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#94862 - 02/27/11 01:25 PM Avian leucosis, Marek's & other diseases
Wieslaw Offline
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Here is the information about connection between slow feathering gene and avian leucosis I've promised before.

Quote:

Recently, the endogenous viral gene ev21 has been shown to be closely linked to the sex-linked dominant slowfeathering gene (K) that is used to feather-sex a large proportion of commercial white-egg-producing chickens (3,20). ev21 has been shown to code for the complete endogenous virus EV21.

If this subgroup E endogenous virus is congenitally transmitted to fast-feathering female progeny that lack gene ev21, these birds could have a reduced immune response to exogenous virus infection. Such a mechanism could lead to the increased ALV infection rate and poor performance observed in fast-feathering female progeny of slow-feathering dams (15).

Certain live poultry vaccines are highly effective when administered on day 18 or 19 of incubation (19). Contamination of these vaccines with infectious endogenous viruses could limit the immune response of vaccinated chickens to exogenous ALV infection. However, a detrimental effect would be expected only if the embryos were susceptible to subgroup E ALV infection and if infection of embryos on day 18 or 19 of incubation rather than on day 6 indeed limits immune response to exogenous ALV.
Since endogenous-virus-induced limitation of immune response
to ALV is clearly specific for that class of viruses (6; Crittenden, unpublished data), the detrimental effects of endogenous-virus expression would not adversely influence chicken flocks that were free of exogenous ALV infection.


It is from here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC254012/pdf/jvirol00094-0092.pdf

Other quotes will follow, but this one has been the easiest to comprehend (by me smile )

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#94943 - 03/04/11 05:57 AM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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Here is another abstract.It is taken from here:

http://www.ncbi.nlm.nih.gov/pubmed/2837753

The difference is in the supposition that the viral insertion in White Leghorns may have happened in the k+ itself.

Quote:
Poult Sci. 1988 Feb;67(2):191-7.

Association of the slow feathering (K) and an endogenous viral (ev21) gene on the Z chromosome of chickens.
Bacon LD, Smith E, Crittenden LB, Havenstein GB.

US Department of Agriculture, Agricultural Research Service, East Lansing, Michigan 48823.

Abstract
A dominant sex-linked gene, K, regulates slow feathering (SF), whereas a recessive allele, k+, determines rapid feathering (RF) in chickens. This trait provides a convenient and inexpensive approach to gender identification of White Leghorn (WL) chicks at hatch, i.e., in a sex-linked mating using k+/k+ males mated with K/- females, the K/k+ male chicks are SF, and the k+/- females are RF. However, in many WL strains, female progeny of SF dams produce fewer eggs and have higher mortality than progeny of RF dams. This loss in productivity has been attributed to higher infection and shedding rates for leukosis viruses (ALV) in SF than in RF dam lines. Because infectious endogenous viruses (EV) can induce immunological tolerance to ALV, we examined the expression and distribution of ev genes in SF and RF siblings from heterozygous K/k+ sires and k+/- dams. Infectious ALV and EV were detected by cocultivation of frozen heparinized blood cells on selected chick embryo fibroblasts and culture supernatants were tested for viral antigen by enzyme-linked immunosorbent assay tests. Specific ev genes were identified as restriction fragment length polymorphisms after hybridization with a recombinant plasmid containing the complete genome of a Rous-associated virus. It was concluded that ev21 and K genes are tightly linked because, in different WL crosses, all SF chicks inherited ev21 but RF siblings uniformly lacked ev21. Alternatively, the K gene in WL may be a mutation resulting from the insertion of ev21 in the k+ gene. The SF chicks which harbor ev21 expressed infectious EV21; evidence that EV21 may influence susceptibility to ALV is presented.


I'm not sure I understand this line:
"This loss in productivity has been attributed to higher infection and shedding rates for leukosis viruses (ALV) in SF than in RF dam lines".

Should it be understood that the SF birds themselves are more succeptible to AVL infection as well?

