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Journal of Virology, September 2004, p. 9544-9551, Vol. 78, No. 17
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.17.9544-9551.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Pathogenesis of Acute Viral Disease Induced in Fish by Carp Interstitial Nephritis and Gill Necrosis Virus

Eli Pikarsky,1 Ariel Ronen,1 Julia Abramowitz,1 Berta Levavi-Sivan,2 Marina Hutoran,1 Yechiam Shapira,2 Michael Steinitz,1 Ayana Perelberg,1,3 Dov Soffer,1 and Moshe Kotler1*

Department of Pathology, The Hebrew University-Hadassah Medical School, Jerusalem,1 Aquaculture Research Station Dor, Ministry of Agriculture and Rural Development, Dor,3 Department of Animal Sciences, The Hebrew University Faculty of Agriculture, Food and Environmental Quality Sciences, Rehovot, Israel2

Received 9 February 2004/ Accepted 5 May 2004

A lethal disease of koi and common carp (species Cyprinus carpio) has afflicted many fish farms worldwide since 1998, causing severe financial losses. Morbidity and mortality are restricted to common carp and koi and appear in spring and autumn, when water temperatures are 18 to 28°C. We have isolated the virus causing the disease from sick fish, propagated it in koi fin cell culture, and shown that virus from a single clone causes lethal disease in carp and koi upon infection. Intraperitoneal virus injection or bathing the fish in virus-containing water kills 85 to 100% of the fish within 7 to 21 days. This virus is similar to the previously reported koi herpesvirus; however, it has characteristics inconsistent with the herpesvirus family, and thus we have called it carp interstitial nephritis and gill necrosis virus. We examined the pathobiology of this disease in carp by using immunohistochemistry and PCR. We found large amounts of the virus in the kidneys of sick fish and smaller amounts in liver and brain. A rapid increase in the viral load in the kidneys was detected by using both immunofluorescence and semiquantitative PCR. Histological analyses of fish at various times after infection revealed signs of interstitial nephritis as early as 2 days postinfection, which increased in severity up to 10 days postinfection. There was severe gill disease evidenced by loss of villi with accompanying inflammation in the gill rakers. Minimal focal inflammation was noted in livers and brains. This report describes the etiology and pathology of a recently described viral agent in fish.

* Corresponding author. Mailing address: Department of Pathology, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel. Phone: 972-2-6757300. Fax: 972-2-6758190. E-mail: mkotler{at}cc.huji.ac.il.

Journal of Virology, September 2004, p. 9544-9551, Vol. 78, No. 17
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.17.9544-9551.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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