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Thread: KHV: Irresponsible People And Ignorance

  1. #11
    Honmei KoiCop's Avatar
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    From the Sep/Oct issue of KOI USA magazine (p. 41), here's a listing of what AKCA and KOI USA have been doing re: KHV research and education:

    KHV, AKCA & KOI USA FACTOIDS
    1998 Mass koi mortalities reported in Israel, England and the United States
    2000 Mass mortalities attributed to newly recognized virus: Koi Herpes Virus (KHV)
    AKCA funded Dr. Andy Goodwin’s KHV research at the University of Arkansas
    2001 AKCA organized and funded its Koi Health Advisor Program; danger of KHV stressed.
    2002 KOI USA published article on KHV by Dr. Sandy Yosha, DVM
    2003 AKCA funded Dr. Branson Richey’s KHV research at University of Georgia
    AKCA funded Dr. Andy Goodwin’s KHV research at the University of Arkansas
    2004 AKCA organized and funded its Project KHV: Donations go exclusively to research & education; AKCA matching funds up to $50k pledged; all organizational and administrative expenses are paid 100% by AKCA; Project KHV fundraising begins.
    KOI USA published articles on KHV by Spike Cover and Dr. Andy Goodwin
    2005 KOI USA published articles on KHV by Dr. Andy Goodwin and Ray Jordan
    2006 KOI USA published articles on KHV by Linda Montgomery, Spike Cover and Ray Jordan
    2007 AKCA funded Denise Petty DVM’s KHV research at U. of Florida
    KOI USA published articles on KHV by L. Porter, Spike Cover and Gene Anderson
    2008 AKCA funded Oregon State University’s trip to Israel to study KHV
    AKCA funded Dr. Ling Jin’s KHV research at Oregon State University
    KOI USA published article on KHV by Joop van Tol
    2009 AKCA funded Dr. Ling Jin’s 2 year KHV research grant at Oregon State University
    KOI USA published articles on KHV by Ray Jordan, Brian Drake and Spike Cover
    2010 KOI USA published articles on KHV by Ray Jordan and Dr. Ling Jin, DVM
    2011 KOI USA published article on KHV by Ray Jordan
    2012 AKCA funded Dr. Ling Jin’s 2 year KHV research grant at Oregon State University KOI USA published article on KHV by Larry Iles
    2013 KOI USA published article on KHV by Rob Hildreth, DVM
    AKCA funded Dr. Ling Jin’s 2 year KHV research grant at Oregon State University
    KOI USA published article on KHV by Dr. Ling Jin, DVM
    TOTALS
    KHV research projects and grants funded by AKCA.............................................. .................................................. ..................9
    KHV articles published in KOI USA magazine.......................................... .................................................. ................................26
    Project KHV Donations received.......................................... .................................................. .......................................$122,893.52
    Project KHV Funds raised via raffles/auctions/etc............................................... ..............................................$ 11,050.88
    Project KHV Research & education funds expended.......................................... ...............................................$11 6,943.39
    Project KHV AKCA matching funds expended.......................................... .................................................. ..........$ 30,000.00
    Project KHV AKCA administrative funds expended.......................................... .................................................. .$ 11,251.27
    As you can see, AKCA and KOI USA weighed in early and often on the threat KHV poses to our hobby. Furthermore, we’ve worked hand in hand with the scientific community to find solutions. With our recently signed two year $30,000 grant with OSU’s Dr. Ling Jin, it’s time once again to start actively fund raising for AKCA’s Project KHV. Please get involved by volunteering and/or donating. We need your support and we look forward to working with you and your clubs.
    Please Contact: Jerry Kyle, AKCA Project KHV Chair [email protected]
    Don Chandler
    Member: AKCA, ZNA, KoiUSA

  2. #12
    Honmei KoiCop's Avatar
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    From the same issue (p. 38), here's Dr. Ling Jin on the latest AKCA funded research grant at Oregon State University:

