IL-18 GENE PROMOTER REGION 607C/A POLYMORPHISM
IN HIV-1 INFECTED NORTH INDIAN POPULATION
Sobti RC1,*, Sharma VL2, Abitew AM2, Berhane N1,
Mahdi SA1, Askari M1, Kuttiat VS3, Wanchu A3
*Corresponding Author: Ranbir C. Sobti, Department of Biotechnology, Panjab University, Chandigarh 160
014 India; Tel.: +172-2534087; +94-1-704-4523; Fax: +172-25341409; E-mail: rcsobti@ pu.ac.in
page: 41
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RESULTS
was done by the physicians
as per the World Health Organization (WHO)
staging guidelines. Accordingly, all the four stages
of HIV/AIDS were found in the cases. Of all the 500
seropositive cases, 74 (14.85%) were at stage I, 143
(28.6%) at stage II, 113 (22.6%) at stage III and 170
(34%) were at stage IV (AIDS) of the disease. The
mean counts of CD4+-T cells at stages I, II, III, and IV
were 331, 268, 206, and 113, respectively.
In all, 500 HIV-1/AIDS patients and an equal
number of controls were studied for –607C>A IL-18
promoter polymorphism. As shown in Figure 1, there
were C/C, C/A and A/A genotypes at position –607.
The PCR products of homozygous individuals showed
a 301 bp DNA segment and those of heterozygous individuals
showed 196 and 301 bp fragments.
The genotypic distributions and allelic frequencies
of –607C>A are presented in Table 2. The genotype
distributions are in agreement with Hardy-Weinberg
equilibrium. A significant increase in frequency of the
wild C/C genotype was observed in patients when compared
to control subjects (43.0 vs. 38.4%, p = 0.040).
The frequency of the C/A genotype was slightly higher
in controls (52.8%) than in cases (51.4%) (p = 0.321)
and that of the A/A genotype was significantly lower
(p = 0.040) in patients (5.6%) than in controls (8.8%).
The frequencies of the C and A alleles were 68.7 and
31.3% in cases and 64.8 and 35.2% in controls (p =
0.071), respectively.
For accounting of the risk assessment the genotypic
data was analyzed with Epi Info software. The
results showed a significantly reduced risk of HIV-1
infection with the homozygous variant –607A>A genotype
when it was computed against healthy controls [odds ratio (OR) = 0.57, 95% confidence interval (95%
CI) = 0.33-0.98, p = 0.040]).Conversely, a statistically
insignificant reduced risk of HIV-1 infection was observed
with the heterozygous –607C>A genotype (OR
= 0.87, 95% CI = 0.66-1.14, p = 0.321). Likewise, a
statistically insignificant association of HIV-1 infection
was observed with the –607A allele (OR = 0.84,
95% CI = 0.69-1.01, p = 0.071).
The genotypic and allelic frequencies of –607C>A
between only seropositive for HIV-1 and seropositive
patients with disease are presented in Table 3. Of the
500 seropositive patients with HIV-1, 330 (66%) were
patients at stages I-III without AIDS and the remaining
170 (34%) were at the AIDS stage. The frequency of
the wild C/C genotype in seropositive patients without
AIDS disease was 130 (26%) as compared to 85 (17%) in HIV-1 patients at at the AIDS stage. The frequency
of the heterozygous C/A genotype was 178 (35.6%)
and 79 (15.8%) for seropositive patients without AIDS
and those at the AIDS stage, respectively. The frequency
of the mutant genotype A/A was 4.4% (22) in
HIV-1 patients without AIDS disease and 1.2% (six)
in patients with AIDS. A statistically insignificant reduced
risk of HIV infection was observed with the C/A
genotype of IL-18-607 (OR = 0.68, 95% CI = 0.47-
1.01, p = 0.057). Moreover, a statistically insignificant
reduced risk of HIV infection was observed with the
homozygous variant A/A genotype (OR = 0.42, 95%
CI = 0.14-1.14, p = 0.098).
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