The population of people living with HIV (PLWH) is growing older with an estimated 4 million over the age of 50 years, a figure which has doubled since the introduction of effective antiretroviral therapy (ART) and which is increasing globally. Despite effective ART, PLWH still experience excess morbidity and mortality compared to the general population with increased prevalence of age-related, non-AIDS illnesses (NAI) such as cardiovascular disease, malignancies, cognitive impairment and reduced bone mineral density, which impact disability and everyday functioning. This review will discuss the challenges presented by comorbidities in ageing PLWH and discuss the aetiology and management of age-related illnesses in this vulnerable population.

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Introduction: Cardiovascular disease (CVD) is one of the leading causes of mortality in virally suppressed people living with HIV (PLWH) and with an ageing population, is likely to become one of the leading challenges in maintaining good health outcomes in HIV infection. However, factors driving risk of CVD in PLWH are multiple and may be different from those of the general population, raising challenges to predicting and managing CVD risk in this population.Areas covered: In this review, we examine the relevant data regarding CVD in HIV infection including that on CVD prevalence, pathogenesis and contributing factors. We review the data regarding CVD risk prediction in PLWH and summarise factors, both general and HIV specific, that may influence CVD risk in this population. And finally we discuss appropriate management of CVD risk in PLWH and explore potential therapeutic pathways which may mitigate CVD risk in the future in this population.Expert opinion: Following a comprehensive review of CVD risk in PLWH, we give our opinion on the primary issues in risk prediction and management of CVD in HIV infected individuals and discuss the future direction of CVD management in this population.

Background Although reports suggest that most individuals with COVID-19 develop detectable antibodies post infection, the kinetics, durability, and relative differences between IgM and IgG responses beyond the first few weeks after symptom onset remain poorly understood. Methods Within a large, well-phenotyped, diverse, prospective cohort of subjects with and without SARS-CoV-2 PCR-confirmed infection and historical controls derived from cohorts with high prevalence of viral coinfections and samples taken during prior flu seasons, we measured SARS-CoV-2 serological responses (both IgG and IgM) using commercially available assays. We calculated sensitivity and specificity, relationship with disease severity and mapped the kinetics of antibody responses over time using generalised additive models. Results We analysed 1,001 samples from 752 subjects, 327 with confirmed SARS-CoV-2 (29.7% with severe disease) spanning a period of 90 days from symptom onset. Sensitivity was lower (44.1-47.1%) early (<10 days) after symptom onset but increased to >80% after 10 days. IgM positivity increased earlier than IgG-targeted assays but positivity peaked between day 32 and 38 post onset of symptoms and declined thereafter, a dynamic that was confirmed when antibody levels were analysed, with more rapid decline observed with IgM. Early (<10 days) IgM but not IgG levels were significantly higher in those who subsequently developed severe disease (signal / cut-off 4.20 (0.75-17.93) versus 1.07 (0.21-5.46), P=0.048). Conclusions This study suggests that post-infectious antibody responses in those with confirmed COVID-19 begin to decline relatively early post infection and suggests a potential role for higher IgM levels early in infection predicting subsequent disease severity

Our HIV Care Cascade model demonstrates that the true numbers of patients NRIC may be significantly lower than previously estimated and once RIC, treatment goals approaching the United Nations Programme on HIV and AIDS targets are possible with 91.5% on treatment and almost 90% of those on treatment virally suppressed. That 40% reengaged following direct contact suggests benefit through regular monitoring and direct contact based on the HIV Care Cascade model.

Objective. To consider the factors which may influence the uptake of routine diabetes care. Methods. A district diabetes register has been analysed to give information on the population not accessing routine diabetes care. The groups of patients with no record of HbA lc or fundoscopy in the previous year were identified and considered for the possible influencing factors of age, sex and socio-economic status designated by DEPCAT score. Results. The results suggested that older patients, over 70 years, and young people, less than 20 years, are less likely to access routine diabetes care. The analysis by deprivation category does not demonstrate the usual poorer uptake in those from deprived areas. In this population uptake was slightly worse from less deprived areas. There was no significant difference between males and females. Conclusions. The data held on the district diabetes register suggests that age does appear to have influence on uptake of routine diabetic review, but the usual influence of deprivation is not demonstrated. Planners of healthcare may need to develop services to meet the needs of the elderly and teenagers as well as giving consideration to the needs of different socio-economic groups.

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Purpose of reviewCardiovascular diseases (CVD) is one of the leading cause of morbidity and mortality in antiretroviral treated people living with HIV (PWH) with risk score algorithms based on traditional risk factors being shown to be consistently unreliable in estimating risk in this population. This review aims to examine recent data published in last 18-24 months exploring biomarkers that may be useful in identifying PWH at risk of developing CVD. Recent findingsOngoing research explores the association of inflammatory biomarkers with subclinical CVD with few studies examining their clinical utility in improving CVD risk prediction. Further mechanistic studies explore the role of monocyte/macrophages in CVD pathogenesis with some studies examining functional assays as better predictors of CVD risk.