HIV-infected treatment-naive participants were randomized to tenofovir-emtricitabine (TDF/FTC) plus atazanavir-ritonavir (ATV/r), darunavir-ritonavir (DRV/r), or raltegravir (RAL) over 96 weeks. Insulin resistance increased rapidly and then plateaued and no differences were found with RAL when compared to ATV/r or DRV/r.

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The mechanisms causing HIV-associated immune activation remain incompletely understood. Alteration of intestinal integrity with subsequent translocation of bacterial products appears to play an important role; however, little is known about the impact of fungal translocation. We assessed the effect of fungal translocation and its association with immune activation in people living with HIV (PLWH) compared with uninfected controls. We measured serum levels of b-D-glucan (BDG) and anti-Saccharomyces cerevisiae antibodies (ASCA) immunoglobulin G (IgG) and immunoglobulin A (IgA) and markers of systemic inflammation and immune activation in virally suppressed PLWH on antiretroviral therapy (ART) and uninfected controls. T-test and Mann-Whitney tests were used to compare markers by HIV status and correlation and regression analyses were used to assess associations of fungal translocation markers with markers of inflammation. One hundred seventysix participants were included (128 HIV+ and 48 HIV-); 72% male, 65% African American, median age was 50 years, and CD4 was 710 cells/cm 3. Levels of BDG tended to be lower in HIV+ when compared with controls (p = .05). No significant difference in levels of ASCA IgG and IgA was seen between groups (p > .75). There was a significant correlation between BDG and several markers of inflammation and immune activation in PLWH, not seen in uninfected controls. In contrast, no correlations were seen between levels of ASCA IgG and IgA with inflammatory markers. PLWH on ART do not have higher levels of BDG or ASCA when compared with uninfected controls, however, the association found between BDG and several inflammation markers suggests a potential role of fungal translocation in the heightened immune activation seen in treated HIV.

Background In HIV-uninfected populations, physical activity decreases mortality and inflammation. Inflammation is a potential cause for co-morbidities in HIV+ adults, the evidence examining the effect of physical activity on cardiometabolic health is limited. This analysis examines the relationship between physical activity, cardiometabolic health and inflammation. Methods We conducted a nested study within the SATURN-HIV trial in which 147 HIV+ adults were randomized to 10 mg daily rosuvastatin or placebo. Measures of physical activity, cardiometabolic health, inflammation, and vascular disease (carotid artery intima media thickness and Computed Tomography-acquired measures pericardial fat volume) were assessed at baseline and through 96 weeks . Spearman correlations and multivariable analyses were used to explore relationships between physical activity, cardiometabolic health and inflammation. Results Median age (Q1, Q3) was 46 (40.4, 52.7) years, 80% were male, 69% were African American and 46% on protease inhibitors. Baseline median physical activity was 44 minutes per week (0, 150), 24% of participants performed greater than 150 minutes per week. At baseline, physical activity correlated with several markers of cardiometabolic health and inflammation (all p≤0.05). Over all time points median physical activity was independently associated with carotid distensibility (β = 2.53, p = 0.008), pericardial fat volume (β = −6.13, p = 0.001) and IL 6 (β = −0.468, p < 0.001). Conclusions Physical activity is associated with vascular disease, endothelial function, and may be an adjuvant to decreasing co-morbidities in HIV+ adults. Further studies should examine long-term effects of physical activity on cardiometabolic health and inflammation in this population.

Background Few reports have been published on the clinical presentation of pediatric patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We aim to shed more light on the clinical presentation of pediatric patients infected with coronavirus disease 2019 (COVID-19), and also potential risk factors for more severe clinical case presentation. Methods We used a large global health research network to gather clinical data extracted from the electronic medical records of pediatric patients aged < 18 years with confirmed SARS-CoV-2 from January 1, 2020 to May 7, 2020. Clinical symptoms at presentation, hospitalization status, associated co-morbidities, and treatments received were reviewed. Results A total of 627 patients with COVID-19 diagnosis (334 were outpatient, 293 were inpatient) were included from a total of 20 organizations across the United States. The mean age of patients was seven years, 48% were females. Inpatients were younger than outpatients (mean age of 5.6 years vs 8.2 years, p<0.001). Sixty-one percent of patients in the inpatient group were < 5 years of age vs. 44% in the outpatient group. Amongst 293 inpatients, 90% (n=265) were non-severe and 10% (n=28) were classified as severe. The percentage of patients <5 years was higher in severe inpatients vs. non-severe (71% vs 60%.) Significantly more patients with a severe illness vs. non-severe illness had a history of co-morbidity including non-congenital heart disease (50% vs 11%, p<0.001) and disease of the respiratory system (86% vs 53%, p< 0.001). Conclusion Clinicians should closely monitor young children with underlying conditions and COVID-19, as they may be more likely to be hospitalized and have a higher severity of the disease.

such as A. baumannii, which can also acquire carbapenemases and have the capacity to survive on dry surfaces for extended periods. 5,8,9 CRE can survive on dry surfaces for extended periods, which indicates that regular and thorough cleaning and disinfection of the patient environment and equipment should be an integral part of strategies to reduce the spread of CRE.

Background Bacterial translocation in HIV is associated with inflammation and metabolic complications; few data exist on the role of fungal translocation. Methods A5260s was a substudy of A5257, a prospective open label randomized trial in which treatment-naïve people with HIV (PWH) were randomized to tenofovir-emtricitabine (TDF/FTC) plus atazanavir-ritonavir (ATV/r), darunavir-ritonavir (DRV/r), or raltegravir (RAL) over 96 weeks. Baseline was assessed, and changes in β-D-glucan (BDG) were assessed at weeks 4, 24, and 96. Wilcoxon rank-sum tests were used to compare distribution shifts in the changes from baseline between treatment arms and linear regression models to assess associations between BDG and measures of inflammation, body composition, and insulin resistance. Results Two hundred thirty-one participants were randomized; 90% were male, the median age was 36 years, HIV-1 RNA was 4.56 log10c/mL, and CD4 cell count was 338 cells/mm3. There was an overall increase in BDG over 96 weeks (1.57 mean fold-change; 95% confidence interval, 1.39 to 1.77) with no differences between arms. Twofold higher BDG levels at week 96 were associated with increases in trunk fat (8%) and total fat (7%) over 96 weeks (P ≤ .035). At week 4, BDG correlated with I-FABP, a marker of enterocyte damage, and zonulin, a marker of intestinal permeability (r = .19–.20; P < .01). Conclusions In treatment-naïve participants initiating antiretroviral therapy (ART) with TDF/FTC and either RAL or ATV/r, DRV/r, BDG, a marker of fungal translocation, increased similarly in all arms over 96 weeks. This may represent continued intestinal damage during ART and resulting fungal translocation. Higher BDG was associated with larger fat gains on ART.

Background: Few studies have investigated metabolic complications in HIV-infected African