Project description:There are 19 differentially expressed microRNAs among new HIV-infected cases, old HIV-infected cases and healthy controls. Five microRNAs show trends in healthy controls, new HIV-infected cases and old HIV-infected cases, they are hsa-miR-1291, and hsa-miR-3609 with up-trends, and hsa-miR-3162-3p, hsa-miR-874-5p and hsa-miR-4258 with down-trends.
Project description:Elite controllers maintain HIV-1 viral loads below the limit of detection. The mechanisms responsible for this phenomenon are poorly understood. As microRNAs (miRNAs) are regulators of gene expression and some of them modulate HIV infection, we have studied the miRNA profile in plasma from HIV elite controllers and chronically infected individuals and compared against healthy donors. Several miRNAs correlate with CD4+ T cell count or with the known time of infection. No significant differences were observed between elite controllers and healthy donors; however, 16 miRNAs were different in the plasma of chronic infected versus healthy donors. In addition, levels of hsa-miR-29b-3p, hsa-miR-33a-5p and hsa-miR-146a-5p were higher in plasma from elite controllers than chronic infected and hsa-miR-29b-3p and hsa-miR-33a-5p overexpression significantly reduced the viral production in MT2 cells. Therefore, levels of circulating miRNAs might be of diagnostic and/or prognostic value for HIV infection. Additionally, hsa-miR-29b-3p and miR-33a-5p may be used in therapeutic strategies. An exploratory cross-sectional study of microRNA levels in EDTA plasma samples. Plasma samples were obtained from 24 subjects and were classified in 3 groups, 9 Elite Controllers (defined as individuals with plasma viral load (PVL) < 50 copies/ml, CD4 count >350/ml), 9 chronic HIV patients (CH) under anti-retroviral treatment and 6 healthy HIV negative donors (HD). This study was approved by the HuM-CM-)sped Foundation Ethics Committee and informed consent was obtained from all subjects.
Project description:Elite controllers maintain HIV-1 viral loads below the limit of detection. The mechanisms responsible for this phenomenon are poorly understood. As microRNAs (miRNAs) are regulators of gene expression and some of them modulate HIV infection, we have studied the miRNA profile in plasma from HIV elite controllers and chronically infected individuals and compared against healthy donors. Several miRNAs correlate with CD4+ T cell count or with the known time of infection. No significant differences were observed between elite controllers and healthy donors; however, 16 miRNAs were different in the plasma of chronic infected versus healthy donors. In addition, levels of hsa-miR-29b-3p, hsa-miR-33a-5p and hsa-miR-146a-5p were higher in plasma from elite controllers than chronic infected and hsa-miR-29b-3p and hsa-miR-33a-5p overexpression significantly reduced the viral production in MT2 cells. Therefore, levels of circulating miRNAs might be of diagnostic and/or prognostic value for HIV infection. Additionally, hsa-miR-29b-3p and miR-33a-5p may be used in therapeutic strategies.
Project description:Despite the use of current antiretroviral therapy (ART) in HIV-1 infected mothers, approximately 5% of new HIV-1 infections still occur in breastfed infants annually. Human Milk (HM) exosomes are highly enriched in maternal microRNAs (miRNAs) and after ingestion and subsequent absorption play an important role in neonatal innate and adaptive immunity. Although, HM exosomes derived from healthy donors are known to inhibit HIV-1 transmission; the effect of HIV-1 on HM exosomal miRNA signatures remains unknown. In the present study, for the first time HM derived exosomal miRNA profiles were determined in HIV-1 infected women.
Project description:In order to detect the expression profile of plasma microRNAs, we have employed microRNA microarray expression profiling as a discovery platform to identify microRNAs with the potential to distinguish the different microRNA profiles from ESCC patients and healthy controls. Three pairs of plasma samples from ESCC patients and healthy controls without any digestive tract disease history were collected for microarray analysis.
Project description:Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis.
Project description:Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis. A 507 protein microarray was employed to provide a broad view of cytokines and chemokines in saliva and plasma in acutely HIV infected subjects as compared to uninfected subjects. A custom array derived from the initial results was refined to highlight those molecules with significant change relative to control subjects indicating the potential for biological impact.
Project description:A 507 protein microarray was employed to provide a broad view of cytokines and chemokines in saliva and plasma in acutely HIV infected subjects as compared to uninfected subjects. A 40 cytokine custom array derived from the initial results was refined to highlight those molecules with significant change relative to control subjects indicating the potential for biological impact. Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis.
Project description:Human immunodeficiency virus type 1 (HIV-1)-induced inflammation and/or long-term antiretroviral drug toxicity may contribute to the evolution of liver disease. We investigated circulating plasma microRNAs (miRNAs) as potential biomarkers of liver injury in patients mono-infected with HIV-1. We performed large-scale deep sequencing analyses of small RNA level on plasma samples from patients with HIV-1 mono-infection that had elevated or normal levels of alanine aminotransferase (ALT) or focal nodular hyperplasia (FNH). Hepatitis C virus (HCV) mono-infected patients were also studied. Compared to healthy donors, patients with HIV-1 or HCV mono-infections showed significantly altered (fold change >2, adjusted p<0.05) level of 25 and 70 miRNAs, respectively. Of the 25 altered miRNAs found in patients with HIV-1, 19 were also found in patients mono-infected with HCV. Moreover, 13 of the 14 most up-regulated miRNAs (range: 9.3-3.4-fold increase) in patients with HCV mono-infections were also up-regulated in patients with HIV-1 mono-infections. Importantly, most of these miRNAs significantly and positively correlated with ALT and aspartate aminotransferase (AST) levels, and liver fibrosis stage (p<0.05). MiR-122-3p and miR-193b-5p were highly up-regulated HIV-1 mono-infected patients with elevated ALT or FNH, but not in HIV-1 patients with normal levels of ALT. These results reveal that HIV-1 infections impacted liver-related miRNA levels in the absence of an HCV co-infection, which highlights the potential of miRNAs as biomarkers for the progression of liver injury in HIV-1 infected patients.
Project description:We carried out a case control study in an attempt to identify changes in circulating microRNAs in patients with intracranial aneurysms (IAs). We selected 40 cases (20 ruptured and 20 unruptured) and 20 healthy controls. We randomly selected 5 samples from each group and combined them into a sample pool. In this way we obtained 12 sample pools and one pool was used for a single microarray. Changes in microRNA levels in the plasma were surveyed with Agilent Human microRNA Microarray (Release 14.0, 8x15K). We identified 20 microRNAs that were unanimously changed in both ruptured and unruptured patients. We included 40 cases (20 ruptured and 20 unruptured) and 20 healthy controls. We randomly selected 5 plasma samples from each group and combined them into a sample pool. In this way we obtained 12 sample pools and one pool was used for a single microarray. Total RNA was isolated from 1 ml plasma from each sample pool and resuspended in the same volume of buffer. A fixed volume of RNA sample was used for microarray detection.