PMID- 10823849
OWN - NLM
STAT- MEDLINE
DCOM- 20000629
LR  - 20190508
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 74
IP  - 12
DP  - 2000 Jun
TI  - Polymorphism in the interleukin-4 promoter affects acquisition of human 
      immunodeficiency virus type 1 syncytium-inducing phenotype.
PG  - 5452-9
AB  - The emergence of syncytium-inducing (SI) variants of human immunodeficiency virus 
      type 1 (HIV-1) in infected individuals is an indicator of poor prognosis and is 
      often correlated with faster CD4(+) cell depletion and rapid disease progression. 
      Interleukin-4 (IL-4) is a pleiotropic cytokine with various immune-modulating 
      functions including induction of immunoglobulin E (IgE) production in B cells, 
      down-regulation of CCR5 (a coreceptor for HIV-1 non-SI [NSI] strains), and 
      up-regulation of CXCR4 (a coreceptor for HIV-1 SI variants). Here we show that 
      homozygosity of a polymorphism in the IL-4 promoter region, IL-4 -589T, is 
      correlated with increased rates of SI variant acquisition in HIV-1-infected 
      individuals in Japan. This mutation was also shown to be associated with elevated 
      serum IgE levels in HIV-1-infected individuals, especially in those at advanced 
      stages of disease. In contrast, neither a triallele polymorphism in IL-10, 
      another Th2 cytokine, nor a biallele polymorphism in the RANTES promoter affected 
      acquisition of the SI phenotype. This finding suggested that IL-4-589T increases 
      IL-4 production in the human body and thus accelerates the phenotypic switch of 
      HIV-1 from NSI to SI and possibly disease progression of AIDS.
FAU - Nakayama, E E
AU  - Nakayama EE
AD  - Department of Infectious Diseases, Institute of Medical Science, University of 
      Tokyo, Tokyo, Japan.
FAU - Hoshino, Y
AU  - Hoshino Y
FAU - Xin, X
AU  - Xin X
FAU - Liu, H
AU  - Liu H
FAU - Goto, M
AU  - Goto M
FAU - Watanabe, N
AU  - Watanabe N
FAU - Taguchi, H
AU  - Taguchi H
FAU - Hitani, A
AU  - Hitani A
FAU - Kawana-Tachikawa, A
AU  - Kawana-Tachikawa A
FAU - Fukushima, M
AU  - Fukushima M
FAU - Yamada, K
AU  - Yamada K
FAU - Sugiura, W
AU  - Sugiura W
FAU - Oka, S I
AU  - Oka SI
FAU - Ajisawa, A
AU  - Ajisawa A
FAU - Sato, H
AU  - Sato H
FAU - Takebe, Y
AU  - Takebe Y
FAU - Nakamura, T
AU  - Nakamura T
FAU - Nagai, Y
AU  - Nagai Y
FAU - Iwamoto, A
AU  - Iwamoto A
FAU - Shioda, T
AU  - Shioda T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Chemokine CCL5)
RN  - 130068-27-8 (Interleukin-10)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Alleles
MH  - Base Sequence
MH  - Chemokine CCL5/genetics
MH  - Disease Progression
MH  - Female
MH  - Gene Frequency/genetics
MH  - Genotype
MH  - Giant Cells/*pathology
MH  - HIV Infections/blood/immunology/*pathology/virology
MH  - HIV-1/immunology/pathogenicity/*physiology
MH  - Haplotypes/genetics
MH  - Hemophilia A
MH  - Heterosexuality
MH  - Humans
MH  - Immunoglobulin E/blood
MH  - Interleukin-10/genetics
MH  - Interleukin-4/*genetics
MH  - Japan
MH  - Male
MH  - Molecular Sequence Data
MH  - Phenotype
MH  - Polymorphism, Genetic/*genetics
MH  - Polymorphism, Restriction Fragment Length
MH  - Promoter Regions, Genetic/*genetics
PMC - PMC112029
EDAT- 2000/05/24 09:00
MHDA- 2000/07/06 11:00
PMCR- 2000/06/01
CRDT- 2000/05/24 09:00
PHST- 2000/05/24 09:00 [pubmed]
PHST- 2000/07/06 11:00 [medline]
PHST- 2000/05/24 09:00 [entrez]
PHST- 2000/06/01 00:00 [pmc-release]
AID - 1317 [pii]
AID - 10.1128/jvi.74.12.5452-5459.2000 [doi]
PST - ppublish
SO  - J Virol. 2000 Jun;74(12):5452-9. doi: 10.1128/jvi.74.12.5452-5459.2000.