Current knowledge on koi herpesvirus (KHV) &ndash; a review

The first outbreaks of a disease connected with high mortality of common carp and koi carp caused by koi herpesvirus (KHV) were reported in 1998 in Israel and in the United States. Since then, several cases have been confirmed all over the world. At present, this viral disease is considered to be one of the most risky factors affecting populations of common carp and koi carp. Affected fish become disoriented and swim erratically with high breathing frequency, swollen gills and partially local skin lesions. The virus was isolated from the tissues of fish showing signs of the disease and subsequently cultured on koi fin (KF-1) cells. Electron microscopic examinations revealed morphological signs identical with viruses of the family Herpesviridae. Analysis of virion polypeptides and gene DNA showed the differences between KHV and the well-known herpesvirus of cyprinids, Herpesvirus cyprini (CHV), and Channel catfish virus (CCV). Water temperature is a factor influencing the onset and severity of disease. Fish seem most susceptible at water temperatures of 18–28°C, no morbidities occur at 13°C and 30°C. At present, diagnosis of KHV is mainly based on detection of viral DNA by PCR method.

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Koi Herpes Virus (KHV) Disease

EDIS ◽

10.32473/edis-vm113-2004 ◽

1969 ◽

Vol 2004 (8) ◽

Author(s):

Kathleen H. Hartman ◽

Roy P.E. Yanong ◽

B. Denise Petty ◽

Ruth Francis-Floyd ◽

Allen C. Riggs

Keyword(s):

Herpes Virus ◽

Viral Disease ◽

The United States ◽

Cooperative Extension Service ◽

Large Animal ◽

Information Sheet ◽

University Of Florida ◽

Koi Herpesvirus ◽

Herpès Virus ◽

Fish Industry

Koi herpes virus (KHV), a viral disease highly contagious to fish, may cause significant morbidity (sickness or disease) and mortality in common carp (Cyprinus carpio) (Hedrick et al., 2000; OATA, 2001). This species is raised as a foodfish in many countries and has been selectively bred for the ornamental fish industry, where it is known as koi. Historically, the first outbreak of KHV was reported in 1998 and confirmed in 1999 in Israel. Since then, other cases have been confirmed in the United States, Europe and Asia (Hedrick et al., 2000; OATA, 2001; Anonymous, 2003). This information sheet is intended to inform veterinarians, biologists, culturists, and hobbyists about KHV. This document is Fact Sheet VM-149, one of a series from the Department of Large Animal Clinical Sciences (College of Veterinary Medicine), Florida Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida. First published: June 2004. VM-149/VM113: Koi Herpesvirus Disease (KHVD) (ufl.edu)

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

Journal of Virology ◽

10.1128/jvi.00146-07 ◽

2007 ◽

Vol 81 (10) ◽

pp. 5058-5065 ◽

Cited By ~ 173

Author(s):

Takashi Aoki ◽

Ikuo Hirono ◽

Ken Kurokawa ◽

Hideo Fukuda ◽

Ronen Nahary ◽

...

Keyword(s):

Common Carp ◽

Direct Repeat ◽

The United States ◽

Membrane Glycoproteins ◽

Genome Sequences ◽

Protein Coding ◽

Channel Catfish Virus ◽

Koi Herpesvirus ◽

Worldwide Production

ABSTRACT 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.

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

Journal of Virology ◽

10.1128/jvi.78.17.9544-9551.2004 ◽

2004 ◽

Vol 78 (17) ◽

pp. 9544-9551 ◽

Cited By ~ 92

Author(s):

Eli Pikarsky ◽

Ariel Ronen ◽

Julia Abramowitz ◽

Berta Levavi-Sivan ◽

Marina Hutoran ◽

...

Keyword(s):

Common Carp ◽

Interstitial Nephritis ◽

Viral Disease ◽

Viral Agent ◽

Fish Farms ◽

Necrosis Virus ◽

Koi Herpesvirus ◽

Single Clone ◽

Gill Disease ◽

Financial Losses

ABSTRACT 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.

