title: RANTES -28G delays and DC-SIGN - 139C enhances AIDS progression in HIV type 1-infected Japanese hemophiliacs.
abstract: The relationships between host immune factors and HIV-1 disease progression are still in dispute. Unlike CCR5Delta32, which has been found to delay disease progression of HIV-1, there still remain several factors whose effect on the clinical course is unconfirmed. To clarify the relationships, we selected seven single-nucleotide polymorphisms (SNPs) out of the previously reported factors, namely, RANTES promoter -28G/-403A, RANTES In1.1C, SDF-1 3'A, IL-4 promoter -589T, and DC-SIGN promoter -139C/-336C, and examined these in Japanese HIV-1-infected hemophiliacs (n = 102). The genotypes were examined by the direct sequencing method, and the distributions of genotype and allelic frequencies were compared between two groups, slow progressors (n = 54) who did not develop AIDS more than 10 years after intravenous infection and others (progressors) (n = 48). The allelic frequency of RANTES -28G was significantly higher in slow progressors (0.185) than in the progressor group (0.074) [p = 0.023, OR = 0.35, 95% CI (0.142, 0.880)]. DC-SIGN promoter -139C, and appeared in progressors with significantly higher allelic frequency (0.333) than slow progressors [0.204, p = 0.040, OR = 1.95, 95% CI (1.039, 3.677)]. With RANTES -403A, RANTES In1.1C, SDF-1 3' A, IL-4 -589T, and DC-SIGN -336C, no significant difference was observed in allelic frequencies between the two groups. These results suggest that RANTES -28G was associated with delayed AIDS progression, while DC-SIGN -139C was associated with accelerated AIDS progression in HIV-1-infected Japanese hemophiliacs.
authors.affiliation: Department of Viral Infection and International Health, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8640, Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Koizumi
authors.forename: Seiji
authors.initials: S
authors.lastname: Kageyama
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Fujiyama
authors.forename: Michiko
authors.initials: M
authors.lastname: Miyashita
authors.forename: Raphael
authors.initials: R
authors.lastname: Lwembe
authors.forename: Keiki
authors.initials: K
authors.lastname: Ogino
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Shioda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ichimura
mesh_terms: D000163:Acquired Immunodeficiency Syndrome; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000235:genetics*; D018946:Chemokine CCL5 / Q000032:analysis / Q000235:genetics*; D018450:Disease Progression; D005787:Gene Frequency; D015658:HIV Infections / Q000150:complications / Q000235:genetics* / Q000503:physiopathology; D015497:HIV-1; D006467:Hemophilia A / Q000150:complications / Q000235:genetics*; D006801:Humans; D015847:Interleukin-4; D007564:Japan; D037181:Lectins, C-Type / Q000032:analysis / Q000235:genetics*; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic; D011956:Receptors, Cell Surface / Q000032:analysis / Q000235:genetics*; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
chemical_list: D015815:Cell Adhesion Molecules; D018946:Chemokine CCL5; D015847:Interleukin-4; D037181:Lectins, C-Type; D011956:Receptors, Cell Surface; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin