AI Article Synopsis

  • Adenoviruses, particularly Human adenovirus serotype 3 (Ad3), produce excess capsid proteins that form free penton complexes crucial for viral entry into host cells.
  • During infection, Ad3 pentons self-assemble into dodecahedral nano-particles, which can effectively penetrate cells and potentially deliver vast amounts of foreign molecules.
  • Understanding the structural and molecular mechanisms behind the assembly and stability of these dodecahedra, including key amino acid residues involved in interactions, is essential for developing them as vectors for drug or gene delivery.

Article Abstract

During the viral life cycle adenoviruses produce excess capsid proteins. Human adenovirus serotype 3 (Ad3) synthesizes predominantly an excess of free pentons, the complexes of pentameric penton base and trimeric fiber proteins, which are responsible for virus penetration. In infected cells Ad3 pentons spontaneously assemble into dodecahedral virus-like nano-particles containing twelve pentons. They also form in insect cells during expression in the baculovirus system. Similarly, in the absence of fiber protein dodecahedric particles built of 12 penton base pentamers can be produced. Both kinds of dodecahedra show remarkable efficiency of intracellular penetration and can be engineered to deliver several millions of foreign cargo molecules to a single target cell. For this reason, they are of great interest as a delivery vector. In order to successfully manipulate this potential vector for drug and/or gene delivery, an understanding of the molecular basis of vector assembly and integrity is critical. Crystallographic data in conjunction with site-directed mutagenesis and biochemical analysis provide a model for the molecular determinants of dodecamer particle assembly and the requirements for stability. The 3.8 Å crystal structure of Ad3 penton base dodecamer (Dd) shows that the dodecahedric structure is stabilized by strand-swapping between neighboring penton base molecules. Such N-terminal strand-swapping does not occur for Dd of Ad2, a serotype which does not form Dd under physiological conditions. This unique stabilization of the Ad3 dodecamer is controlled by residues 59-61 located at the site of strand switching, the residues involved in putative salt bridges between pentamers and by the disordered N-terminus (residues 1-47), as confirmed by site directed mutagenesis and biochemical analysis of mutant and wild type protein. We also provide evidence that the distal N-terminal residues are externally exposed and available for attaching cargo.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3457955PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0046075PLOS

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