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Koi herpesvirus and carp oedema virus: Infections and coinfections during mortality events of wild common carp in the United States

Journal of Fish Diseases ◽

10.1111/jfd.13082 ◽

2019 ◽

Vol 42 (11) ◽

pp. 1609-1621 ◽

Cited By ~ 5

Author(s):

Soumesh K. Padhi ◽

Isaiah Tolo ◽

Margaret McEachran ◽

Alexander Primus ◽

Sunil K. Mor ◽

...

Keyword(s):

United States ◽

Common Carp ◽

The United States ◽

Virus Infections ◽

Koi Herpesvirus

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SUSCEPTIBILITY OF CYPRINID AND NON-CYPRINID FISH CELL LINES TO KOI HERPESVIRUS (KHV)

Indonesian Aquaculture Journal ◽

10.15578/iaj.4.2.2009.131-137 ◽

2009 ◽

Vol 4 (2) ◽

pp. 131

Author(s):

Tuti Sumiati ◽

Agus Sunarto

Keyword(s):

Cell Lines ◽

Common Carp ◽

Cyprinid Fish ◽

Fish Cell ◽

Post Inoculation ◽

Koi Carp ◽

Koi Herpesvirus ◽

Emerging Virus ◽

Infected Cells ◽

Culture Supernatants

Koi herpesvirus (KHV) is an emerging virus that infects koi and common carp (Cyprinus carpio) with mortality up to 95% within 7 days. The disease is rapidly spreading worldwide including to Indonesia. However, it has only been documented in koi and common carp. The aim of this research was to evaluate the susceptibility of fish cell cultures originated from cyprinid and non-cyprinid fish to KHV. Koi Fin (KF-1) and Koi Tail (KT-2) cell lines derived from koi carp and SSN-1 cells originated from fry of striped snakehead were used in this study. The cells were inoculated with tissue extract of KHV-infected koi carp (experiment 1) and virus stock of KHV (experiment 2). The cultures were incubated at 22oC and the onset and type of cytophatic effect (CPE) were observed for 21 days post inoculation. The results of experiment 1 showed that CPE was observed in KT-2 at day 6 post inoculation. In the experiment 2, however CPE was observed in KF-1 and KT-2 cells at day 4 post infection. CPE was not observed in SSN-1 of either experiment 1 or experiment 2. CPE was characterized by extensive vacuolization of the infected cells. Polymerase chain reaction (PCR) assay of cell and tissue culture supernatants confirmed that KF-1 and KT-2 showing CPE were indeed infected with KHV. The results indicated that KF-1 and KT-2 cells were susceptible and SSN-1 was resistant to KHV. The implication of these findings was also discussed in the paper.

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Electron Microscopic Analysis of Myonecrosis Induced by a Pure Component Isolated From Rattlesnake Venom

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100091445 ◽

1976 ◽

Vol 34 ◽

pp. 292-293

Author(s):

Charlotte L. Ownby ◽

David Cameron ◽

Anthony T. Tu

Keyword(s):

Gel Filtration ◽

Microscopic Analysis ◽

The United States ◽

Exchange Chromatography ◽

Pure Component ◽

Electron Microscopic Level ◽

Electron Microscopic ◽

Mouse Muscle ◽

Major Health Problem ◽

Rattlesnake Venom

In the United States the major health problem resulting from snakebite poisoning is local tissue damage, i.e. hemorrhage and myonecrosis. Since commercial antivenin does not usually prevent such damage to tissue, a more effective treatment of snakebite-induced myonecrosis is needed. To aid in the development of such a treatment the pathogenesis of myonecrosis induced by a pure component of rattlesnake venom was studied at the electron microscopic level.The pure component, a small (4,300 mol. wt.), basic (isoelectric point of 9.6) protein, was isolated from crude prairie rattlesnake (Crotalus viridis viridis) venom by gel filtration (Sephadex G-50) followed by cation exchange chromatography (Sephadex C-25), and shown to be pure by electrophoresis. Selection of the myotoxic component was based on light microscopic observations of injected mouse muscle.

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