    Eliminating KHV latency by blocking
    ORF6 protein expression during latency
    Specific Aim:
    Cyprinid herpesvirus 3, or koi herpesvirus (KHV), is a deadly virus that affects koi and carp worldwide. It causes severe gill necrosis and nephritis, dermal ulceration , hemorrhage, and mass mortality of up to 100% of affected fish. Fish that survive KHV infection are latently infected lifelong carriers. Little is known about the molecular mechanisms and control of latency of KHV Our previous work has demonstrated that in KHV-infected koi, the virus becomes latent in leukocytes, specifically in circulating IgM+ B cells. Similar to many mammalian herpesviruses, a latency-associated viral gene, ORF6, was also recently identified in KHV-infected B cells, that likely encodes a transcriptional regulator. Our recent work demonstrated that ORF6 protein is made during latent infection and is sumoylated during productive infection. In this research application, we hypothesize that ORF6 protein is required for maintaining the latent infection, and blocking ORF6 protein expression will result termination of KHV latency. To test our hypothesis, we propose the following specific aims:
    1) Determine the role of ORF6 protein during latency. Our preliminary studies demonstrated ORF6 gene of KHV was detected in B cells from KHV latently infected koi. The predicted 752 aa protein from ORF6 contains a conserved domain that has homology to the conserved domain of Epstein-Barr Virus Nuclear Antigen 3B (EBNA-3B). We hypothesize that ORF6 has a similar function to EBNA-3B, which plays an important role in latency establishment and reactivation from latency. To determine the role of ORF6 in latency and reactivation, we will infect koi with three strains of KHV: unmodified, ORF6-deletion mutant, and ORF6 dleletion/ EBNA-3B-insertion mutant to determine ORF6 role in latency establishment and latency reactivation.
    2) Eliminating KHV latent infection by treating koi with PMO. To determine whether ORF6 is required for latency maintenance, ORF 6 expression will be blocked during latency by anti-sense technology with vivo-morpholino (PMO). KHV latency will be compared between PMO treated and un-treated groups of koi. Through this aim we will know if ORF6 can serve as treatment target to eliminate latent infection.
    Research Strategy
    A. Significance
    Herpesvirus Latency:
    Latency has classically been divided into establishment, maintenance, and reactivation phases and is characterized by a dormant viral genome and limited gene expression. For alphaherpeviruses, such as HSV-1 and Bovine herpesvirus-1 (BHV-1) which become latent mainly in the trigeminal nerve ganglion, the only viral gene expressed during latency is the latency-associated transcript (LAT) or latency related transcripts (LR). For betaherpesvirus latency, such as CMV which becomes latent mainly in myeloid progenitor cells, a few more genes are expressed, such as the CMV latency transcripts, US 28, vIL10, LUNA, and UL138 loci. During gammaherpesvirus latency, such as Epstein–Barr virus (EBV) which becomes latent in B cells, up to nine virally encoded proteins are expressed in latently infected B cells which include the EBV nuclear antigens (EBNA-1, -2, -3A, -3B, -3C, and -LP) and the latent membrane proteins (LMP-1, -2A, and -2B). Genes that are identified during latency can be divided into three groups: 1) transcriptional regulation, such as LMP-1 and Interferon regulatory factor 7, which regulates viral gene expression during latency, 2) anti- apoptosis genes, such as LAT, which can block apoptosis of infected cells during virus replication, and 3) immunomodulatory genes, examples of which include vIL10 and M2 of MHV68, which can dampen immune detection of the virus and mitigate clearance of latently infected cells. In addition to viral genes detected during latency, microRNAs (miRNAs) derived from the viral genome have been identified during latency. Although miRNA functions are still under investigation, they may play crucial roles in latency, such as transcription and translation activations. It is logical to speculate that anti-apoptosis, immune modulation, transcription and translation regulation are properties that a latent virus needs to influence in order to co-exist within its host. The elusive question that remains is how viruses accomplish all these functions with such a limited expression profile during latency. The relative simplicity of the fish immune system (vs. mammals) is a key advantage in dissecting the molecular basis of KHV modulatation of immune responses during latency and reactivation.
    KHV:
