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CCR5 32 delta deletion gene mutation (Read 8186 times)
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CCR5 32 delta deletion gene mutation
Apr 19th, 2012 at 3:10pm
 
This is the big deal with Atheists and Evodelusionists and Creationists don't like this either.   
This CCR5 delta 32 deletion mutations is now found to have bad effects in over 9 genetically caused deaths and diseases.

If you have both parents with this gene you  will get it.  It is a deletion of 32 base pairs in


Cell Mol Neurobiol. 2009 Dec;29(8):1205-9.
CCR5-delta 32 allele is associated with the risk of developing multiple sclerosis in the Iranian population.
Shahbazi M, Ebadi H, Fathi D, Roshandel D, Mahamadhoseeni M, Rashidbaghan A, Mahammadi N, Mahammadi MR, Zamani M.
Source
Medical Cellular & Molecular Research Center, Golestan University of Medical Sciences, Gorgan, Iran. shahbazimajid@yahoo.co.uk

Abstract
The 32-base pair deletion on the C-C chemokine receptor 5 gene (CCR5-delta 32) is known as a protective allele against immune system disorders. We have studied this variation in Iranian multiple sclerosis (MS) patients and healthy controls. DNA samples were prepared from the whole blood of 254 patients with MS and 380 healthy controls. We amplified the fragment including the CCR5-delta 32 polymorphism and visualized the products in a documentation system after agarose gel electrophoresis. Data were analysed using one-way ANOVA and Fisher's exact tests with SPSS-v13 and STATA-v8 software. The delta 32 allele was more frequent in MS patients when compared with controls (OR = 2.3, P < 0.0001). Also, we found a significant difference in the frequency of the delta 32/delta 32 genotype among patients and controls (OR = 7.4, P < 0.001). The mean age at onset and progression index was not significantly different between patients with various genotypes. According to our study, the delta 32 allele of the CCR5 gene might be a predisposing factor for MS development in the Iranian population. However, there were no associations between this polymorphism and the clinical course of the disease in this study.

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CCR5 (chemokine receptor-5) DNA-polymorphism influences the severity of rheumatoid arthritis.
(PMID:11196706)
Abstract
Citations
BioEntities
Related Articles
Zapico I, Coto E, Rodríguez A, Alvarez C, Torre JC, Alvarez V
Servicio de Reumatología, Hospital Central de Asturias, Oviedo, Spain.
Genes and Immunity [2000, 1(4):288-9]
Type:  Journal Article, Research Support, Non-U.S. Gov't

DOI: 10.1038/sj.gene.6363673 

Abstract      Highlight Terms
  Gene Ontology(1)   Diseases(4)   Genes/Proteins(2)  Species(1)
Chemokines are critical for the inflammatory process in autoimmune diseases such as rheumatoid arthritis (RA). The chemokine receptor-5 (CCR5) mediates chemotaxis by CC-chemokines and is expressed by lymphocytes with the Th1 phenotype and monocyte/macrophages. A 32 bp deletion in the CCR5 (CCR5-delta 32 allele) abolishes receptor expression in homozygotes, while CCR5-delta 32 carriers would express less receptor than wild-type homozygotes. This polymorphism is related to the resistance to HIV-1 infection and progression towards AIDS. We hypothesized that the CCR5-delta 32 allele may modulate the severity of disease in RA. A total of 160 RA-patients (71 and 89 with severe and non-severe phenotypes, respectively) and 500 healthy individuals from the same Caucasian population (Asturias, northern Spain) were genotyped. Carriers of the CCR5-delta 32 allele were at a significantly higher frequency (P = 0.012) in non-severe compared to severe patients (17% vs 4%). Our results suggest that the CCR5-delta 32 polymorphism is a genetic marker related to the severity of RA.
-------------------------------

CCR5-32 mutation is strongly associated with primary sclerosing cholangitis

R Eri1, J R Jonsson2, N Pandeya3, D M Purdie3, A D Clouston2, N Martin4, D Duffy4, E E Powell2,5, J Fawcett6, T H J Florin1,7 and G L Radford-Smith1,8



---------------------------------------
1 of 2A Risk of Diabetic Nephropathy in Type 1 Diabetes Is Associated With Functional Polymorphisms in RANTES Receptor Gene (CCR5)
A Sex-Specific Effect
Wojciech M. Mlynarski123, Grzegorz P. Placha12, Pawel P. Wolkow12, Jacek P. Bochenski12, James H. Warram1 and Andrzej S. Krolewski12

"Similarly, male carriers of the 32-bp deletion, which causes truncation of the protein, had significantly higher risk of diabetic nephropathy than noncarriers"