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#94975 - 03/05/11 06:03 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Sigi Offline
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Yes, my experience. Slow deaths in slow feathering birds, lethargic and most around 5-6 months in my case. They just wasted away, it was not 'leukosis' but another viral blood cancer is what the vet suspected afther the 6th case in one line of slow feathering Serama. I never bred the cockerels anyway, but I remembered their father was very slow in feathering, also in mature feathers, at 6 months he still didn't developed a full tail with the 2 main sickles, actually his tail was always short.
Not all of his children died. But I culled them all, remembering the ALV21 story which was horror in poultry industry late 90s.
David knows more about this. It was discussed on an international poultry congress.

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#94986 - 03/06/11 08:40 AM Re: Avian leucosis, Marek's & other diseases [Re: Sigi]
KazJaps Offline
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Both R.Okimoto and D.Caveny have discussed the issue of K locus and ALV in the past (if you want to do a search). From memory, I think it might be discussed in "Poultry Breeding & Genetics" also. On a side note, R.Okimoto mentioned that the K mutation reverts back to wild type at a high rate (another reason why not so good for large scale commercial use for sexing day-olds)

The following suggests that it is the close linkage between K and ev21 loci giving the correlations of late-feathering / poor ALV resistance, ie hasn't been determined that K mutation alone gives the poor ALV resistance (ie possibly the ev21 allele mutation alone):

Quote:
Although the LF phenotype facilitates the sexing of chicks, the K allele is also associated with a reduction in egg production, an increase in infection by lymphoid leucosis virus [7], and an increase in the mortality rate [8]. These negative side effects may be caused by the presence of the endogenous retrovirus 21 (ev21) [8]. Concordance between expression of ev21 and the LF phenotype indicated a linkage of less than 0.3 cM between K and the ev21 locus [9,10]. The ev21 locus consists of an integration site that can be occupied (ev21+) or unoccupied (ev21-). EF animals were found to have only one unoccupied site per Z chromosome; whereas, LF animals have at least one Z chromosome with an unoccupied and an occupied site [11]. A study on the organization of the K allele concluded the integration of ev21 into one of two large homologous segments located on the Z chromosome of LF chickens [12]. EF revertants carrying an occupied site have been observed; therefore, it was concluded that ev21 itself could not be the sole cause of the LF phenotype [13].

.......Although the LF phenotype facilitates the sexing of chicks at hatching, expression of ev21 is associated with the negative side effects of the K allele [7,8]. The establishment of a line where late-feathering is not associated with decreased egg production and tolerance to exogenous avian leucosis virus infection would be of prime commercial interest. Obviously, the search for the K allele lacking the occupied site is an effective approach. This search for revertants and the establishment of a line can be done by combining the TaqMan K test and the ev21 test proposed by Tixier-Boichard [15].

* so it has been determined that ev21 doesn't give the K - late feathering phenotype.

Partial duplication of the PRLR and SPEF2 genes at the late feathering locus in chicken.
Elferink MG, Vallée AA, Jungerius AP, Crooijmans RP, Groenen MA.
BMC Genomics. 2008 Aug 20;9:391.
full paper
*As the paper title indicates, they have narrowed down the K locus gene to two candidates: PRLR & SPEF2 genes.

------------------
The following was an interesting study on a strain of very late feathering chickens from Indonesia:

A deleted retroviral insertion at the ev21-K complex locus in Indonesian chickens.
Tixier-Boichard M, Boulliou-Robic A, Morisson M, Coquerelle G, Horst P, Benkel B.
Poult Sci. 1997 May;76(5):733-42.
full paper
*this phenotype (& genotype) more complex.

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#95036 - 03/08/11 05:54 AM Re: Avian leucosis, Marek's & other diseases [Re: KazJaps]
Wieslaw Offline
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Kazjaps, WOW!, that is a nice piece of information , thanks.