    Cyprinid herpesvirus 3, commonly known as koi herpesvirus (KHV), is a newly identified pathogen of koi and common carp (Cyprinus carpio) that causes significant disease and a high mortality in fish. KHV has been classified as a member of Alloherpesviridae, under the order Herpesvirales. KHV latency has also been demonstrated in koi that have recovered from an initial viral infection 15 years ago. Our recent study has demonstrated that KHV becomes latent mainly in IgM+ B cells in koi. Similarly to many mammalian herpesviruses, a latency-associated transcript, ORF6, was also detected in KHV-latent B cells of koi. The ORF6 transcript encodes a conserved domain in the predicted 752 aa protein that has homology to consensus sequences within the EBNA-3B conserved domain and the N-terminal regulator domain of the herpesvirus transcriptional regulator ICP4. During latency, EBV expresses three related nuclear proteins: EBNA-3A, -3B, and -3C. Both the EBNA-3A and -3C genes are essential for EBV immortalization, but EBNA-3B is dispensable in vitro. It is speculated that EBNA-3B is important for successful EBV infection in vivo, perhaps by regulating expression of host genes important for acute or latent EBV infection. It is significant that KHV expresses a gene during latency with a conserved domain with homology to EBNA-3B of EBV. It is possible that KHV’s ORF6 plays a similar role as EBNA-3B during latency. The proposed work will determine whether ORF6 functions similarly as EBNA-3B and has a role in latency and reactivation.
    C. Approach:
    Preliminary studies:
    Identifying ORF 6 protein in latently infected B cells.
    Our previous studies had demonstrated that RNA of ORF 6 is expressed in IgM+ B cells from KHV latently infected koi. To determine if ORF6 protein is expressed during latency in B cells, IgM+ B cells from koi latently infected with KHV is stained by an ORF6 peptide antibody, made with a peptide predicted by Antigen Profiler as antigenic peptide (Thermo Scientific, Pierce-Antibodies). Only cells infected by KHV and IgM+ B cells from KHV latently infected koi were stained (white arrow) by the ORF6 peptide antibody in the nucleus. No specific staining was observed in uninfected cells or IgM- B cells from uninfected control koi. In addition, expression vector containing the entire ORF6 spliced transcript can produce a correct size of protein that can be recognized by the ORF6 peptide antibody (data not shown). It suggests the ORF6 gene indeed codes a protein.
    Research design and methods:
    Aim 1: Determine the role of ORF6 protein during latency.
    Rationale:
    Our preliminary studies demonstrated that KHV ORF6 was detected in B cells from latently infected koi. The predicted 752 aa protein from ORF6 contains a conserved domain that has homology to the conserved domain of Epstein-Barr Virus Nuclear Antigen 3B (EBNA-3B). We hypothesize that the latency-associated ORF6 has a similar function as EBNA-3B, and that it plays an important role in latency establishment and reactivation from latency. To test its role in latency, we will measure latent infection in koi infected with three strains of KHV: unmodified, ORF6-deletion mutant, and ORF6-deletion/EBNA-3B-insertion mutant.
    Construction of ORF6 plasmid, ORF6-, and ORF6-/EBNA-3B+ plasmid:
    To make TOPO-ORF6 plasmid the entire ORF6 gene, flanking sequences ORF6L and ORF6R will be amplified by PCR and cloned into PCR-TOPO2.1. To make the ORF6 deletion construct (TOPO-ORF6-), the TOPO-ORF6 plasmid will be cut by Pst I, which removes most of the ORF6 coding region (235 nt and 1574 nt). To make the ORF6 deletion and ENBA-3B insertion construct, the EBNA-3B sequence will be amplified from Plasmid MSCV-N EBNA-3B (addgene) with Pst I restriction sites at the end, then sub-cloned into TOPO-ORF6- plasmid to generate the ORF6-/EBNA-3B+ plasmid. Restriction digestion and DNA sequencing will be used to confirm the final plasmid.
    Generation of ORF6 deletion and EBNA3B insertion mutants:
    The linearized pTOPO-ORF6- or pTOPO-ORF6-/EBNA-3B+ (cut with EcoRI) will be co-transfected with KHV genomic DNA into KF-1 cells to generate the KHV-ORF6- mutant or KHV-ORF6-/ENBA-3B+ mutant by homologous recombination as we previously described. Briefly, viral DNA (approximately 2 to 3 μg/ml) and linearized plasmid (cut with EcoRI) (10 to 15 μg/ml) will be co-transfected by the calcium phosphate method into monolayers of KF-1 cells. Individual viral plaques will be screened by PCR and Southern Blot as previously described. The EBNA-3B insertion mutant will place EBNA-3B 80 bp down40 KOI USA
    stream of the ATG site of ORF6. To generate the rescue mutant, the ORF6 gene will be placed back into the KHV-ORF6- mutant. The rescue mutant will be made similarly by homologous recombination between KHV-ORF6- mutant and TOPO-ORF6 plasmid. Restriction digestion and DNA sequencing will be used to confirm the recombinant. Recombinant viruses will be subjected to at least three rounds of plaque purification and stored at −70°C.
