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Review
. 2007 Nov;81(21):11554-9.
doi: 10.1128/JVI.01178-07. Epub 2007 Aug 22.

Polyomaviruses of birds: etiologic agents of inflammatory diseases in a tumor virus family

Reimar Johne  1 , Hermann Müller
Affiliations
Review

Polyomaviruses of birds: etiologic agents of inflammatory diseases in a tumor virus family

Reimar Johne et al. J Virol. 2007 Nov.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Comparison of genome sequences of mammalian polyomaviruses and polyomaviruses of birds. (A) Schematic view of the genomes of SV40 and APV. Regions of low sequence similarity between these viruses are shown as crosshatched boxes. Indicated are the origin of replication (ori) and the regions encoding the small tumor antigen (sT-Ag), large tumor antigen (lT-Ag), agnoprotein (agno), and VP1 through 4. Despite having the same designation, VP4 of SV40 and VP4 of APV have no structural or functional similarities. (B) Phylogenetic relationship of 15 polyomaviruses based on the complete amino acid sequences of large tumor antigen. Abbreviations of the virus names are as in Table 1. The alignment was performed using the Clustal W algorithm of the MegAlign module of DNASTAR software package (LASERGENE).
FIG. 2.
FIG. 2.
Schematic map of VP4 of APV. General characteristics of the amino acid composition are shown above the map. Leucine residues (L) involved in the formation of a leucine zipper-like structure and phosphorylation sites (P) are indicated. Functional domains involved in induction of apoptosis (apoptosis), DNA binding, and the proposed multimerization of VP4 are labeled in italics. The numbers beneath the map refer to amino acid positions. Amino acids 70 to 132 are deleted in the splicing variant VP4Δ.
See this image and copyright information in PMC

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