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#95124 - 03/12/11 06:14 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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Originally Posted By: Kazjaps
On a side note, R.Okimoto mentioned that the K mutation reverts back to wild type at a high rate (another reason why not so good for large scale commercial use for sexing day-olds)


Originally Posted By: R.Okimoto
Some mutations are very frequent and happen all the time. The sex-linked late-feathering locus in chickens mutates back to wild-type early feathering at a rate of 1 in a thousand. Commercial late-feathering lines developed for feather sexing have to be constantly screened for early feathering revertants.


It is in this thread .


While we are at slow feathering: the gene has the tendency to mutate back. But what about the other way around? Do the rapid feathering mutate to slow feathering with increased frequency(compared to other genes)? Any known reports?

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#107721 - 01/13/13 01:32 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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I have not forgotten this thread, I just have been too busy to update it. In the meantime , I have found some articles you need to read.

http://www.ncbi.nlm.nih.gov/pubmed/20979123
http://www.ncbi.nlm.nih.gov/pubmed/22332987

and this
http://www.ncbi.nlm.nih.gov/pubmed/10502478

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#107723 - 01/13/13 02:11 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Marina Offline
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Wieslaw - thanks for the links. Very interesting.

Is there a way I can read the whole article, not just the abstract?

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#107724 - 01/13/13 02:51 PM Re: Avian leucosis, Marek's & other diseases [Re: Marina]
Wieslaw Offline
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Usually there is a place you can read the whole article if you follow some links, but you have to pay for the access.

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#107734 - 01/13/13 07:42 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
jonnydot Offline
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I "think" this is related and I have some questions ..http://www.ncbi.nlm.nih.gov/pubmed/16457736BMC Genomics. 2006 Feb 5;7:19.
Complete association between a retroviral insertion in the tyrosinase gene and the recessive white mutation in chickens.
Chang CM, Coville JL, Coquerelle G, Gourichon D, Oulmouden A, Tixier-Boichard M.
Source

UMR Génétique et Diversité Animales, INRA/INA P-G, Centre de Recherches de Jouy, 78352 Jouy-en-Josas, France. chang@dga2.jouy.inra.fr
Abstract
BACKGROUND:

In chickens, three mutant alleles have been reported at the C locus, including the albino mutation, and the recessive white mutation, which is characterized by white plumage and pigmented eyes. The albino mutation was found to be a 6 bp deletion in the tyrosinase (TYR) gene. The present work describes an approach to identify the structural rearrangement in the TYR gene associated with the recessive white mutation.
RESULTS:

Molecular analysis of the chicken TYR gene has revealed a major structural difference (Restriction Fragment Length Polymorphism, RFLP) in the genomic DNA of the recessive white chicken. A major size difference of 7.7 kb was found in intron 4 of the TYR gene by long-range PCR. Molecular cloning and sequencing results showed the insertion of a complete avian retroviral sequence of the Avian Leukosis Virus (ALV) family. Several aberrant transcripts of the tyrosinase gene were found in 10 week old recessive white chickens but not in the homozygous wild type colored chicken. We established a rapid genotyping diagnostic test based on the discovery of this retroviral insertion. It shows that all homozygous carriers of this insertion had a white plumage in various chicken strains. Furthermore, it was possible to distinguish heterozygous carriers from homozygous normal chickens in a segregating line.
CONCLUSION:

In this study, we conclude that the insertion of a complete avian retroviral sequence in intron 4 of the tyrosinase gene is diagnostic of the recessive white mutation in chickens. This insertion causes aberrant transcripts lacking exon 5, and we propose that this insertion is the causal mutation for the recessive white allele in the chicken.

PMID:
16457736
[PubMed - indexed for MEDLINE]
PMCID:
PMC1373650

Free PMC Article

Images from this publication.See all images (11) Free text
Figure 1
Figure 10
Figure 11
Figure 2
Figure 3
Publication Types, MeSH Terms, Substances
LinkOut - more resources ...........My questions are ...does this mean that this virus is still active ? or has it just changed dna ,and if it is active would it mean that in those c/c birds that leak straw the virus is not as prolific as in those that are a clean white and does it mean that if a leaky bird was over a clean white bird that the offspring would get a stronger dose of the virus ? sorry if I have asked in the wrong place

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#107767 - 01/14/13 03:37 PM Re: Avian leucosis, Marek's & other diseases [Re: jonnydot]
Wieslaw Offline
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You have asked the correct place, but it is not sure you will get an answer right now. I think people who keep recessive whites should be asked to express their opinion on general health and longevity of the birds, whether they observed something 'suspect'compared to other birds.

