The emergence of the novel coronavirus disease known as COVID-19 creates another health burden for people living with HIV (PLWH) who face multiple morbidities and may be at heightened risk for severe physical health illness from COVID-19. Our abilities to address these morbidities in PLWH must be considered alongside the socially-produced burdens that both place this population at risk for COVID-19 and heighten the likelihood of adverse outcomes. These burdens can affect the physical, emotional, and social well-being of PLWH and interfere with the delivery of effective healthcare and access to HIV treatment. We posit that a syndemic framework can be used to conceptualize the potential impact of COVID-19 among PLWH to inform the development of health programming services.

Objective(s): Some but not all studies indicate that individuals with HIV infection are at an increased risk of fracture. We systematically reviewed the literature to investigate whether incidence of fracture (both overall and fragility) differs between individuals with and without HIV. Design: A systematic review and meta-analysis. Methods: Medline, Scopus and the Cochrane Library databases for all studies ever published up to 28 September 2012 and electronically available conference abstracts from CROI, ASBMR, IAS and AIDS were searched. All studies reporting incidence of all fracture and fragility fracture in HIV-infected adults were included. A random effects model was used to calculate pooled estimates of incidence rate ratios (IRRs) for studies that presented data for HIV-infected and controls. For all studies, incidence rates of fracture and predictors of fracture among HIV-infected individuals were summarized. Results: Thirteen eligible studies were analysed, of which seven included controls. Nine studies reported all incident fractures and 10 presented incident fragility fractures. The pooled IRR was 1.58 [95% confidence interval (CI) 1.25–2.00] for all fracture and 1.35 (95% CI 1.10–1.65) for fragility fracture . Smoking, white race and older age were consistent predictors for fragility fractures. Conclusion: Our results indicate that HIV infection is associated with a modest increase in incident fracture. Future research should focus on clarifying risk factors, designing appropriate interventions and the long-term implications of this increased risk for an ageing HIV-infected population.

Cryptococcus neoformans is a ubiquitous environmental fungus that can cause life-threatening meningitis and fungemia, often in the presence of acquired immunodeficiency syndrome (AIDS), liver cirrhosis, diabetes mellitus, or other medical conditions. To distinguish risk factors from comorbidities, we performed a hospital-based, density-sampled, matched case-control study. All new-onset cryptococcal meningitis cases and cryptococcemia cases at a university hospital in Taiwan from 2002–2010 were retrospectively identified from the computerized inpatient registry and were included in this study. Controls were selected from those hospitalized patients not experiencing cryptococcal meningitis or cryptococcemia. Controls and cases were matched by admission date, age, and gender. Conditional logistic regression was used to analyze the risk factors. A total of 101 patients with cryptococcal meningitis (266 controls) and 47 patients with cryptococcemia (188 controls), of whom 32 patients had both cryptococcal meningitis and cryptococcemia, were included in this study. Multivariate regression analysis showed that AIDS (adjusted odds ratio [aOR] = 181.4; p < 0.001), decompensated liver cirrhosis (aOR = 8.5; p = 0.008), and cell-mediated immunity (CMI)-suppressive regimens without calcineurin inhibitors (CAs) (aOR = 15.9; p < 0.001) were independent risk factors for cryptococcal meningitis. Moreover, AIDS (aOR = 216.3, p < 0.001), decompensated liver cirrhosis (aOR = 23.8; p < 0.001), CMI-suppressive regimens without CAs (aOR = 7.3; p = 0.034), and autoimmune diseases (aOR = 9.3; p = 0.038) were independent risk factors for developing cryptococcemia. On the other hand, diabetes mellitus and other medical conditions were not found to be risk factors for cryptococcal meningitis or cryptococcemia. The findings confirm AIDS, decompensated liver cirrhosis, CMI-suppressive regimens without CAs, and autoimmune diseases are risk factors for invasive C. neoformans diseases.

Objective: There is growing evidence that fracture risk is increased in individuals with HIV and/or hepatitis C virus (HCV) infection. We systematically reviewed the literature to determine whether prevalence of osteoporosis and incidence of fracture is increased in HIV/HCV-coinfected individuals. Design: A systematic review and meta-analysis. Methods: A search was performed of Medline, Scopus and the Cochrane Library databases, as well as of abstracts from annual retroviral, liver and bone meetings (up to 2013) for studies with bone mineral density (BMD) or bone fracture data for HIV/HCV-coinfected individuals. Osteoporosis odds ratios (ORs) and fracture incidence rate ratios (IRRs) were estimated from studies with data on HIV-monoinfected or HIV/HCV-uninfected comparison groups. Results: Of 15 included studies, nine reported BMD data and six reported fracture data. For HIV/HCV-coinfected, the estimated osteoporosis prevalence was 22% [95% confidence interval (95% CI) 12–31] and the crude OR for osteoporosis compared with HIV-monoinfected was 1.63 (95% CI 1.27–2.11). The pooled IRR of overall fracture risk for HIV/HCV-coinfected individuals was 1.77 (95% CI 1.44–2.18) compared with HIV-monoinfected and 2.95 (95% CI 2.17–4.01) compared with uninfected individuals. In addition to HIV/HCV-coinfection, older age, lower BMI, smoking, alcohol and substance use were significant predictors of osteoporosis and fractures across studies. Conclusion: HIV/HCV coinfection is associated with a greater risk of osteoporosis and fracture than HIV monoinfection; fracture risk is even greater than uninfected controls. These data suggest that HIV/HCV-coinfected individuals should be targeted for fracture prevention through risk factor modification at all ages and DXA screening at age 50.

The latent viral reservoir is the major obstacle to achieving HIV remission and necessitates life-long antiretroviral therapy (ART) for HIV-infected individuals. Studies in adults and children have found that initiating ART soon after infection is associated with a reduction in the size of the HIV-1 reservoir. Here we quantified cell-associated HIV-1 DNA in early-treated but currently older HIV-infected children suppressed on ART. The study participants comprised of a cohort of 146 early-treated children with HIV-1 RNA <50 copies/ml enrolled as part of a clinical trial in Johannesburg, South Africa. A stored buffy coat sample collected after a median 4.3 years on ART and where HIV-1 RNA was <50 copies/ml was tested for cell-associated HIV-1 DNA levels. An in-house, semi-nested real-time quantitative hydrolysis probe PCR assay to detect total HIV-1 subtype C proviral DNA was used. Children were followed prospectively for up to 3 years after this measurement to investigate subsequent HIV-1 RNA rebound/failure while remaining on ART. Age at ART initiation, HIV-1 RNA decline prior to HIV-1 DNA measurement and other factors were investigated. A gradient between age at ART initiation and later HIV-1 DNA levels was observed. When ART was started 50 copies/ml whilst on ART within 3 years after the DNA measurement was 2.07 (95% CI: 1.352–3.167) times greater if the HIV-1 DNA level was above the median of 55 copies/10⁶ cells. Cell-associated HIV-1 DNA levels measured after more than 4 years on ART were lower the younger the age of the child when ART was initiated. This marker of the size of the viral reservoir also predicted subsequent viral rebound/treatment failure while ART was sustained. The results provide additional evidence of the benefits of prompt diagnosis and early ART initiation in newborns and infants.