Search

To evaluate clinical value of metagenomic next-generation sequencing (mNGS) in people living with HIV/AIDS (PLWHA) who had CNS disorders. Cerebrospinal fluid (CSF) samples from 48 PLWHA presenting with CNS disorders were sequenced using mNGS and compared with clinical conventional diagnostic methods. In total, 36/48 ss(75%) patients were diagnosed with pathogen(s) infection by mNGS, and the positive detection proportion by mNGS was higher than that by clinical conventional diagnostic methods (75% vs 52.1%, X2 = 5.441, P = 0.020). Thirteen out of 48 patients (27.1%) were detected with 3–7 pathogens by mNGS. Moreover, 77 pathogen strains were detected, of which 94.8% (73/77) by mNGS and 37.0% (30/77) by clinical conventional methods (X2 = 54.206, P < 0.001). The sensitivity and specificity of pathogens detection by mNGS were 63.9% (23/36) and 66.7% (8/12), respectively, which were superior to that by clinical conventional methods (23/36 vs 9/25, X2 = 4.601, P = 0.032; 8/12 vs 5/23, X2 = 5.029, P = 0.009). The application of mNGS was superior for its ability to detect a variety of unknown pathogens and multiple pathogens infection, and relatively higher sensitivity and specificity in diagnosis of CNS disorders in PLWHA. [ABSTRACT FROM AUTHOR]

The identification of circulating proteins associated with acquired immunodeficiency syndrome‐related non‐Hodgkin lymphoma (AIDS‐NHL) may help in the development of promising biomarkers for screening, diagnosis, treatment, and prognosis. Here, we used quantitative liquid chromatography‐tandem mass spectrometry (LC–MS/MS) to identify differentially expressed proteins (DEPs) in plasma collected from patients with AIDS‐NHL and human immunodeficiency virus (HIV)‐infected patients without NHL (HIV+). Proteins with a log2 (fold change) in abundance >0.26 and p < 0.05 were considered differentially abundant. In total, 84 DEPs were identified, among which 20 were further validated as potential biomarkers, with immunoglobulin and complement components being the most common proteins. Some of the proteins were further verified in a retrospective analysis of the medical records of patients in a larger cohort. These markedly altered proteins were found to mediate pathophysiological pathways that likely contribute to AIDS‐NHL pathogenesis, such as the humoral immune response, complement activation, and complement and coagulation cascades. Our findings provide a new molecular understanding of AIDS‐NHL pathogenesis and provide new evidence supporting the identification of these proteins as possible biomarkers in AIDS‐NHL. [ABSTRACT FROM AUTHOR]

Background: Human immunodeficiency virus (HIV)-infected individuals are at high risk of contracting tuberculosis (TB) disease, and current methods for diagnosing TB infection are less effective in this population. We developed and evaluated a new interferon-gamma release assay (IGRA), named A.TB, in HIV-infected individuals, with and without active TB, in a setting of high TB burden and low HIV prevalence. Methods: A total of 255 subjects were divided into 3 groups according to their HIV and TB status: HIV + without active TB (n = 123), HIV +/TB + (n = 79), and HIV-/TB + (n = 65). The A.TB assay was performed in parallel with the QuantiFERON-TB Gold In-Tube (QFT-GIT) and tuberculin skin test (TST). Results: The positive rate was 59.3% (n = 123) by A.TB and 53.8% (n = 106) by QFT-GIT. We observed a strong concordance of 81.2% (k = 0.612) between the two IGRAs. The QFT-GIT results were affected by low CD4+ cell count (p= 0.013), while A.TB results were not. A.TB was also performed in patients with active TB (n = 65) and patients with active TB and HIV co-infection (n = 79). The sensitivity of A.TB in these groups was 80.0% and 81.0%, respectively. Conclusion: The A.TB results were not affected by low CD4+ cell count in the co-infected cohort. With further evaluation,A.TB may prove to be a valuable tool for diagnosing TB in HIV-infected patients. [ABSTRACT FROM AUTHOR]

Summary Objectives To investigate the prevalence, incidence of abnormal liver function tests (LFTs), and mortality during anti-TB treatment in patients multi-infected with HIV, tuberculosis (TB), and hepatitis virus (hepatitis B virus (HBV) and hepatitis C virus (HCV)). Methods Three hundred and sixty-one HIV-positive TB patients were enrolled and divided into an HIV/TB group, HIV/TB/HBV group, and HIV/TB/HCV group; 1013 HIV-negative TB patients were selected randomly as controls. Results One hundred and seventeen (32.4%) HIV-positive TB patients were infected with HBV and/or HCV, compared with 90 (8.9%) HIV-negative TB patients ( p = 0.000). HIV-positive TB patients had a higher incidence of anti-TB drug-induced hepatotoxicity than HIV-negative TB patients (4.2% vs. 1.0%, odds ratio (OR) 4.348, 95% confidence interval (CI) 1.935–9.769, p = 0.000). The incidence of abnormal LFTs in the HIV/TB/HBV group and HIV/TB/HCV group were significantly higher than in the HIV/TB group (40.7% vs. 11.1%, OR 5.525, 95% CI 2.325–13.131, p = 0.000; 20.0% vs. 11.1%, OR 2.009, 95% CI 1.057–3.820, p = 0.031). A total of 68.4% of patients with HBV-DNA >1.0 × 10 5 copies/ml and 42.9% of patients with HCV-RNA >1.0 × 10 5 copies/ml had abnormal LFTs. Twenty-three (19.7%) patients multi-infected with HIV, TB, and hepatitis virus died during anti-TB treatment. Conclusions HIV, HBV, and HCV are risk factors for the development of abnormal LFTs and mortality during anti-TB treatment. TB patients co-infected with HIV and hepatitis virus need close follow-up. [ABSTRACT FROM AUTHOR]