Genetics, Vol. 152, 1387-1396, August 1999, Copyright © 1999

A Novel Virus Family, the Rudiviridae: Structure, Virus-Host Interactions and Genome Variability of the Sulfolobus Viruses SIRV1 and SIRV2

David Prangishvilia, Hans Peter Arnolda, Dorothee Götza, Ulrike Ziesea, Ingelore Holza, Jakob K. Kristjanssonb, and Wolfram Zilliga
a Max-Planck-Institut für Biochemie, D 82152 Martinsried, Germany
b Technological Institute of Iceland, Keldnaholt, IS 112, Reykjavik, Iceland

Corresponding author: David Prangishvili, Max-Planck-Institut für Biochemie, Am Klopferspitz 18a, 82152 Martinsried, Germany., prangish{at}biochem.mpg.de (E-mail)

Communicating editor: P. BLUM

The unenveloped, stiff-rod-shaped, linear double-stranded DNA viruses SIRV1 and SIRV2 from Icelandic Sulfolobus isolates form a novel virus family, the Rudiviridae. The sizes of the genomes are 32.3 kbp for SIRV1 and 35.8 kbp for SIRV2. The virions consist of a tube-like superhelix formed by the DNA and a single basic 15.8-kD DNA-binding protein. The tube carries a plug and three tail fibers at each end. One turn of the DNA-protein superhelix measures 4.3 nm and comprises 16.5 turns of B DNA. The linear DNA molecules appear to have covalently closed hairpin ends. The viruses are not lytic and are present in their original hosts in carrier states. Both viruses are quite stable in these carrier states. In several laboratory hosts SIRV2 was invariant, but SIRV1 formed many different variants that completely replaced the wild-type virus. Some of these variants were still variable, whereas others were stable. Up to 10% nucleotide substitution was found between corresponding genome fragments of three variants. Some variants showed deletions. Wild-type SIRV1, but not SIRV2, induces an SOS-like response in Sulfolobus. We propose that wild-type SIRV1 is unable to propagate in some hosts but surmounts this host range barrier by inducing a host response effecting extensive variation of the viral genome.





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