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Journal of Virology, May 2007, p. 5058-5065, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.00146-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Genome Sequences of Three Koi Herpesvirus Isolates Representing the Expanding Distribution of an Emerging Disease Threatening Koi and Common Carp Worldwide{triangledown}

Takashi Aoki,1 Ikuo Hirono,1 Ken Kurokawa,2 Hideo Fukuda,1 Ronen Nahary,3 Avi Eldar,4 Andrew J. Davison,5* Thomas B. Waltzek,6 Herve Bercovier,3 and Ronald P. Hedrick6

Laboratory of Genome Science, Tokyo University of Marine Science and Technology, Konan 4-5-7 Minato, 108-8477 Tokyo, Japan,1 Laboratory of Comparative Genomics, Nara Institute of Science and Technology, Keihanna Science City, 8916-5, Takayama-cho, Ikoma, Nara 630-0192, Japan,2 Institute of Microbiology, Department of Clinical Microbiology, The Hebrew University-Hadassah Medical School, Ein Karen, Jerusalem, Israel,3 Kimron Veterinary Institute, Bet Dagan, Israel,4 MRC Virology Unit, Church St., Glasgow G11 5JR, United Kingdom,5 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, California 956166

Received 22 January 2007/ Accepted 20 February 2007

Since the mid-1990s, lethal infections of koi herpesvirus (KHV) have been spreading, threatening the worldwide production of common carp and koi (both Cyprinus carpio). The complete genome sequences of three KHV strains from Japan, the United States, and Israel revealed a 295-kbp genome containing a 22-kbp terminal direct repeat. The finding that 15 KHV genes have clear homologs in the distantly related channel catfish virus (ictalurid herpesvirus 1) confirms the proposed place of KHV in the family Herpesviridae, specifically in the branch with fish and amphibian hosts. KHV thus has the largest genome reported to date for this family. The three strains were interpreted as having arisen from a wild-type parent encoding 156 unique protein-coding genes, 8 of which are duplicated in the terminal repeat. In each strain, four to seven genes from among a set of nine are fragmented by frameshifts likely to render the encoded proteins nonfunctional. Six of the affected genes encode predicted membrane glycoproteins. Frameshifts or other mutations close to the 3' ends of coding sequences were identified in a further six genes. The conclusion that at least some of these mutations occurred in vivo prompts the hypothesis that loss of gene functions might be associated with emergence of the disease and provides a basis for further investigations into the molecular epidemiology of the virus.

* Corresponding author. Mailing address: MRC Virology Unit, Institute of Virology, Church St., Glasgow G11 5JR, United Kingdom. Phone: 44 141 330 6263. Fax: 44 141 337 2236. E-mail: a.davison{at}mrcvu.gla.ac.uk

{triangledown} Published ahead of print on 28 February 2007.

Journal of Virology, May 2007, p. 5058-5065, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.00146-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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