Uganda Virus Research Institute

About: Uganda Virus Research Institute is a facility organization based out in Entebbe, Uganda. It is known for research contribution in the topics: Population & Acquired immunodeficiency syndrome (AIDS). The organization has 569 authors who have published 957 publications receiving 47051 citations. The organization is also known as: Yellow Fever Research Institute & East African Virus Research institute.

Discovery and refinement of loci associated with lipid levels

Abstract: Levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides and total cholesterol are heritable, modifiable risk factors for coronary artery disease. To identify new loci and refine known loci influencing these lipids, we examined 188,577 individuals using genome-wide and custom genotyping arrays. We identify and annotate 157 loci associated with lipid levels at P < 5 × 10(-8), including 62 loci not previously associated with lipid levels in humans. Using dense genotyping in individuals of European, East Asian, South Asian and African ancestry, we narrow association signals in 12 loci. We find that loci associated with blood lipid levels are often associated with cardiovascular and metabolic traits, including coronary artery disease, type 2 diabetes, blood pressure, waist-hip ratio and body mass index. Our results demonstrate the value of using genetic data from individuals of diverse ancestry and provide insights into the biological mechanisms regulating blood lipids to guide future genetic, biological and therapeutic research.

Rates of HIV-1 Transmission per Coital Act, by Stage of HIV-1 Infection, in Rakai, Uganda

Abstract: Background. We estimated rates of human immunodeficiency virus (HIV)‐1 transmission per coital act in HIV-discordant couples by stage of infection in the index partner. Methods. We retrospectively identified 235 monogamous, HIV-discordant couples in a Ugandan populationbased cohort. HIV transmission within pairs was confirmed by sequence analysis. Rates of transmission per coital act were estimated by the index partner’s stage of infection (recent seroconversion or prevalent or late-stage infection). The adjusted rate ratio of transmission per coital act was estimated by multivariate Poisson regression. Results. The average rate of HIV transmission was 0.0082/coital act (95% confidence interval [CI], 0.0039‐ 0.0150) within ∼2.5 months after seroconversion of the index partner; 0.0015/coital act within 6‐15 months after seroconversion of the index partner (95% CI, 0.0002‐0.0055); 0.0007/coital act (95% CI, 0.0005‐0.0010) among HIV-prevalent index partners; and 0.0028/coital act (95% CI, 0.0015‐0.0041) 6‐25 months before the death of the index partner. In adjusted models, early- and late-stage infection, higher HIV load, genital ulcer disease, and younger age of the index partner were significantly associated with higher rates of transmission. Conclusions. The rate of HIV transmission per coital act was highest during early-stage infection. This has implications for HIV prevention and for projecting the effects of antiretroviral treatment on HIV transmission. Model estimates suggest that the rate of heterosexual HIV-1 transmission per coital act follows a U-shaped curve, being highest during the postseroconversion period, lower during latency, and increasing with advancing disease [1‐4]. This is supported by findings that blood HIV load, which is higher during the postseroconversion period and during advanced disease, is the principal predictor of heterosexual transmission [5‐

Common variants associated with plasma triglycerides and risk for coronary artery disease

Abstract: Triglycerides are transported in plasma by specific triglyceride-rich lipoproteins; in epidemiological studies, increased triglyceride levels correlate with higher risk for coronary artery disease (CAD). However, it is unclear whether this association reflects causal processes. We used 185 common variants recently mapped for plasma lipids (P < 5 × 10(-8) for each) to examine the role of triglycerides in risk for CAD. First, we highlight loci associated with both low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, and we show that the direction and magnitude of the associations with both traits are factors in determining CAD risk. Second, we consider loci with only a strong association with triglycerides and show that these loci are also associated with CAD. Finally, in a model accounting for effects on LDL-C and/or high-density lipoprotein cholesterol (HDL-C) levels, the strength of a polymorphism's effect on triglyceride levels is correlated with the magnitude of its effect on CAD risk. These results suggest that triglyceride-rich lipoproteins causally influence risk for CAD.