Neurobehavioral HIV medicine最新文献

BACKGROUND: The prevalence of Human immunodeficiency virus (HIV)-associated dementia (HAD) has continued to rise even as incidence has fallen. Several host genetic variants have been identified that modify risk for HAD. However, the findings have not been replicated consistently and most studies did not consider the multitude of factors that might themselves confer risk for HAD. In the current study, we sought to replicate the findings of previous studies in a neurologically and behaviorally well-characterized cohort. METHODS: The sample consisted of 143 HIV+ individuals enrolled in the National NeuroAIDS Tissue Consortium (NNTC). Based on consensus diagnosis, 117 were considered neurologically normal upon study entry, and 26 had HAD. Seven single-nucleotide polymorphisms (SNPs) were genotyped within seven genes (CCL2, CCL3, CCL5, interleukin-1α [IL-1α], IL-10, stromal cell-derived factor 1, and tumor necrosis factor-α). Logistic regression analysis was used to predict group membership (normal vs HAD), with predictor variables including length of infection, age, current drug dependence, current depression, and genotype. RESULTS: The two groups were statistically similar with regards to demographic characteristics, current drug use, and disease factors. The HAD group had significantly greater number of individuals with current depression. Only one SNP, rs1130371 within the gene for CCL3, was entered into the analysis as the others showed symmetric distribution between groups. Logistic regression indicated that current depression and CCL3 genotype were significant predictors of HAD. Depression conferred a fivefold greater risk of HAD, while the TT genotype for CCL3 SNP (rs1130371) was associated with twofold risk for HAD. CONCLUSION: Depression and CCL3 genotype predicted HAD. The fact that SNPs previously found to be associated with HAD were not in our analysis, and that rs1130371 is in high linkage disequilibrium with neighboring genes indicates that more dense genotyping in significantly larger cohorts is required to further characterize the relationship between genotype and risk for HAD.

Gender and racial differences in infection rates for chlamydia and gonorrhea have been reported within community-based populations, but little is known of such differences within juvenile offending populations. Moreover, while research has demonstrated that certain individual-level and community-level factors affect risky behaviors associated with sexually transmitted disease (STD), less is known about how multi-level factors affect STD infection, particularly among delinquent populations. The present study investigated gender and racial differences in STD infection among a sample of 924 juvenile offenders. Generalized linear model regression analyses were conducted to examine the influence of individual-level factors such as age, offense history, and substance use and community-level factors such as concentrated disadvantage, ethnic heterogeneity, and family disruption on STD status. Results revealed significant racial and STD status differences across gender, as well as interaction effects for race and STD status for males only. Gender differences in individual-level and community-level predictors were also found. Implications of these findings for future research and public health policy are discussed.