Genetics in Medicine (2004) 6, 126–131; doi:10.1097/01.GIM.0000127274.45301.54

Association of CCR5 Δ32 deletion with early death in multiple sclerosis

Radhika Gade-Andavolu1, David E Comings2, James MacMurray2, Masoud Rostamkhani2, Li S -C Cheng3, Wallace W Tourtellotte4 and Lawrence A Cone1,5

1Genetic Research Institute of the Desert, Eisenhower Medical Center, Rancho Mirage, California
2Department of Medical Genetics, City of Hope Medical Center, Duarte, California
3Department of Bio statistics, City of Hope Medical Center, Duarte, California
4Neurology & Research Services, VA, West Los Angeles Healthcare Center & Department of Neurology, UCLA, Los Angeles, California
5Sections of Immunology and Infectious Diseases, Eisenhower Medical Center, Rancho Mirage, California
Correspondence: Dr. Lawrence A. Cone, >39000 Bob Hope Drive, Eisenhower Medical Center, Probst # 308, Genetic Research Institute of the Desert, Rancho Mirage, CA 92270.

Received 21 November 2003; Accepted 17 February 2004

Top of page
Abstract
Purpose: The interaction between chemokines and their receptors is extremely important in controlling T cell migration into sites of CNS inflammation. Because trafficking of inflammatory T cells into the central nervous system (CNS) is a key player in the pathogenesis of multiple sclerosis (MS), we investigated the possible association of CCR5 Δ32 deletion in this disorder.

Methods: DNA isolated from postmortem brain tissue samples of 132 patients with MS and from blood tissue samples of 163 gender and ethnicity-matched healthy controls was used to screen for the CCR5 Δ32 deletion allele.

Results: An increased frequency of 32-bp deletion allele was found to be associated with early death (P = 0.00005) and with a progressive reduction in the years of survival (onset to death). The death hazard ratio of CCR5 with deletion versus no deletion was 2.12, suggesting that MS patients with the 32-bp deletion have twice the mortality rate of patients with the normal genotype. This effect was more significant in females (hazard ratio 3.58).

Conclusion: A strong association of the CCR5 Δ32 deletion with early death could serve as a prognostic marker for MS.

Keywords: multiple sclerosis; polymerase chain reaction; chemokine receptor; experimental autoimmune encephalomyelitis

-----------------------------



"Does the CCR5-delta32 mutation have an entirely positive/protective role?
Probably not. In patients with abdominal aortic aneurysm (AAA), the major risk is a sudden rupture - which is quite often fatal. Individuals with the delta 32 variant are more likely to have aneurysms than non-carriers, and among patients with aneurysms, delta 32 carriers are more likely to rupture than to be diagnosed in time for surgical repair. [PMID 15557916]"

-------------------------------

Association Between the CCR5 32-bp Deletion Allele and Late Onset of Schizophrenia
Henrik Berg Rasmussen; Sally Timm; August G. Wang; Karen Søeby; Henrik Lublin; Mogens Fenger; Ralf Hemmingsen; Thomas Werge
Am J Psychiatry 2006;163:507-511. 10.1176/appi.ajp.163.3.507

--------------------------------------

1 of 2 Here's another:
Association of CCR5 Δ32 deletion with early death in multiple sclerosis
Radhika Gade-Andavolu1, David E Comings2, James MacMurray2, Masoud Rostamkhani2, Li S -C Cheng3, Wallace W Tourtellotte4 and Lawrence A Cone1,5
1Genetic Research Institute of the Desert, Eisenhower Medical Center, Rancho Mirage, California
2Department of Medical Genetics, City of Hope Medical Center, Duarte, California
3Department of Bio statistics, City of Hope Medical Center, Duarte, California

2 of 2 4Neurology & Research Services, VA, West Los Angeles Healthcare Center & Department of Neurology, UCLA, Los Angeles, California
5Sections of Immunology and Infectious Diseases, Eisenhower Medical Center, Rancho Mirage, California