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#107775 - 01/15/13 04:27 AM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
ssc Offline
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Could some strains of Copper Black Marans carry recessive white?

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#107787 - 01/15/13 04:25 PM Re: Avian leucosis, Marek's & other diseases [Re: ssc]
Wieslaw Offline
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Originally Posted By: ssc
Could some strains of Copper Black Marans carry recessive white?


Why not? There are recessive white Marans.

Here is another horror, this time with Marek's

http://www.ncbi.nlm.nih.gov/pubmed/21320336

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#108268 - 02/01/13 05:05 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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#109438 - 04/24/13 03:47 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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I have found an easy to understand abstract.

Quote:

Institute for Animal Health, Compton, Newbury, Berks, RG20 7NN, United Kingdom

ABSTRACT

Three species of avian retrovirus cause disease in poultry: the avian leukosis/sarcoma virus
(ALSV), reticuloendotheliosis virus (REV), and lymphoproliferative disease virus (LPDV) of turkeys. The
ALSV can be classified as slowly transforming viruses, which lack a viral oncogene, and acutely transforming
viruses, which possess a viral oncogene. Slowly transforming viruses induce late onset leukoses of the B cell
lymphoid, erythroid, and myeloid cell lineages, and other tumors, by viral promoter insertion into the
genome of a host cell and activation of a cellular protooncogene. The various acutely transforming leukemia and sarcoma viruses induce leukotic or other tumors rapidly and carry one or another (sometimes two) viral oncogenes, of which some 15 have been identified. The ALSV fall into six envelope subgroups, A through E, and the recently recognized J subgroup, which induces myeloid leukosis. With the exception of Subgroup E viruses, these viruses spread vertically and horizontally as infectious virions, and are termed exogenous viruses. Subgroup E viruses are usually spread genetically as DNA proviruses (often defective) in host germ cell genome, and are termed endogenous viruses. Several other families of endogenous viruses also exist, one of which, endogenous avian retrovirus (EAV), is related to Subgroup J ALV. Exogenous viruses, and sometimes endogenous viruses, can have detrimental effects on commercially important production traits. Exogenous viruses are currently controlled by virus eradication schemes. Reticuloendotheliosis virus, which lacks a viral oncogene, causes chronic B cell and T-cell lymphomas in chickens, and also chronic lymphomas in turkeys and other species of birds. An acutely transforming variant of REV, Strain T, carries a viral oncogene, and induces reticuloendotheliosis within a few days. In chickens and turkeys, REV spreads vertically and horizontally. No commercial control schemes are operated. In turkeys, LPDV infection has occurred in several countries, where it caused a lymphoproliferative disease of uncertain nature

It is from here:

http://www.poultryscience.org/ps/paperpdfs/98/ps981204.pdf

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#111531 - 01/24/14 05:11 AM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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A propos recessive white viral insertion: I have read, that it is inserted "backwards"(provided I understood correctly), thus should not make a bird more succeptible to avian leucosis(?)

Here is another interesting link

http://www.ncbi.nlm.nih.gov/pubmed/8202427

Quote:
Male-mediated venereal transmission of endogenous avian leukosis virus.
Smith EJ, Fadly AM.
Author information USDA, Agricultural Research Service, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.

