RANTES -28G delays and DC-SIGN -139C enhances AIDS progression in HIV type 1-infected Japanese hemophiliacs

Yusuke Koizumi, Seiji Kageyama, Yoshihide Fujiyama, Michiko Miyashita, Raphael Lwembe, Keiki Ogino, Tatsuo Shioda, Hiroshi Ichimura

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40 Citations (Scopus)


The relationships between host immune factors and HIV-1 disease progression are still in dispute. Unlike CCR5Δ32, 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 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.

Original languageEnglish
Pages (from-to)713-719
Number of pages7
JournalAIDS Research and Human Retroviruses
Issue number5
Publication statusPublished - May 2007
Externally publishedYes

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Infectious Diseases


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