---------------------------------------

CCR5 Expression Influences the Progression of Human Breast Cancer in a p53-dependent Manner
Santos Mañes 1 , Emilia Mira 1 , Ramón Colomer 2 , Sagrario Montero 2 , Luis M. Real 4 , Concepción Gómez-Moutón 1 , Sonia Jiménez-Baranda 1 , Alfredo Garzón 3 , Rosa Ana Lacalle 1 , Keith Harshman 1 , Agustín Ruíz 4 , and Carlos Martínez-A. 1
+ Author Affiliations
1Department of Immunology and Oncology, Centro Nacional de Biotecnología, Universidad Autonoma de Madrid, E-28049 Madrid, Spain
2Medical Oncology, Hospital Universitario 12 de Octubre, E-28041 Madrid, Spain
3Pathology Department, Hospital Universitario 12 de Octubre, E-28041 Madrid, Spain
4Department of Structural Genomics, Neocodex, E-41020 Seville, Spain
Address correspondence to Santos Mañes, Department of Immunology and Oncology, Centro Nacional de Biotecnología, Campus de Cantoblanco, Universidad Autonoma de Madrid, E-28049 Madrid, Spain. Phone: 34-91-585-4660; Fax: 34-91-372-0493; e-mail: smanes@cnb.uam.es
ABSTRACT

Chemokines are implicated in tumor pathogenesis, although it is unclear whether they affect human cancer progression positively or negatively. We found that activation of the chemokine receptor CCR5 regulates p53 transcriptional activity in breast cancer cells through pertussis toxin–, JAK2-, and p38 mitogen–activated protein kinase–dependent mechanisms. CCR5 blockade significantly enhanced proliferation of xenografts from tumor cells bearing wild-type p53, but did not affect proliferation of tumor xenografts bearing a p53 mutation. In parallel, data obtained in a primary breast cancer clinical series showed that disease-free survival was shorter in individuals bearing the CCR5Δ32 allele than in CCR5 wild-type patients, but only for those whose tumors expressed wild-type p53. These findings suggest that CCR5 activity influences human breast cancer progression in a p53-dependent manner.

----------------------------------

Further, all the subjects (controls and patients) were divided in two groups on the basis of age and were termed as early onset (aged 0–49 years) and late onset (aged 50 onwards) patients. On analysing the frequency distribution of genotypes in early and late onset patients, distribution of genotypes in early and late onset groups was almost similar in healthy controls. On comparing the frequency distribution among early and late onset group, variation in the frequency of CCR5+/Δ32 genotype in early onset group was observed. In the patients having early onset of the disease the frequency distribution of CCR5+/Δ32 genotype was 3.0% in control while it was 15.6% in GBC. This vast difference was statistically significant and was conferring extremely high risk for the disease (P = 0.006, OR = 6.24, CI = 1.6–13.0). At allele level also CCR5 Δ32 allele frequency was high in GBC patient with early onset of the disease when compared with controls of the same age group (10.0% and 1.5%). However, in the GBC patients having late onset of the disease, the frequency distribution of all the genotypes as well as alleles was almost similar in patient and control group and no significant disparity in the distribution pattern was observed (Table 5).
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Re: CCR5 32 delta deletion gene mutation
Reply #1 - Apr 19th, 2012 at 4:50pm
 
Genetics in Medicine (2004) 6, 126–131; doi:10.1097/01.GIM.0000127274.45301.54

Association of CCR5 Δ32 deletion with early death in multiple sclerosis

Radhika Gade-Andavolu1, David E Comings2, James MacMurray2, Masoud Rostamkhani2, Li S -C Cheng3, Wallace W Tourtellotte4 and Lawrence A Cone1,5

1Genetic Research Institute of the Desert, Eisenhower Medical Center, Rancho Mirage, California
2Department of Medical Genetics, City of Hope Medical Center, Duarte, California
3Department of Bio statistics, City of Hope Medical Center, Duarte, California
4Neurology & Research Services, VA, West Los Angeles Healthcare Center & Department of Neurology, UCLA, Los Angeles, California
5Sections of Immunology and Infectious Diseases, Eisenhower Medical Center, Rancho Mirage, California
Correspondence: Dr. Lawrence A. Cone, >39000 Bob Hope Drive, Eisenhower Medical Center, Probst # 308, Genetic Research Institute of the Desert, Rancho Mirage, CA 92270.

Received 21 November 2003; Accepted 17 February 2004

Top of page
Abstract
Purpose: The interaction between chemokines and their receptors is extremely important in controlling T cell migration into sites of CNS inflammation. Because trafficking of inflammatory T cells into the central nervous system (CNS) is a key player in the pathogenesis of multiple sclerosis (MS), we investigated the possible association of CCR5 Δ32 deletion in this disorder.

Methods: DNA isolated from postmortem brain tissue samples of 132 patients with MS and from blood tissue samples of 163 gender and ethnicity-matched healthy controls was used to screen for the CCR5 Δ32 deletion allele.

