scholarly journals Frequency of the CCR5-delta 32 chemokine receptor gene mutation in the Lebanese population

2004 ◽  
Vol 10 (4-5) ◽  
pp. 671-675
Author(s):  
W. Karam ◽  
R. Jurjus ◽  
N. Khoury ◽  
H. Khansa ◽  
C. Assad ◽  
...  

A direct correlation between HIV infection and mutation in the chemokine receptor [CCR5] gene has been established. However, such correlation has never been investigated in Lebanon. We report the frequency of the CCR5-delta 32 mutation in a r and om sample of 209 healthy, HIV-1 seronegative Lebanese aged 19-68. Overall, 4.8% were heterozygous for the mutation. Homozygosity was absent from our sample. The frequency for the CCR5-delta 32 allele was 2.5%. Distribution of the mutation was unaffected by sex, age, religion or educational level. The frequency in the Lebanese population is consistent with that in the origin of the mutation in northern Europe. This could be attributed to a gene flow into the Middle East from northern Europe

Blood ◽  
2000 ◽  
Vol 96 (8) ◽  
pp. 2887-2894 ◽  
Author(s):  
Weiping Shen ◽  
Baoqun Li ◽  
Michele A. Wetzel ◽  
Thomas J. Rogers ◽  
Earl E. Henderson ◽  
...  

Abstract Interactions between cell surface receptors are important regulatory elements in the complex host responses to infections. In this study, it is shown that a classic chemotactic factor, the bacterial chemotactic peptide N-formyl-methionyl-leucylphenyl-alanine (fMLF), rapidly induced a protein-kinase-C–mediated serine phosphorylation and down-regulation of the chemokine receptor CCR5, which serves as a major human immunodeficiency virus (HIV)-1 coreceptor. The fMLF binding to its receptor, formyl peptide receptor (FPR), resulted in significant attenuation of cell responses to CCR5 ligands and in inhibition of HIV-1-envelope-glycoprotein–mediated fusion and infection of cells expressing CD4, CCR5, and FPR. The finding that the expression and function of CCR5 can be regulated by peptides that use an unrelated receptor may provide a novel approach to the design of anti-inflamatory and antiretroviral agents.


2006 ◽  
Vol 118 (2) ◽  
pp. 518-521 ◽  
Author(s):  
William T. Shearer ◽  
Jaime G. DeVille ◽  
Pearl M. Samson ◽  
John H. Moye Jr. ◽  
Courtney V. Fletcher ◽  
...  

2000 ◽  
Vol 48 (2) ◽  
pp. 308-309 ◽  
Author(s):  
Koji KONISHI ◽  
Kiyoshi IKEDA ◽  
Kazuo ACHIWA ◽  
Hiroo HOSHINO ◽  
Kiyoshi TANAKA

Blood ◽  
1999 ◽  
Vol 93 (6) ◽  
pp. 1838-1842 ◽  
Author(s):  
Charles S. Rabkin ◽  
Quan-en Yang ◽  
James J. Goedert ◽  
Giao Nguyen ◽  
Hiroaki Mitsuya ◽  
...  

Normal B-lymphocyte maturation and proliferation are regulated by chemotactic cytokines (chemokines), and genetic polymorphisms in chemokines and chemokine receptors modify progression of human immunodeficiency virus-1 (HIV-1) infection. Therefore, 746 HIV-1–infected persons were examined for associations of previously described stromal cell-derived factor 1 (SDF-1) chemokine and CCR5 and CCR2 chemokine receptor gene variants with the risk of B-cell non-Hodgkin’s lymphoma (NHL). The SDF1-3′A chemokine variant, which is carried by 37% of whites and 11% of blacks, was associated with approximate doubling of the NHL risk in heterozygotes and roughly a fourfold increase in homozygotes. After a median follow-up of 11.7 years, NHL developed in 6 (19%) of 30 SDF1-3′A/3′A homozygotes and 22 (10%) of 202 SDF1-+/3′A heterozygotes, compared with 24 (5%) of 514 wild-type subjects. The acquired immunodeficiency syndrome (AIDS)-protective chemokine receptor variant CCR5-▵32 was highly protective against NHL, whereas the AIDS-protective variant CCR2-64I had no significant effect. Racial differences in SDF1-3′A frequency may contribute to the lower risk of HIV-1–associated NHL in blacks compared with whites. SDF-1 genotyping of HIV-1–infected patients may identify subgroups warranting enhanced monitoring and targeted interventions to reduce the risk of NHL.


Retrovirology ◽  
2011 ◽  
Vol 8 (1) ◽  
Author(s):  
Rakhi Malhotra ◽  
Liangyuan Hu ◽  
Wei Song ◽  
Ilene Brill ◽  
Joseph Mulenga ◽  
...  

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