Background Indonesia is a tropical country, warm and humid, with numerous environmental fungi. Data on fungal disease burden help policymakers and clinicians. Objectives We have estimated the incidence and prevalence of serious fungal diseases. Methods We found all published and unpublished data and estimated the incidence and prevalence of fungal diseases based on populations at risk. HIV data were derived from UNAIDS (2017), pulmonary tuberculosis (PTB) data from 2013–2019, data on chronic pulmonary aspergillosis (CPA) were used to estimate CPA prevalence and likely deaths, COPD data from Hammond (2020), lung cancer incidence was from Globocan 2018, and fungal rhinosinusitis was estimated using community data from India. Results Overall ~7.7 million Indonesians (2.89%) have a serious fungal infection each year. The annual incidence of cryptococcosis in AIDS was 7,540. Pneumocystis pneumonia incidence was estimated at 15,400 in HIV and an equal number in non‐HIV patients. An estimated 1% and 0.2% of new AIDS patients have disseminated histoplasmosis or Talaromyces marneffei infection. The incidence of candidaemia is 26,710. The annual incidence of invasive aspergillosis was estimated at 49,500 and the prevalence of CPA is at 378,700 cases. Allergic bronchopulmonary aspergillosis prevalence in adults is estimated at 336,200, severe asthma with fungal sensitisation at 443,800, and fungal rhinosinusitis at 294,000. Recurrent vulvovaginal candidiasis is estimated at 5 million/year (15–50 years old). The incidence of fungal keratitis around 40,050. Tinea capitis prevalence in schoolchildren about 729,000. Conclusions Indonesia has a high burden of fungal infections.
Altered T cell profiles have been linked with metrics of persistent cytomegalovirus (CMV) infections in healthy aging and older HIV patients stable on antiretroviral therapy (ART). In this study, we use CMV DNA to identify active infections, and levels of CMV-reactive antibody to assess the persistent burden of CMV in a longitudinal study of 78 young adult patients beginning ART in Jakarta, Indonesia, with <200 CD4 T cells/μL. CMV antibodies, inflammatory markers (C-reactive protein [CRP], soluble interferon-α/β receptor) and T cell phenotypes were assessed before ART (V0) and after 1, 3, 6, and 12 months (V1-V12). CMV DNA was detected in 41 patients (52%) at V0, irrespective of CD4 T cell counts, gender, age, or plasma HIV RNA. CMV DNA+ patients had higher levels of antibody reactive with CMV Immediate Early 1 (IE-1) at V0 and V12 (p = 0.04), and with CMV lysate at V12 (p = 0.01). Detectable CMV DNA did not align with inflammatory markers, but associated with lower CD4/CD8 ratios until V3. CMV antibody levels correlated inversely with proportions of naive CD4 and CD8 T cells, and directly with proportions of CD57 and activated memory T cells (CD3 CD45RA) after 3-12 months on ART. Overall, active CMV replication is common in HIV patients beginning ART in Indonesia and associates with low CD4/CD8 ratios. Elevated levels of CMV-reactive antibody measured on ART also mark a depletion of naive T cells, accumulation of memory T cells, and may be a stable metric of the burden of CMV.
ART reduces the prevalence of OPC, and the total fungal and C. albicans burden. Levels of salivary β-defensin-2 may associate with OPC in HIV patients responding to ART.
Objectives: Atherosclerosis has been linked with periodontitis in the general population and with persistent immune activation and a high burden of cytomegalovirus (CMV) in HIV patients responding to antiretroviral therapy (ART). Here, we assess risk factors for cardiovascular changes in younger HIV patients representative of patient populations in Asia. Study Design: HIV-infected adults (n = 82) with <200 CD4 T-cells/μl were examined as they began ART at Cipto Mangunkusumo Hospital, Jakarta, and after 3 months. 32 patients were re-assessed after 5 years, alongside 32 age-matched healthy controls. Methods: We assessed the community periodontal index of treatment needs, carotid -thickness (cIMT), plasma markers of immune activation (using commercial enzyme-linked immunosorbent assay) and CMV antibodies by in-house enzyme-linked immunosorbent assay. Results: Periodontitis persisted in 16/32 patients after 5 years and was potentiated by greater age (P = 0.03) and poor oral hygiene (P = 0.05), with no effect of smoking, pulmonary tuberculosis, oral candidiasis, or low CD4+ T-cell counts (P > 0.05). After 5 years on ART, right and left cIMT were greater in HIV patients with periodontitis (P = 0.02, 0.006, respectively). Moreover, cIMT values were higher in patients with periodontitis (P = 0.05–0.01) than in equivalent controls. Simple linear regressions showed that patients with periodontitis had greater right (P = 0.01) and left (P = 0.004) cIMT than those without periodontitis. Multiple linear regressions showed that periodontitis and CMV antibody levels optimally predicted poor right and left cIMT (Adjusted R2 = 0.36, P = 0.0013; Adjusted R2 = 0.40, P = 0.001, respectively). Conclusions: Our data identify periodontitis and CMV as independent predictors of atherosclerosis in young adult HIV patients.
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