots of the complex. Here, we report development and application of a structural bioinformatics protocol to design peptides that can inhibit RdRp complex formation by targeting the interface of its core subunit nonstructural protein (nsp) 12 with accesory factor nsp7. We adopt a top-down approach for protein design by using interaction hotspots of the nsp7-nsp12 complex obtained from a long molecular dynamics trajectory as template. A large library of peptide sequences constructed from multiple hotspot motifs of nsp12 is screened in silico to determine peptide sequences with highest shape and interaction complementarity for the nsp7-nsp12 interface. Two lead designed peptide are extensively characterized using orthogonal bioanalytical methods to determine their suitability for inhibition of RdRp complexation and anti-viral activity. Their binding affinity to nsp7 (target), as determined from surface plasmon resonance (SPR) assay, is found to be comparable to that of the nsp7-nsp12 complex. Further, one of the designed peptides gives 46 % inhibition of nsp7-nsp12 complex at 10:1 peptide:nsp7 molar concentration (from ELISA assay). Further optimization of cell penetrability and target affinity of these designed peptides is expected to provide lead candidates with high anti-viral activity against SARS-CoV-2.

bioinformatics↗