Epidemiological, immunological and virological characteristics, and disease progression of HIV-1/HCV-co-infected patients from a southern Brazilian population.

A cross-sectional study was carried out in order to describe the epidemiological, immunological and virological characteristics, and the disease progression of hepatitis C virus (HCV)/human immunodeficiency virus type 1 (HIV-1)- co-infected patients from a southern Brazilian population. Of 778 HIV-1-infected individuals enrolled in the study from September 2001 to December 2003, and followed up until June 2004, 757 were tested for anti-HCV antibodies. Of these, 159 (21.0%) showed positive results for anti-HCV. Males, individuals in the 25 to 34 year age range, and individuals of lower economic levels were more likely to be seropositive for both viruses [prevalence rate (PR), 2.04; 95% confidence interval (95% CI), 1.43-2.92; p<0.001]. The anti-HCV reactivity was also associated with blood routes of transmission (PR, 2.20; 95% CI, 1.28-3.77; p<0.001), intravenous drug use (PR, 5.79; 95% CI, 4.74-7.07; p<0.001), self-reported previous sexually transmitted diseases (PR, 1.55; 95% CI, 1.18-2.04; p=0.002), VDRL positivity (PR, 2.87; 95% CI, 2.40-3.43; p<0.001), and anti-HTLV I/II reactivity (PR, 5.09; 95% CI, 4.16-6.23; p<0.001). In the follow-up period, the HCV/HIV-1-co-infected patients showed a trend toward lower CD4+ T-cell counts, higher HIV-1 RNA plasma viral load and faster disease progression than patients infected only with HIV-1, but significant differences were not observed. Although there were proportionately more deaths in the HCV/HIV-1-co-infected group, the use of highly active antiretroviral therapy (HAART) was a string predictor of increased CD4+ T-cell counts and decreased HIV-1 RNA plasma levels, suggesting that HAART is more important to the immunological and virological outcomes in HIV-1 infection than is HCV co-infection status.

Frequency of CCR5-Delta32 deletion in human immunodeficiency virus type 1 (HIV-1) in healthy blood donors, HIV-1-exposed seronegative and HIV-1-seropositive individuals of southern Brazilian population.

The frequency of CCR5-Delta32 allele in human immunodeficiency virus type 1 (HIV-1) infection in the southern Brazilian population was determined in a cross-sectional study carried out from October 2001 to June 2004. Genomic DNA was extracted from peripheral blood cells of 134 healthy blood donors, 145 HIV-1-exposed seronegative individuals, 152 HIV-1-seropositive asymptomatic individuals, and 478 HIV-1-seropositive individuals with AIDS. A fragment with 225 base-pairs of the CCR5 gene was amplified by polymerase chain reaction. The CCR5-Delta32 homozygous deletion was observed in 2 (1.5%) blood donors and in 1 (0.7%) individual HIV-1-exposed seronegative, and was absent among all the HIV-1-seropositive individuals (Fisher's exact test, p=0.0242). The frequency of the homozygous CCR5-Delta32 deletion in the HIV-1-exposed did not differ when compared with that observed in the HIV-1 seronegative blood donors (Fisher's exact test, p=0.6093; OR: 2.18, 95% CI: 0.11-129.6). The wild-type genotype CCR5/CCR5 frequency was higher among the HIV-1-seropositive with AIDS compared to HIV-1 seropositive asymptomatic individuals (Chi-square test, p=0.0263; OR: 2.02, 95% CI: 1.03-3.97). The absence of the homozygous deletion of CCR5-Delta32 among HIV-1-seropositive individuals underscored that this genotype is an important genetic factor associated with the decreased susceptibility to HIV-1 infection. The higher frequency of heterozygosity for the CCR5-Delta32 and the CCR5-Delta32 allele in HIV-1 seropositive asymptomatic compared to HIV-seropositive with AIDS individuals also underscored that this deletion could be associated with the delay of the HIV-1 disease progression in this population. However, the low frequency of CCR5-Delta32 homozygosity observed among HIV-1-exposed seronegative individuals shows that the allele could not explain, by itself, the natural resistance to HIV-1 infection and different mechanisms of protection against HIV-1 infection that must be involved in this population.

The effect of stromal cell-derived factor 1 (SDF1/CXCL12) genetic polymorphism on HIV-1 disease progression.

The human immunodeficiency virus type 1 (HIV-1) epidemic is increasing in Brazil, and little information has been reported about the genetic host factors related to HIV-1 infection in the Brazilian population. A polymorphism in the conserved 3' untranslated region of the stromal cell-derived factor 1 (SDF1/CXCL12) gene has been related either to resistance to HIV-1 infection and delayed progression to AIDS or to rapid disease progression and death. A longitudinal study was conducted to evaluate the association of the SDF1 polymorphism and the progression of HIV-1 infection in 161 asymptomatic patients infected with HIV-1 (ASYMPT) and 617 patients with AIDS (SYMPT) from Londrina and the surrounding region, southern Brazil. The endpoints used were the development of AIDS, death, and the slopes of the CD4+ T cell counts and HIV-1 RNA plasma levels. Among the 161 ASYMPT patients, all of the 7 patients (4.3%) homozygous for the mutation remained asymptomatic (p=0.1906); 6 of them had not initiated antiretroviral therapy. Among the 617 patients with AIDS, 40 (6.5%) progressed to death. Of these, 33/388 (8.5%) did not have the SDF1-3'A allele, 6/196 (3.1%) were heterozygous and 1/33 (3.0%) was homozygous for the SDF1-3'A allele (p=0.029). The SDF1 genotypes were not associated with the surrogate markers of HIV-1 disease progression such as the CD4+ T cell decline and plasma HIV-1 RNA levels. The results observed in this study support the hypothesis that the mutation of SDF1-3'A could have a possible late-stage protective effect on HIV-1 disease progression in the Brazilian population.