Results: An increased frequency of 32-bp deletion allele was found to be associated with early death (P = 0.00005) and with a progressive reduction in the years of survival (onset to death). The death hazard ratio of CCR5 with deletion versus no deletion was 2.12, suggesting that MS patients with the 32-bp deletion have twice the mortality rate of patients with the normal genotype. This effect was more significant in females (hazard ratio 3.58).

Conclusion: A strong association of the CCR5 Δ32 deletion with early death could serve as a prognostic marker for MS.

Keywords: multiple sclerosis; polymerase chain reaction; chemokine receptor; experimental autoimmune encephalomyelitis
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Re: CCR5 32 delta deletion gene mutation
Reply #2 - May 27th, 2012 at 3:52am
 
More:

Association of Polymorphisms in MCP-1, CCR2, and CCR5 Genes with the Risk and Clinicopathological Characteristics of Prostate Cancer
To cite this article:
Canan Kucukgergin, Ferruh K. Isman, Bedia Cakmakoglu, Oner Sanli, and Sule Seckin. DNA and Cell Biology.
" CCR5 Δ32/wt genotype and CCR5 Δ32 allele were also found to be involved in the susceptibility to prostate cancer"
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Re: CCR5 32 delta deletion gene mutation
Reply #3 - Jun 9th, 2012 at 1:58am
 
Association of Polymorphisms in MCP-1, CCR2, and CCR5 Genes with the Risk and Clinicopathological Characteristics of Prostate Cancer
To cite this article:
Canan Kucukgergin, Ferruh K. Isman, Bedia Cakmakoglu, Oner Sanli, and Sule Seckin. DNA and Cell Biology. -Not available-, ahead of print. doi:10.1089/dna.2012.1716.

" CCR5 Δ32/wt genotype and CCR5 Δ32 allele were also found to be involved in the susceptibility to prostate cancer (p=0.028 and p=0.030, respectively)."
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Re: CCR5 32 delta deletion gene mutation: More
Reply #4 - Jul 4th, 2012 at 3:51am
 
Increase in CCR5 Δ32/Δ32 genotype in multiple sclerosis

K. Pulkkinen1,4, M. Luomala2, H. Kuusisto3,5, T. Lehtimäki2, M. Saarela1,2,3, T. O. Jalonen1,4,5, I. Elovaara1,3,5
Article first published online: 10 DEC 2003

DOI: 10.1046/j.1600-0404.2003.00233.x

Chemokines and their receptors participate in the development of multiple sclerosis (MS) by guiding immune cells into the brain tissue. A CCR5 Δ32 deletion mutation abolishes functional CCR5 on the cell surface and may reduce cell entry into the lesion sites. To analyse the significance of this mutation in MS, we compared the frequencies of CCR5 genotype in peripheral blood mononuclear cells from 89 MS patients and 119 healthy controls. The CCR5 genotype was further compared with the CCR5 RNA and surface protein expression in 48 MS patients and their controls. In all MS patients, the Δ32/32 genotype was found with 6.7% frequency, whereas it was present only in 0.8% of the controls (6/89 vs 1/119, P = 0.01). Specifically, the Δ32/Δ32 genotype was increased (11.5%, P = 0.05) among primary progressive MS patients, whereas it was present only in 4.8% in other MS subtypes and only in 0.8% of the controls. The amount of CCR5 protein on CD4+ cells analysed in 48 MS patients (nine primary progressive MS, 18 secondary progressive MS, 21 relapsing–remitting MS) and 13 controls decreased with genotype, being 8.9% in wt/wt, 7.7% in wt/Δ32 and 4.3% in Δ32/Δ32. CCR5 surface expression analysed on these 48 MS patients and 13 controls was significantly decreased in Δ32/Δ32 MS patients as compared with that in wt/wt genotype individuals (P = 0.004). The significantly increased number of Δ32/Δ32 individuals among our MS patients suggests that this genotype could contribute as a general risk factor for MS. However, neither the levels of RNA or surface protein correlated with MS subtype, neurological disability as expressed by expanded disability status scale, or disease progression index. Our results suggest that the lack of CCR5 does not protect from MS, but rather it may predispose to the chronic course of the disease. This would further imply that in view of the redundancy in the chemokine system, CCR5 ligands must be assumed to function through other closely related chemokine receptors.
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Re: CCR5 32 delta deletion gene mutation
Reply #5 - Jul 4th, 2012 at 3:56am
 
Effects of the CCR5-Δ32 mutation on antiviral treatment in chronic hepatitis C

Golo Ahlenstiel, Thomas Berg, Rainer P Woitas, Frank Grünhage, Agathe Iwan, Lothar Heß, Hans H Brackmann, Bernd Kupfer, Andrea Schernick, Tilman Sauerbruch, Ulrich Spengler

Abstract
Background/Aims: The CC-chemokine receptor (CCR) 5-Δ32 mutation may predispose to chronic liver disease and high level viremia in hepatitis C. However, it is unclear whether CCR5-Δ32 also affects the response to antiviral treatment.

