Twenty-four weeks of rosuvastatin therapy significantly decreased the level of Lp-PLA2, a vascular-specific, inflammatory enzyme that predicts cardiovascular events in the general population. Statins may hold promise as a means of attenuating CVD risk in HIV-infected individuals by decreasing Lp-PLA2 levels.

Purpose of review-Weight gain and obesity among people living with HIV (PLWH) is a serious problem that occurs often after initiation of antiretroviral therapy but may be worse with integrase strand transfer inhibitors (INSTIs). This paper comprehensively reviews available data and summarizes our current understanding of the topic.Recent findings-Recent studies support the concept that weight gain and treatment emergent obesity are worse with INSTI-based regimens, particularly dolutegravir. Women and non-whites appear to be the most at risk, and the accompanying nucleoside reverse transcriptase inhibitor may play a role. Lipohypertrophy, an abnormal accumulation of visceral fat and/or ectopic fat depots, continues to be a problem among PLWH, but the role of INSTIs is inconsistent. The pathogenesis of weight gain and changes in body composition in HIV, especially with INSTIs, is poorly understood but may lead to serious co-morbidities, such as cardiovascular disease and diabetes.Summary-Although INSTI-based regimens are highly efficacious for viral suppression, they appear to cause more weight gain and treatment emergent obesity than non-INSTI-based regimens and may increase the risk of weight-related co-morbidities. More studies are needed to understand the pathogenesis of weight gain with INSTIs in PLWH, in order to prevent this serious complication.

The benefits of long-term antiretroviral therapy (ART) are recognized all over the world with infected children maturing into adults and HIV infection becoming a chronic illness. However, the improved survival is associated with serious metabolic complications, including lipodystrophy (LD), dyslipidemia, insulin resistance, lactic acidosis and bone loss. In addition, the dyslipidemia mainly seen with protease inhibitors may increase the risk of cardiovascular disease in adulthood and potentially in children as they mature into adults. Nucleoside reverse transcriptase inhibitors, particularly stavudine, zidovudine and didanosine are linked to development of LD and lactic acidosis. Perinatally infected children initiate ART early in life; they require lifelong therapy with multiple drug regimens leading to varying toxicities, all potentially impacting their quality of life. LD has a significant impact on the mental health of older children and adolescents leading to poor self-image, depression and subsequent poor adherence to therapy. Reduced bone mineral density (BMD) is reported in both adults and children on ART with the potential for children to develop more serious bone complications than adults due to their rapid growth spurts and puberty. The role of vitamin D in HIV-associated osteopenia and osteoporosis is not clear and needs further study. Most resource-limited settings are unable to monitor lipid profiles or BMD, exposing infected children and adolescents to on-going toxicities with unclear long-term consequences. Improved interventions are urgently needed to prevent and manage these metabolic complications. Longitudinal cohort studies in this area should remain a priority, particularly in resource-limited settings where the majority of infected children reside.

Metabolic complications relating to complex effects of viral and immune-mediated mechanisms are now a focus of clinical care among persons living with human immunodeficiency virus (PLHIV), and obesity is emerging as a critical problem. To address knowledge gaps, the US National Institutes of Health sponsored a symposium in May 2018 entitled “Obesity and Fat Metabolism in HIV-infected Individuals.” Mechanisms relating to adipose dysfunction and fibrosis, immune function, inflammation, and gastrointestinal integrity were highlighted as contributors to obesity among PLHIV. Fibrotic subcutaneous adipose tissue is metabolically dysfunctional and loses its capacity to expand, leading to fat redistribution, including visceral obesity and ectopic fat accumulation, promoting insulin resistance. Viral proteins, including viral protein R and negative regulatory factor, have effects on adipogenic pathways and cellular metabolism in resident macrophages and T cells. HIV also affects immune cell trafficking into the adipose compartments, with effects on adipogenesis, lipolysis, and ectopic fat accumulation. Key cellular metabolic functions are likely to be affected in PLHIV by gut-derived cytokines and altered microbiota. There are limited strategies to reduce obesity specifically in PLHIV. Enhancing our understanding of critical pathogenic mechanisms will enable the development of novel therapeutics that may normalize adipose tissue function and distribution, reduce inflammation, and improve insulin sensitivity in PLHIV.

Objective:To describe system failures potentially contributing to perinatal HIV transmission in the state of Georgia, United States, between 2005 and 2012.Design:A retrospective chart review of antenatal and postnatal records of HIV-infected infants between 1 January 2005 and 31 December 2012.Methods:Study participants included all HIV-infected infants referred for specialized management to the Ponce Family and Youth Clinic within Grady Health Systems in Atlanta. Main outcomes included identification of maternal, perinatal, and neonatal risk factors associated with vertical transmission.Results:Twenty-seven cases were identified; 89% of mothers were African–American between 16 and 30 years of age. Seventy-four percent of women knew their HIV status prior to pregnancy, 44% had no prenatal care, and 52% did not receive combination antiretroviral therapy during pregnancy or intrapartum zidovudine. HIV-1 RNA near the time of delivery was available in only 10 of 27 mothers, and of those, only three had an undetectable HIV-1 RNA level. Caesarean section was performed in 70% of women. Of the 27 children, the mean gestational age was 37 (SD: 2.9) weeks, with 33% requiring neonatal ICU admission. Fifty-nine percent were men, and only 67% received postnatal zidovudine prophylaxis.Conclusion:Mother-to-child transmission of HIV continues to occur in Georgia at unacceptable levels. Increased education with adherence to existing national guidelines, as well as coordinated efforts between healthcare and public health providers to improve linkage and retention in medical care are urgently needed to prevent further vertical transmission events in Georgia.

Vitamin D supplementation decreased markers of T-cell activation/exhaustion and monocyte activation in HIV-infected youth, with subjects given the highest dose (120,000 IU/month) showing the greatest decreases. These data suggest that high-dose vitamin D supplementation may attenuate immune activation and exhaustion, and serve as adjuvant therapy to antiretroviral therapy in HIV. ClinicalTrials.gov identifier: NCT01523496.

Obesity emerged as a risk factor for morbidity and mortality related to 2009 pandemic influenza A (H1N1) infection. However, few studies examine the immune responses to H1N1 vaccine among children and adults of various body mass indices (BMI). Pooling data from 3 trials of unadjuvanted split-virus H1N1 A/California/07/2009 influenza vaccines, we analyzed serologic responses of participants stratified by BMI grouping. A single vaccine dose produced higher hemagglutination inhibition antibody titers at day 21 in obese compared to nonobese adults, but there were no significant differences in responses to H1N1 vaccine among children or adults of various BMI following 2 doses.

Purpose of the review Because of antiretroviral therapy, people are living with HIV infection longer than ever before. As this patient group ages, it is expected that medical co-morbidities such as osteoporosis and fragility fractures will increase. The purpose of this review is to address the epidemiology and what is known regarding the pathogenesis of bone loss in people living with HIV infection with a focus on recently published literature. Recent findings HIV-infected individuals are at increased risk for low bone mineral density and bone fractures. The cause of bone loss in HIV is multifactorial including traditional risk factors some of which disproportionately affect HIV-infected individuals and alterations in bone metabolism due to antiretroviral therapy (ART), HIV viral proteins and chronic inflammation. Lifestyle modification, changing ART, calcium and vitamin D supplementation and pharmacologic treatment for osteoporosis may all be employed to abrogate bone loss in this patient group. Summary Clinicians should be aware of the contributors to bone loss in people living with HIV in order to recognize high risk individuals and to take appropriate steps to address modifiable risk factors to prevent future fracture.