PMID- 22587568
OWN - NLM
STAT- MEDLINE
DCOM- 20130429
LR  - 20120727
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Linking)
VI  - 80
IP  - 2
DP  - 2012 Aug
TI  - Interleukin-18 and interferon-gamma polymorphisms are implicated on proviral load 
      and susceptibility to human T-lymphotropic virus type 1 infection.
PG  - 143-50
LID - 10.1111/j.1399-0039.2012.01887.x [doi]
AB  - Interleukin-18 (IL-18) and interferon-gamma (IFN-gamma) exert important functions in 
      both innate and adaptive immune responses against intracellular pathogens and 
      viruses. Previous studies suggested that host genetic factors, including 
      cytokines gene polymorphisms, could be involved in the pathogenesis of human 
      T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic 
      paraparesis (HAM/TSP). Thus, we analyzed -137C/G and -607A/C of the IL-18 
      promoter and +874T/A of the IFN-gamma in DNA samples from 98 HTLV-1-infected 
      individuals exhibiting or not clinical symptoms and 150 healthy control 
      individuals. The IL-18 promoter -607CC genotype was significantly lower in HTLV-1 
      asymptomatic carriers (HAC) and HTLV-1-infected individuals (HAC + HAM/TSP) than 
      healthy control group. In contrast, the -607AC genotype was significantly higher 
      in HAC and HTLV-1-infected individuals group compared to the healthy control 
      group. The -137G/-607A IL-18 haplotype was higher in infected group than healthy 
      control group, and the -137C/-607C IL-18 haplotype was increased in the healthy 
      control group compared to the others. Finally, the IFN-gamma polymorphism analysis 
      showed that the HTLV-1-infected individuals with +874AT genotype presented higher 
      proviral load than +874AA genotype. These data indicate that the IL-18-607AC 
      genotype and -137G/-607A haplotype could be a risk factor for HTLV-1 infection, 
      whereas the protective effect could be conferred by -607CC genotype and 
      -137C/-607C haplotype. Also, the IFN-gamma could be implicated on the proviral load 
      levels.
CI  - (c) 2012 John Wiley & Sons A/S.
FAU - Rocha-Junior, M C
AU  - Rocha-Junior MC
AD  - Hemocentro de Ribeirao Preto, Universidade de Sao Paulo (USP), Ribeirao Preto, 
      Sao Paulo CEP: 14051-140, Brazil.
FAU - Haddad, R
AU  - Haddad R
FAU - Ciliao Alves, D C
AU  - Ciliao Alves DC
FAU - de Deus Wagatsuma, V M
AU  - de Deus Wagatsuma VM
FAU - Mendes-Junior, C T
AU  - Mendes-Junior CT
FAU - Deghaide, N H S
AU  - Deghaide NH
FAU - Takayanagui, O M
AU  - Takayanagui OM
FAU - Covas, D T
AU  - Covas DT
FAU - Donadi, E A
AU  - Donadi EA
FAU - Kashima, S
AU  - Kashima S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120515
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (Interleukin-18)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - Case-Control Studies
MH  - Disease Susceptibility
MH  - Gene Frequency
MH  - Haplotypes
MH  - Human T-lymphotropic virus 1/*immunology
MH  - Humans
MH  - Interferon-gamma/*genetics/immunology
MH  - Interleukin-18/*genetics/immunology
MH  - Male
MH  - Middle Aged
MH  - Paraparesis, Tropical Spastic/*genetics/immunology/virology
MH  - Polymorphism, Genetic
MH  - Promoter Regions, Genetic
MH  - *Proviruses
MH  - Real-Time Polymerase Chain Reaction
MH  - Risk Factors
MH  - Viral Load
EDAT- 2012/05/17 06:00
MHDA- 2013/04/30 06:00
CRDT- 2012/05/17 06:00
PHST- 2012/05/17 06:00 [entrez]
PHST- 2012/05/17 06:00 [pubmed]
PHST- 2013/04/30 06:00 [medline]
AID - 10.1111/j.1399-0039.2012.01887.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2012 Aug;80(2):143-50. doi: 10.1111/j.1399-0039.2012.01887.x. 
      Epub 2012 May 15.