    Virus infection in Koi and Latency establishment:
    To assess the function of ORF6 in virus infection and latency establishment, four groups of ten adult koi 10-12 inches long (3-5 years old) will be infected with 1 × 104 PFU/ml of KHV-ORF6-, KHV-ORF6-/EBNA-3B+, rescue mutant or wild-type KHV. The infection will be monitored daily during the first two weeks. Gill or droppings from all groups will be swabbed and examined on days 1, 3, 5, 7, 10 and 14 post-infection. The amount of infectious virus in each swab or droppings will be determined by a standard plaque assay on KF-1 cell monolayers. To determine whether the ORF6 has any effect on establishment of latency, B cells will be harvested from surviving koi on day 30 post-infection, and KHV DNA copy number will be determined in these B cells, using Taqman real-time PCR as described previously. In addition, viral gene expression will be investigated as described in Aim 1 in B cells from koi infected by the mutants and wild type virus, respectively.
    Assess the role of ORF6 and EBNA-3B in reactivation under heat stress:
    Our laboratory has previously shown that KHV reactivates under temperature stress. To determine whether ORF6 gene participates in reactivation from latency, four groups of koi (n = 20 per group), will be infected with the ORF6 deletion mutant, KHV-ORF6-/EBNA-3B+, the rescue mutant, and wild type virus as discussed above. Health and mortality of these fish will be monitored for 30 days, after which surviving fish within each group will be stressed by heating. Briefly, the koi tank water temperature will be increased from 12°C to 23°C at a rate of 1°C per day, then the temperature will be held constant for four days at 23°C before dropping back to 12°C at a rate of 1°C per day. KHV reactivation can cause death as well as virus shedding in the tissues and droppings. Virus reactivation will be monitored by virus detection in gill swabs and collected droppings by standard plaque assays.
    Aim 2:
    Eliminating KHV latent infection by treating koi with PMO
    To determine whether ORF6 can be targeted to block latency, ORF6 expression will be blocked by an anti-sense oligo specific to ORF6 RNA near the start codon (ATG). Through this aim we will gain insight into the degree of importance and viral species-specificity of ORF6 function in KHV latency.
    Design vivo morpholino (PMO):
    The PMO will be designed and manufactured against ORF 6 translation by a local company (GeneTools, LLC). Its efficacy against ORF6 protein synthesis will be tested in vitro first as reported before.
    Comparing the KHV latency in koi treated and un-treated with ORF6-PMO:
    To evaluate the effect of blocking ORF6 translation with ORF6-PMO, two groups (10 each) of koi will be injected via i.v. with PMO at a concentration of 10 uM based on previous in vivo study. One group will be given ORF6 specific PMO, the other group with be given a control PMO for a week daily. Following treatment, KHV latency in B cell will be monitored at day 1, 3, 5, 7 and 14 days post-treatment. The KHV genome copy number will be estimated by TaqMan real-time PCR as described previously.
    Expected results:
    If ORF6 gene function is required for establishment of latency, we expect koi infected with KHV-ORF6- will have reduced latency in B cells. Therefore, B cells recovered from KHV-ORF6- infection will carry undetectable or low levels of the KHV genome. If ORF expression is required for maintenance of KHV, blocking ORF6 expression with ORF6 PMO will result in reduced KHV latency in B cells, which may discover a therapeutic target for interfering herpesvirus latency. If ORF6 gene is essential for the virus reactivation, no mortality or virus shedding should be observed in groups infected with KHV-ORF6- mutant following heat stress. If ORF6 is a homolog of EBNA-3B, we expect the KHV-ORF6-/EBNA-3B+ mutant to behave the same as KHV wild type virus and rescue mutant in latency establishment and reactivation. The difference in viral gene expression between mutant and wild type virus will lead us to develop a focused research hypothesis to investigate the role of viral genes during latency and reactivation.
    Potential difficulties and alternative approaches:
    We have ample experience making similar mutants of HSV-1 as well as porcine herpesvirus. We don’t anticipate difficulty making the mutants. Although we have used PMO in vivo before in mice, PMO treatment in koi has not been reported before. The PMO dosage is based on our previous studies in mice and cotton rats. An effective dosage in koi may be different from the dosage we discovered in mice. A pilot study will be conducted before treating the koi with PMO to determine the optimal dosage in koi.

