Search bioRxiv⌕ Search

Biology subjects

Codina, N.

Publications and source records attributed to Codina, N..

2 recordsLinked to original sources

De novo design of ACE2 protein decoys to neutralize SARS-CoV-2

There is an urgent need for the ability to rapidly develop effective countermeasures for emerging biological threats, such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes the ongoing coronavirus disease 2019 (COVID-19) pandemic. We have developed a generalized computational design strategy to rapidly engineer de novo proteins that precisely recapitulate the protein surface targeted by biological agents, like viruses, to gain entry into cells. The designed proteins act as decoys that block cellular entry and aim to be resilient to viral mutational escape. Using our novel platform, in less than ten weeks, we engineered, validated, and optimized de novo protein decoys of human angiotensin-converting enzyme 2 (hACE2), the membrane-associated protein that SARS-CoV-2 exploits to infect cells. Our optimized designs are hyperstable de novo proteins ([~]18-37 kDa), have high affinity for the SARS-CoV-2 receptor binding domain (RBD) and can potently inhibit the virus infection and replication in vitro. Future refinements to our strategy can enable the rapid development of other therapeutic de novo protein decoys, not limited to neutralizing viruses, but to combat any agent that explicitly interacts with cell surface proteins to cause disease.

biochemistry↗

Insights into the stability of a therapeutic antibody Fab fragment by molecular dynamics and its stabilization by computational design

Successful development of protein therapeutics depends critically on achieving stability under a range of conditions, while retaining their specific mode of action. Gaining a deeper understanding of the drivers of instability across different stress conditions, will potentially enable the engineering of protein scaffolds that are inherently manufacturable and stable. Here, we compared the structural robustness of a humanized antibody fragment (Fab) A33 using atomistic molecular dynamics simulations under two different stresses of low pH and high temperature. RMSD calculations, structural alignments and contact analysis revealed that low pH unfolding was initiated through loss of contacts at the constant domain interface (CL-CH1), prior to CL domain unfolding. By contrast, thermal unfolding began with loss of contacts in both the CL-CH1 and variable domain interface (VL-VH), followed by domain unfolding of CL and also of VH, thus revealing divergent unfolding pathways. FoldX and Rosetta both agreed that mutations at the CL-CH1 interface have the greatest potential for increasing the stability of Fab A33. Additionally, packing density calculations found these residues to be under-packed relative to other inter-domain residues. Two salt bridges were identified that possibly drive the conformational change at low pH, while at high temperature, salt bridges were lost and reformed quickly, and not always with the same partner, thus contributing to an overall destabilization. Sequence entropy analysis of existing Fab sequences revealed considerable scope for further engineering, where certain natural mutations agreed with FoldX and Rosetta predictions. Lastly, the unfolding events at the two stress conditions exposed different predicted aggregation-prone regions (APR), which would potentially lead to different aggregation mechanisms. Overall, our results identified the early stages of unfolding and stability-limiting regions of Fab A33, which provide interesting targets for future protein engineering work aimed at stabilizing to both thermal and pH-stresses simultaneously.\n\nAuthor SummaryCurrently, antibody-based products are the most rapidly growing class of pharmaceuticals due to their high specificity towards their targets, such as biomarkers on the surface of cancer cells. However, they tend to aggregate at all stages of product development, which leads to decreased efficiency and could elicit an immunological response. Improvements in the stability of therapeutic antibodies are generally made during the development phase, by trial and error of the composition of the formulated product, which is both costly and time consuming. There is great demand and potential for identifying the drivers of instability across different stress conditions, early in the discovery phase, which will enable the rational engineering of protein scaffolds. This work elucidated the stability-limiting regions of the antibody fragment Fab A33 using several computational tools: atomistic molecular dynamics simulations, in-silico mutational analysis by FoldX and Rosetta, packing density calculators, analysis of existing Fab sequences and predictors of aggregation-prone regions. Results identified particular regions in which mutagenesis has the potential to stabilize Fab against both thermal and pH-stresses simultaneously. Overall, the methodology used here could improve the developability screening of candidate antibody products for many diseases, such as cancer, chronic inflammatory diseases and infectious diseases.

biophysics↗