Figure 1 (Left) Computer rendering of a particle of murine polyomavirus strain A2. (Center) Capsomer bonding relations. Each icosahedral asymmetric unit comprises six Vp1 subunits, including one (a) from a pentavalent pentamer. The six symmetrically different subunits are designated a, a′, a″, b, b′ and c, corresponding to three different bonding states. (Right) Computer graphics representation of the surface of the capsid of murine polyomavirus strain A2. Five Vp1 subunits form the basis of a polyomavirus capsomer, and 72 capsomers link together in a 12 pentavalent/60 hexavalent arrangement, conveying icosahedral capsid structure.
(Left and center, from Salunke, D.M., Casper, D.L.D. and Garcea, R.L. (1986). Cell46, 895–904; right, from Eckhart W. (1991). In Fundamental Virology, 2nd edn (B.N. Fields and D.M. Knipe, Eds.), Raven Press, New York; with permission.)
Figure 2 Electron micrographs of: (left) brain tissue from a progressive multifocal leukoencephalopathy (PML) patient showing the assembly of JC polyomavirus (JCPyV) particles in the nucleus of an infected oligodendrocyte; and (right) composite of virus-like particles (VLP) self-assembled from recombinant Vp1 of BK polyomavirus (BKPyV) (rBKVp1), purified by CsCl ultracentrifugation from supernatants of Sf9 insect cell cultures infected with recombinant BKVp1-baculovirus. The particles were negatively stained with 2% phosphotungstic acid. The composite includes an insert showing an enlargement of a single VLP. Bar=100 nm.
Figure 3 Diagram of representative polyomavirus genomes and encoded proteins, SV40 (left) and MPyV (right). The grey circles represent the viral dsDNAs. The origin of DNA replication (ORI) is indicated. Arrows indicate protein-coding regions and their direction of transcription. Introns are denoted by solid lines. Note that the non-coding region in the vicinity of ORI also includes the regulatory region. Alternative splicing is a common characteristic of polyomavirus coding regions. The multiple large T gene products all share identical amino termini.
Figure 4 The Compass: A schematic diagram of the relationships between JC polyomavirus (JCPyV) regulatory region sequences published worldwide. JCPyV variant regulatory regions are grouped into quadrants (I-S, I-R, II-S and II-R) with ace sequence-units lightly shaded. Upper quadrant variant types (I) have no additional sequence integrated into the ace units (no inserts). Lower quadrant variant types (II) have dark integrated sequence sections (inserts), b (23 bp) and d (66 bp). Both types I and II are divided into singular (S) and repeat (R) forms by the left and right quadrants, respectively. Unshaded boxes are TATA boxes. Dots represent sites of possible deletions. Unshaded diamonds contain the nucleotide that occupies the 49th position in sequence section c (nt 85 of I-S, or 108 of II-S), which is adenine (A) in type I variants, but predominantly guanine (G) in type II variants. Right quadrants (R-forms) have dark dashes where sequence is deleted and ⊕ where additional repeats may occur. The * in the lower right quadrant (II-R) identifies one reported sequence that retains the second TATA box (Ciappi et al., 1999). JCPyV tropism common to all variant regulatory region forms is contained in the dark central circle. Specific JCPyV tropisms are contained in the dark corner triangles. Cells from tonsil are either (L) lymphocytes, or (S) stromal cells (Monaco et al., 1998). Cells in bone marrow that contain JCPyV have been identified as B-lymphocytes
(Houff et al., 1988).
Figure 5 Phylogentic relationships of polyomaviruses. The figure shows a concatenated data set of maximum likelihood (ML) trees that were obtained for each of VP1, VP2 and T antigen. Branch lengths are proportional to genetic divergence. The scale bars indicate nuclear substitutions per site.
(After Krumbholz, A. et al. (2009). Infect. Genet. Evol., 9, 784–799.)