Alasdair Steven (Structural Biology, National Institute for Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, USA)
Abstract:The architectures of many viruses are distinguished by having capsids of uniquely specified size, shape, and molecular complement. Other systems accommodate a limited degree of structural variability (polymorphism), and still others a high degree of polymorphism. In each assembly pathway, one may distinguish three phases: initiation, elongation, and completion. Once initiated, assembly tends to proceed rapidly and not in synchrony. This makes study difficult, as assembly intermediates do not accumulate. This talk will discuss the hypothesis that polymorphism has its basis in multiple alternative initiation complexes that serve as launching-pads from which assembly may proceed along differing lines towards differing end-points. It will be illustrated with data relating to capsid assembly in systems that exhibit minimal polymorphism (cystovirus f6); moderate polymorphism (a hepadnavirus, hepatitis B virus, bacteriophage T4); and extreme polymorphism (retroviruses Rous Sarcoma Virus and Human Immunodeficiency Virus).
[1] Uetrecht et al., High Resolution Mass Spectrometry of Viral Assemblies: Molecular Compositions and Stability of Dimorphic Hepatitis B Virus Capsids, Proc. Nat'l. Acad. Sci. USA 105 9216-20 (2008)