  3. #13
    Sansai
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    Quote Originally Posted by KoiCop View Post
    Mike's post is spot on: There is no cure for Koi Herpes Virus (KHV). Infected koi who survive the heat treatment become lifelong KHV carriers and a threat to naive koi.

    As our own Brian Sousa wrote in his "Word from the Editor" in KOI BITO 10 (2005):

    Now that KHV appears poised to become pandemic, all but the most optimistic would tend to fear the worst. What will become of our beloved hobby? Rumors abound and the public is wary of buying. Although mostly unfounded, uncertaintity breeds fear, and in the wake of the events of the past few years, the present is a dangerous time for the existence of nishikigoi. Efforts have been underway to combat and keep this disease in check, yet we still have no vaccine to this day. If you're considering supporting further research, now is the time. The more we learn and understand, the greater the chance that we uncover the cure.
    No vaccine for AIDS,not likely to bother about KHV.

    Big AIDS conference in Durban at the moment.

    Rid the world of HIV by 2030 .

    News headlines.

    A lot the sex workers are making their way to the conference city. Not to be cured I don't think.

    Purely gossip yesterday, 3 Koi breeders in UK reported with KHV outbreaks????

    Garfield

  4. #14
    Oyagoi yerrag's Avatar
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    So koi that have recovered from KHV are immune, right? If so, how does one go about getting their koi infected with KHV, and then make them immune by recovering from it?Would KHV-immune Oyagoi confer immunity on offsprings? Are there many strains of KHV? If so, there is no guarantee that being immunized from KHV means there is absolute certainty that the koi will not fall to another strain of KHV to which it has no developed immunity.

  5. #15
    Daihonmei MikeM's Avatar
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    Now, Yerrag, I'm sure you can figure out how to have a pond full of survivors. However, experience has been that heat treatment does not save all the infected fish. So, you would have to be willing to gamble on losing the ones you like the most.... and be willing to be ostracized by the hobby. The least impact on hobbyists with survivors is the standard that KHV survivors are not allowed to be entered in shows. Far greater is being viewed as harboring the source of death. The person keeping KHV carriers should be excluded from all aspects of the hobby. That is the reason for my initial post.

    There are several strains of KHV. There are indications that rates of mortality vary, but all are high. I am not aware of research focused on re-infection by different strains. I would guess it might be similar to flu. A new infection is possible, but the effects are milder due to the immune system being able to respond more quickly.
    MCA likes this.

  6. #16
    Daihonmei MikeM's Avatar
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    KoiCop: Thanks for posting. Project KHV has made a lasting contribution to the hobby. I hope the work can continue for many years.

  7. #17
    Oyagoi yerrag's Avatar
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    The mis-information is on their website. The latency of the KHV virus has been established in the studies made by Dr. Jin and colleagues at Oregon State University. The abstract from one study is very clear:

    "Koi herpesvirus (KHV) has recently been classified as a member of the family of Alloherpesviridae within the order of Herpesvirales. One of the unique features of Herpesviridae is latent infection following a primary infection. However, KHV latency has not been recognized. To determine if latency occurs in clinically normal fish from facilities with a history of KHV infection or exposure, the presence of the KHV genome was investigated in healthy koi by PCR and Southern blotting. KHV DNA, but not infectious virus or mRNAs from lytic infection, was detected in white blood cells from investigated koi. Virus shedding was examined via tissue culture and reverse transcription-PCR (RT-PCR) testing of gill mucus and feces from six koi every other day for 1 month. No infectious virus or KHV DNA was detected in fecal secretion or gill swabs, suggesting that neither acute nor persistent infection was present. To determine if KHV latent infections can be reactivated, six koi were subjected to a temperature stress regime. KHV DNA and infectious virus were detected in both gill and fecal swabs by day 8 following temperature stress. KHV DNA was also detectable in brain, spleen, gills, heart, eye, intestine, kidney, liver, and pancreas in euthanized koi 1 month post-temperature stress. Our study suggests that KHV may become latent in leukocytes and other tissues, that it can be reactivated from latency by temperature stress, and that it may be more widespread in the koi population than previously suspected."
    Thus study establishes the latency of KHV of koi previously that survived infection with KHV. Subjected to temperature stress (whatever that is), KHV infections were reactivated.