Methods: We determined CCR5 genotypes in patients with hepatitis C treated with either interferon-α (N=78) or interferon and ribavirin (N=78). In each group, rates of end of treatment responses (ETRs) and sustained virological responses (SVRs) were compared between CCR5-Δ32 carriers and homozygous CCR5 wildtype patients.

Results: ETR and SVR were achieved in 25 and 12 patients with interferon-α and in 52 and 45 patients with interferon/ribavirin treatment, respectively. CCR5-Δ32 carriers had significantly lower ETR rates than homozygous CCR5 wildtype patients (10.5 vs. 39.0%; P=0.02), whereas SVR rates only showed a non-significant trend (5.3 vs. 18.6%). Multivariate analysis confirmed CCR5-Δ32 carriage as an independent negative predictor for ETR in interferon-α monotherapy (odds ratio: 0.16; 95% confidence limits: 0.032–0.82; P=0.03). In interferon/ribavirin treated patients CCR-Δ32 carriers and CCR5 wildtype patients had similar ETR rates [19.2% vs. 23.1%] and SVR rates [20.0% vs. 21.2%].

Conclusions: Response rates to interferon-α monotherapy are reduced in hepatitis C virus (HCV)-infected patients carrying the CCR5-Δ32 mutation. However, interferon/ribavirin combination treatment may overcome this negative effect of CCR5-Δ32.
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Re: CCR5 32 delta deletion gene mutation
Reply #6 - Oct 2nd, 2012 at 8:32am
 
Dabelić, Sanja; Crkvenac Gregorek Andrea; Crkvenac Gornik Kristina; Stupin Polančec Darija
Title:      Impact of gene polymorphisms on the formation of abdominal aortic aneurysm in humans
Source:      11th Croatian Biological Congress with International Participation - Proceedings of Abstracts / Jelaska, Sven ; Klobučar, Goran ; Šerić Jelaska, Lucija ; Leljak Levanić, Dunja ; Lukša, Žaklin (ed). - Zagreb : Hrvatsko biološko društvo 1885 , 2012. 126-127.
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Re: CCR5 32 delta deletion gene mutation
Reply #7 - Nov 9th, 2012 at 9:13pm
 
Samson et al. (1996) identified a heterozygous 32-bp deletion in the CMKBR5 gene ..... (2006) concluded that
CCR5 delta-32 is a risk factor for symptomatic WNV infection.
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Re: CCR5 32 delta deletion gene mutation
Reply #8 - Jan 15th, 2013 at 1:07am
 
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0053515

Characterization In Vitro and In Vivo of a Pandemic H1N1 Influenza Virus from a Fatal Case

In addition, examination of chemokine receptor 5 (CCR5) genotype, recently reported as involved in severe influenza virus disease, revealed that the F virus-infected patient was homozygous for the deleted form of CCR5 receptor (CCR5Δ32).

The chemokine receptor CCR5 is expressed on activated macrophages and plays an important role in the macrophage response to influenza virus infection since knock out mice for Crc5 gene display increased mortality rates [37]. Moreover, critically ill patients infected with pandemic H1N1 virus showed a large proportion of heterozygosity for a deleted allele of CCR5 that prevents the surface expression of the protein (CCR5Δ32)

Therefore the F patient was infected with a potential highly pathogenic virus and its genetic background of CCR5Δ32 homozygous could contribute to the severity of the infection.
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Re: CCR5 32 delta deletion gene mutation
Reply #9 - Feb 22nd, 2013 at 10:30pm
 
MCP-1, CCR2 and CCR5 Polymorphisms
in Tunisian Patients with Atopic Asthma
Tarak Dhaouadi1, Imen Sfar1, Hajer Aounallah-Skhiri2, Saloua Jendoubi-Ayed1,
Hend Bouacha3, Taieb Ben Abdallah1, and Yousr Gorgi1
1Laboratory of Research in Immunology of Renal Transplantation and Immunopathology,
Charles Nicolle Hospital, Tunis El Manar University, Tunis, Tunisia
2National Institute of Public Health, Tunis, Tunisia
3Pneumonology Department, Charles Nicolle Hospital, Tunis, Tunisia
Received: 3 November 2011; Received in revised form: 8 May 2012; Accepted: 8 August 2012

http://www.ncbi.nlm.nih.gov/pubmed/23454776
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