Hepatitis C virus (HCV) genome encodes for one long polyprotein that is processed by cellular and viral proteases to generate 10 polypeptides. The viral structural proteins include the core protein, and the envelope glycoproteins E1 and E2, present at the surface of HCV particles. Non-structural (NS) proteins consist of NS1, NS2, NS3, NS4A, NS4B, NS5a, and NS5b and have a variable function in HCV RNA replication and particle assembly. Recent findings evidenced the capacity of HCV virus to modulate host cell factors to create a favorable environment for replication. Indeed, increasing evidence has indicated that the presence of HCV is significantly associated with aberrant miRNA expression in host cells, and HCV structural and non-structural proteins may be responsible for these alterations. In this review, we summarize the recent findings on the role of HCV structural and non-structural proteins in the modulation of host cell miRNAs, with a focus on the molecular mechanisms responsible for the cell re-programming involved in viral replication, immune system escape, as well as the oncogenic process. In this regard, structural and non-structural proteins have been shown to modulate the expression of several onco-miRNAs or tumor suppressor miRNAs.

Heart failure (HF) is a complex and multifactorial syndrome with high morbidity and mortality rates worldwide. Accumulative evidence suggests that microRNAs (miRNAs) play critical roles in maintaining cardiac homeostasis. The dysregulation of various miRNAs has been reported in different studies on failing human hearts. However, little is known about their circulatory profile. In this study, comprehensive miRNA profiling was performed by next-generation sequencing for plasma samples of 24 HF and 24 age and sex-matched, non-HF patients. A total of 1391 miRNAs were detected, of which 228 miRNAs and 261 miRNAs were commonly expressed in the HF and non-HF groups, respectively. Eight miRNAs (hsa-let-7b-3p, hsa-miR-92b-5p, hsa-miR-145-3p, hsa-miR-206, hsa-miR-664a-5p, hsa-miR-1307-5p, hsa-miR-1908-5p, and hsa-miR-3074-5p) were found to be dysregulated between HF and non-HF patients. The expression of another seven miRNAs (hsa-miR-589-5p, hsa-miR-30b-5p, hsa-miR-654-3p, hsa-miR-1292-5p, hsa-miR-659-5p, hsa-miR-548d-5p, and hsa-miR-7847-3p) was frequently observed in HF patients but not in non-HF cases. Subsequent analyses of target gene prediction and associated pathways revealed the enrichment of pathways related to vascular development, the cell cycle, and transcriptional activity. These data reveal the expression profile and the dysregulation of circulating miRNAs in our patients with HF.

Background and Objectives: Shellfish allergies are common in Vietnam. The basophil activation test (BAT) is a powerful tool in the diagnosis of food allergies. We aimed to evaluate the application of BAT to distinguish shrimp allergy in comparison with skin prick test and specific IgE measurement. Materials and Methods: We recruited adult shrimp- or prawn-allergic subjects from the University Medical Center (Vietnam). BAT was performed using the in-house crude extracts for two allergens: black tiger shrimp Penaeus monodon (shrimp) and giant freshwater prawn Macrobrachium rosenbergii (prawn). The percentages of CD63 in response to shrimp and prawn were recorded. The results of skin prick tests (SPT) and the specific IgE (sIgE) levels in response to commercial shrimp/prawn were noted. Receiver operating characteristic (ROC) analysis and area under the curve (AUC) were calculated. Results: Of 43 recruited subjects, 9 (26.5%) subjects had a specific allergy to shrimp, 2 (5.9%) subjects had a specific allergy to prawn, and 23 (67.6%) subjects had both shrimp and prawn allergy. Basophil CD63% was significantly increased in subjects with allergy to shrimp and prawn (p < 0.05% for all). Compared with SPT and sIgE, CD63 expression-based BAT was better in discriminating subjects with allergies to these species from their non-allergic counterparts (AUC/sensitivity/specificity = 0.88/77%/89% for shrimp, and 0.74/88%/77% for prawn, p < 0.05 for all). The addition of SPT and BAT improved the diagnostic power. A positive BAT could help identify shrimp/prawn allergy among cases with negative SPT/sIgE to shrimp/prawn. BAT facilitated the diagnosis of shrimp allergy among prawn-allergic subjects (100% accurate). Conclusions: The BAT test can help predict clinical reactions to shrimp and prawn in allergic patients, and enhance diagnostic accuracy in cases where SPT or specific IgE tests yield negative results.