    I would like there to be a follow-up study of similar design on koi previously uninfected by KHV(established by PCR testing), to determine if KHV infections would occur. As a control group.

    If the study fails to find KHV infection occurring on this control group, that would validate further the orthodoxy of stigamatizing koi keepers that elected on saving their KHV-infected koi.

    If the study finds otherwise, it probably would not make much of a difference still, in terms of protocols in koi shows. Bio-security protocols would still be maintained, and the former practice of mixing koi from different owners would not be re-established. But it may lead us to confront KHV from a different perspective. The perspective may simply be that KHV is latent in all koi population, and avoiding its expression would be the focus. If proper care can be consistently maintained, preventing its expression would be the best thing to do.

    If it does occur to a prized koi that is worthy of koi shows, and the recovery of the koi is complete, and this koi goes on to become an oyagoi, I hope it and its offsprings would not be stigmatized.

    Yet, in the real world, where a majority of ponds are not exactly the paragon of superb koi care, it would be hard to avoid cases of KHV fatalities that simply go undetected. A fatality would simply be chucked to the dustbin of "All
    koi die eventually. Some earlier. Some later." This would be a convenient explanation, as being a superb koi keeper is not a realistic expectation for all. To make it any more complicated would drive away many potential koi hobbyists.

  8. #18
    MCA
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    Honmei MCA's Avatar
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    I would have hoped the hobby had gotten pass keeping known KHV survivors/carriers over 15 years ago.

  9. #19
    Daihonmei MikeM's Avatar
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    Quote Originally Posted by yerrag View Post
    Thus study establishes the latency of KHV of koi previously that survived infection with KHV. Subjected to temperature stress (whatever that is), KHV infections were reactivated.

    I would like there to be a follow-up study of similar design on koi previously uninfected by KHV(established by PCR testing), to determine if KHV infections would occur. As a control group.

    If the study fails to find KHV infection occurring on this control group, that would validate further the orthodoxy of stigamatizing koi keepers that elected on saving their KHV-infected koi.

    If the study finds otherwise, it probably would not make much of a difference still, in terms of protocols in koi shows. Bio-security protocols would still be maintained, and the former practice of mixing koi from different owners would not be re-established. But it may lead us to confront KHV from a different perspective. The perspective may simply be that KHV is latent in all koi population, and avoiding its expression would be the focus. If proper care can be consistently maintained, preventing its expression would be the best thing to do.

    If it does occur to a prized koi that is worthy of koi shows, and the recovery of the koi is complete, and this koi goes on to become an oyagoi, I hope it and its offsprings would not be stigmatized.

    Yet, in the real world, where a majority of ponds are not exactly the paragon of superb koi care, it would be hard to avoid cases of KHV fatalities that simply go undetected. A fatality would simply be chucked to the dustbin of "All
    koi die eventually. Some earlier. Some later." This would be a convenient explanation, as being a superb koi keeper is not a realistic expectation for all. To make it any more complicated would drive away many potential koi hobbyists.
    I think I must not understand. It seems you want a study to see if naïve koi can be infected by carriers? Do you doubt that a naïve koi would be infected by a koi shedding the virus?

    KHV is not latent in all the koi population. Numerous koi have been tested with no KHV DNA in their systems.

    In theory, over numerous generations, it would be possible to develop carp whose immune systems could combat KHV. In the process, one would discard the genetics of refinement that created Nishikigoi and then start over. I do not know who would do that work, since all the experienced breeders would be bankrupted and the hobby dead.

  10. #20
    Daihonmei MikeM's Avatar
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    Quote Originally Posted by MCA View Post
    I would have hoped the hobby had gotten pass keeping known KHV survivors/carriers over 15 years ago.
    Agreed. But as long as folks like Doc Johnson talk the way they do, the misplaced 'compassion' for the carrier will be with us.

    It is so strange to me to have people's sympathies lead them to save a carrier. If they feel that strongly about killing a fish, why do they keep koi at all? The entire process of producing koi is about killing millions of 'innocent babies' to produce marketable ones. The issue should never be the 'cruelty' of killing the carrier. They can be euthanized painlessly. The cruel act is keeping a carrier that inherently endangers the healthy koi of one's friends and neighbors.

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