Reactivation of koi herpesvirus infections in common carp Cyprinus carpio

Abstract

Two co-habitation studies with common carp were conducted to determine whether latent infections of koi herpesvirus (KHV) exist. Fish were exposed to KHV using 2 different temperature profiles, which induced low and high initial mortality. Subsequently, certain groups of fish were co-habited with naïve fish while others were not. Koi herpesvirus was reactivated in fish from 3 of the 5 experimental tanks. Reactivation of the virus occurred regardless of the initial mortality associated with the virus or whether fish were co-habited with naïve fish. The reactivation of the virus in our experiments occurred several months after the initial exposure to KHV and appeared to be temperature dependent. KEY WORDS: Koi herpesvirus · KHV · Latent infections · Reactivation · Common carp · Co-habitation Resale or republication not permitted without written consent of the publisherDis Aquat Org 67: [15][16][17][18][19][20][21][22][23] 2005 virus can infect fish and remain in an inactive state until conditions are more favourable.Exposure of carp to KHV at non-permissive temperatures (less than 17°C or greater than 28°C) has been used in the Koi carp industry to induce immunity to the virus (Ronen et al. 2003). Data suggest that at the high end of the non-permissive temperature range, exposed fish develop specific immunity, which upon rechallenge, affords protection. However, there is much debate as to whether this strategy of inducing a 'natural immunity' produces latent infections in fish (Walster 2003), and whether these fish can subsequently transmit the virus to naïve fish.The objectives of this study were to determine whether KHV can persist in common carp after initial virus exposure, and whether the virus can be transmitted to naïve fish by co-habitation. MATERIALS AND METHODSVirus isolate. The UK D-132 Koi herpesvirus isolate (CEFAS) was used to challenge fish in both exposure experiments in this study. The virus was propagated on a koi fin cell line (Hedrick et al. 2000).Fish maintenance. Fig. 1 provides a schematic diagram of the experimental tanks used in this study. All tanks, unless otherwise stated, were on a flow-through system utilizing approximately 2 l min -1 of de-chlorinated bore-hole water. Fish were fed a maintenance diet of 1% bodyweight d -1 throughout the experiment. Fish were monitored for mortalities 2 times d -1 during the course of the study.KHV Exposure 1. Fish: One thousand common carp were purchased from a private farm with no history of KHV. The fish ranged from juveniles (aged ~1 yr), weighing between 25 and 30 g, to older fish that weighed between 150 and 200 g. One hundred fish were placed in each of two 300 l tanks (Tanks 1A and 2A) and served as controls. The 800 remaining fish were placed in a 900 l tank (Tank 1B). Prior to starting the study, fish were brought up to a temperature of 21°C from 10°C (1°C d -1 for 11 d). Ten fish were euthanized prior to exposure to KHV and blood was collected from the caudal vein. Serum was tested for KHV-specific antibodies using an ELISA (se...

Development of mRNA-specific RT-PCR for the detection of koi herpesvirus (KHV) replication stage

“…The latency-associated transcript (LAT), which plays a role in inhibiting apoptosis and maintaining latency by promoting the survival of infected neurons, has been detected in HSV-1 (Perng et al 2000). However, few reports have been conducted on latent infection of herpesvirus in aquatic animals, although it has been suggested that carp surviving KHV infection may become a carrier of the virus (St-Hilaire et al 2005, Dishon et al 2007). Currently, we are studying the state of the virus in the main internal organs of carp surviving KHV infection.…”

Phylogenetic relationships in the family Alloherpesviridae

“…The best evidence comes from studies of the Lucké tumor, in which RaHV1 nucleic acid and proteins have been demonstrated in non-infectious, virus-free tumor tissue that, upon temperature manipulation, can yield infectious virus (Biggs 1972, Naegele & Granoff 1980, Tweedell 1989. Moreover, evidence for a long-term carrier state, which may or may not involve latency, has been described in several fish HVs, including IcHV1 (Wise et al 1985, Boyle & Blackwell 1991, Baek & Boyle 1996, Gray et al 1999, Thompson et al 2005, SalHV2 (Gou et al 1991, Kimura & Yoshimizu 1998), CyHV1 (Sano et al 1993), AngHV1 (van Nieuwstadt et al 2001, Shih 2004, and CyHV3 (Adkison et al 2005, Bercovier et al 2005, St-Hilaire et al 2005. These reports, and others of an anecdotal nature, indicate the existence of long-term infections (perhaps latency) caused by a wide selection of viruses in the family Alloherpesviridae.…”

Koi Herpes Virus: A Review and Risk Assessment of Indian Aquaculture

“…A progressive increase in anti-KHV antibodies in naturally exposed koi is seen by ELISA [69]. These antibodies are detected in the serum at 3 weeks after experimental infection and in survivors after 1 year following a natural infection [1,39,78,81]. KHV infection induces a high prevalence (54 %) of KHV specific antibodies in surviving wild fish population [83]; while studies in farmed fish of England show almost 85-93 % of fish are seropositive by ELISA, even 1 year after disease outbreak [81].…”

“…In wild populations, KHV can remain as carrier in asymptomatic fish and act as reservoir of infection [83]. Several months after initial exposure to the virus, temperature-dependent reactivation of KHV infection can occur in exposed fish [19,78]. This latency feature of KHV probably contributes in the spread of this pathogen to new geographic locations.…”