Abstract

Congenital transmission of avian leukosis viruses (ALV) occurs readily through the egg, but transmission of ALV through male seminal fluid is considered to be nonexistent or rare. Progeny from mating endogenous late-feathering (LF), K/k+ males carrying an endogenous virus gene (ev21) with virgin early-feathering (EF) k+/w females were examined for the presence of infectious endogenous virus EV21 using an enzyme-labeled immunoassay for viral capsid antigen p27. All 177 LF chicks expressed EV21, p27, and 171 of 175 EF chicks did not express p27. Blood from the four p27-positive EF chicks revealed only infectious Subgroup E ALV as determined by subgroup-specific virus assays. Southern blot DNA hybridizations, however, ruled out germline integration of EV21 among the four infected EF progeny. Virus EV21 was not shed in albumens of the dams. Moreover, antibodies against ALV Subgroups A and E were not detected in dams 17 wk after the first insemination. Chicks infected with EV21 were found only in the first two of six hatches. Data suggested direct infection of the embryos from viremic semen rather than congenital infection through infected hens. Direct male transmission of EV21 to progeny may be the basis for persistence of refractory lines noted in some ALV eradication programs. Based on the absence of recombinants among 352 progeny, ev21 and K appear to be less than .3 cM apart.

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#111593 - 01/30/14 12:39 AM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Redcap Online   content
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In the meanwhile it is known, that infection or reinfection can happen in adult chicken
http://www.ncbi.nlm.nih.gov/pubmed/17039834
or even in turkeys
http://veterinaryrecord.bmj.com/content/171/23/602.1.extract
http://www.ncbi.nlm.nih.gov/pubmed/11918050

Therefore is has been suggest to revaccinate chicken - best results can be reached with homologous vaccines
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643530/
_________________________

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#116907 - 11/09/17 02:57 PM Re: Avian leucosis, Marek's & other diseases [Re: Redcap]
Wieslaw Offline
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A new article on avian influenza

Identifying the genetic basis for resistance to avian influenza in commercial egg layer chickens
https://www.ncbi.nlm.nih.gov/pubmed/29103391

Abstract

Two highly pathogenic avian influenza (HPAI) outbreaks have affected commercial egg production flocks in the American continent in recent years; a H7N3 outbreak in Mexico in 2012 that caused 70% to 85% mortality and a H5N2 outbreak in the United States in 2015 with over 99% mortality. Blood samples were obtained from survivors of each outbreak and from age and genetics matched non-affected controls. A total of 485 individuals (survivors and controls) were genotyped with a 600 k single nucleotide polymorphism (SNP) array to detect genomic regions that influenced the outcome of highly pathogenic influenza infection in the two outbreaks. A total of 420458 high quality, segregating SNPs were identified across all samples. Genetic differences between survivors and controls were analyzed using a logistic model, mixed models and a Bayesian variable selection approach. Several genomic regions potentially associated with resistance to HPAI were identified, after performing multidimensional scaling and adjustment for multiple testing. Analysis conducted within each outbreak identified different genomic regions for resistance to the two virus strains. The strongest signals for the Iowa H5N2 survivor samples were detected on chromosomes 1, 7, 9 and 15. Positional candidate genes were mainly coding for plasma membrane proteins with receptor activity and were also involved in immune response. Three regions with the strongest signal for the Mexico H7N3 samples were located on chromosomes 1 and 5. Neuronal cell surface, signal transduction and immune response proteins coding genes were located in the close proximity of these regions.


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#116909 - 11/10/17 04:51 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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Livestock and poultry density and childhood cancer incidence in nine states in the USA.


https://www.ncbi.nlm.nih.gov/pubmed/28858758

Abstract
BACKGROUND:
Parental occupational and childhood exposures to farm animals have been positively associated with childhood brain tumors, whereas associations with childhood leukemia are equivocal. The developing immune system may be influenced by allergen, virus, or other exposures from animal sources, which may contribute to childhood cancer incidence.

RESULTS:
We found positive associations between AML and broiler chicken densities (RRper 10AU/km2 = 1.14, 95% CI = 1.02-1.26). ALL rates increased with densities of hog operations (RRper operation/100km2 = 1.06, 95% CI = 1.02-1.11). PNS cancer rates were inversely associated with layer chicken density (RRper log of AU/km2 = 0.94, 95% CI = 0.89-0.99). No association was found between any cancer type and densities of cattle, equine, or goats

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#116912 - 11/13/17 11:55 AM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Redcap Online   content
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