Tăng sản thượng thận bẩm sinh (TSTTBS) là bệnh di truyền lặn trên nhiễm sắc thể thường do thiếu hụt enzyme 21-hydroxylase. Sự thiếu hụt enzyme 21-hydroxylase xảy ra do các đột biến trên gen CYP21A2. Khoảng 20-25% bệnh nhân TSTTBS mang các đột biến về thay đổi số lượng bản sao như mất đoạn, lặp đoạn hoặc đảo đoạn gen CYP21A2. Nghiên cứu được thực hiện với mục tiêu khảo sát mất đoạn gen CYP21A2 gây bệnh TSTTBS bằng kỹ thuật MLPA. 30 bệnh nhân được chẩn đoán mắc bệnh tăng sản thượng thận bẩm sinh thể thiếu enzyme 21-OH; DNA được tách chiết từ mẫu máu; kỹ thuật MLPA được thực hiện để xác định mất/lặp đoạn gen. Kết quả phát hiện 6 bệnh nhân (20%) đột biến mất đoạn đồng hợp tử và 6 bệnh nhân (20%) có mất đoạn dị hợp tử. Trong các đột biến mất đoạn đồng hợp tử, mất đoạn từ exon 1 đến exon 3 chiếm tỷ lệ cao nhất (50%), thứ hai là mất đoạn từ exon 1 đến exon 7 (33,3%) và còn lại là kiểu gen mất đoạn từ exon 4 đến exon 7 (16,7%).

Congenital adrenal hyperplasia (CAH) is an autosomal recessive disorder usually caused by a deficiency of the enzyme 21-hydroxylase. The deficiency of the enzyme 21-hydroxylase occurs due to mutations in the CYP21A2 gene, of which about 60% of CAH patients carry point mutations in the CYP21A2 gene. The study was carried out with the aim of screening point mutations on CYP21A2 gene using Sanger sequencing technique. 30 patients were diagnosed with congenital adrenal hyperplasia with 21- hydroxylase deficiency was collected; DNA extracted from blood samples was carried out; PCR and Sanger sequencing was performed to identify mutations. Results: 11 patients carry genetic mutations that cause CAH were found, including 10 patients with the salt-wasting phenotype and 1 patient with the simple virilization phenotype. The most common mutation is I2G (16.7%), followed by p.R356W (5%) and p.R426C (5%), the remaining mutations range from 1.7% - 3%. Tăng sản thượng thận bẩm sinh (TSTTBS) là bệnh di truyền lặn trên nhiễm sắc thể thường do thiếu hụt enzyme 21-hydroxylase. Sự thiếu hụt enzyme 21-hydroxylase xảy ra do các đột biến trên gen CYP21A2, trong đó khoảng 60% bệnh nhân TSTTBS mang các đột biến điểm trên gen CYP21A2. Nghiên cứu được thực hiện với mục tiêu khảo sát đột biến điểm trên gen CYP21A2 bằng kỹ thuật giải trình tự Sanger. 30 bệnh nhân được chẩn đoán mắc bệnh tăng sản thượng thận bẩm sinh thể thiếu enzyme 21-OH; DNA được tách chiết từ mẫu máu; kỹ thuật PCR và giải trình tự Sanger được thực hiện để xác định đột biến điểm. Kết quả nghiên cứu phát hiện 11 bệnh nhân mang đột biến gen gây bệnh TSTTBS, trong đó 10 bệnh nhân mang kiểu hình mất muối và 1 bẹnh nhân mang kiểu hình nam hóa đơn thuần. Đột biến phổ biến nhất là I2G (16,7%), theo sau là p.R356W (5%) và p.R426C (5%), các đột biến còn lại chiếm tỉ lệ từ 1,7% - 3%.