2022/07/22 by Mattia Bacca, Bacca, Mattia · 1 citation
Biochemistry, Genetics and Molecular Biology · Environmental Science · Medicine · #Bacteriophages and microbial interactions #Biological Physics (physics.bio-ph) #FOS: Physical sciences #Lipid Membrane Structure and Behavior #Monoclonal and Polyclonal Antibodies Research
paper · pdf · doi:10.48550/arxiv.2207.10907
openalex publication_date 2022/07/22 · openalex created_date 2022/07/28 · openalex updated_date 2026/07/28
Budding allows virus replication and macromolecular secretion in cells. It involves the formation of a bud, i.e. an outgrowth from the cell membrane that evolves into an envelope. The largest energetic barrier to bud formation is membrane deflection and is trespassed primarily thanks to nucleocapsid-membrane adhesion. Transmembrane proteins (TPs), which later form the virus ligands, are the main promotors of adhesion and can accommodate membrane bending thanks to an induced spontaneous curvature. Adhesive TPs must diffuse across the membrane from remote regions to gather on the bud surface, thus, diffusivity controls the kinetics. This paper proposes a simple model to describe diffusion-mediated budding unraveling important size limitations and size-dependent kinetics. The predicted optimal virion radius, giving the fastest budding, is validated against experiments for Coronavirus, HIV, Flu, and Hepatitis. Assuming exponential replication of virions and hereditary size, the model can predict the size distribution of a virus population. This is verified against experiments for SARS-CoV-2. All the above comparisons rely on the premise that budding poses the tightest size constraint. This is true in most cases, as demonstrated in this paper, where the proposed model is extended to describe virus infection via receptor- and clathrin-mediated endocytosis, and via membrane fusion.