No abstract

Human SARS-CoV-2 and avian infectious bronchitis virus (IBV) are highly contagious and deadly coronaviruses, causing devastating respiratory diseases in humans and chickens. The lack of effective therapeutics exacerbates the impact of outbreaks associated with SARS-CoV-2 and IBV infections. Thus, novel drugs or therapeutic agents are highly in demand for controlling viral transmission and disease progression. Mesenchymal stem cells (MSC) secreted factors (secretome) are safe and efficient alternatives to stem cells in MSC-based therapies. This study aimed to investigate the antiviral potentials of human Wharton’s jelly MSC secretome (hWJ-MSC-S) against SARS-CoV-2 and IBV infections in vitro and in ovo. The half-maximal inhibitory concentrations (IC50), cytotoxic concentration (CC50), and selective index (SI) values of hWJ-MSC-S were determined using Vero-E6 cells. The virucidal, anti-adsorption, and anti-replication antiviral mechanisms of hWJ-MSC-S were evaluated. The hWJ-MSC-S significantly inhibited infection of SARS-CoV-2 and IBV, without affecting the viability of cells and embryos. Interestingly, hWJ-MSC-S reduced viral infection by >90%, in vitro. The IC50 and SI of hWJ-MSC secretome against SARS-CoV-2 were 166.6 and 235.29 µg/mL, respectively, while for IBV, IC50 and SI were 439.9 and 89.11 µg/mL, respectively. The virucidal and anti-replication antiviral effects of hWJ-MSC-S were very prominent compared to the anti-adsorption effect. In the in ovo model, hWJ-MSC-S reduced IBV titer by >99%. Liquid chromatography-tandem mass spectrometry (LC/MS-MS) analysis of hWJ-MSC-S revealed a significant enrichment of immunomodulatory and antiviral proteins. Collectively, our results not only uncovered the antiviral potency of hWJ-MSC-S against SARS-CoV-2 and IBV, but also described the mechanism by which hWJ-MSC-S inhibits viral infection. These findings indicate that hWJ-MSC-S could be utilized in future pre-clinical and clinical studies to develop effective therapeutic approaches against human COVID-19 and avian IB respiratory diseases.

Several studies were performed to evaluate the degree of liver fibrosis by non-invasive markers. We aimed to assess the diagnostic value of both biglycan (BGN) and osteopontin (OPN) as non-invasive markers of hepatic fibrosis in patients with chronic hepatitis B (CHB) and chronic hepatitis C (CHC). This study was performed on 100 patients with CHB virus, 100 patients with CHC virus and 100 normal controls. All participants were subjected to the following laboratory tests: hemoglobin, platelet, alanine aminotransferase, aspartate aminotransferase, albumin, international normalized ratio, HBs Ag, hepatitis C virus (HCV) antibody, hepatitis B virus DNA, HCV RNA, liver biopsy, BGN and OPN. We found that BGN level was significantly increased in the CHB group compared with the controls (p<0.001), but the level was not different between the CHC group and the controls (p<0.96). OPN was increased in both the CHB and CHC groups compared with the controls (p<0.001). Positive correlation was found between fibrosis stages and BGN level of the CHB group (r=0.64; p<0.001) and between fibrosis stages and OPN level of the CHB (r=0.63; p<0.001) and CHC (r=0.59; p<0.03) groups. The area under the curve (AUC), sensitivity and specificity of BGN were 1.0, 100% and 100% in predicting fibrosis in patients with CHB, and 0.50, 26% and 78% in predicting fibrosis in patients with CHC. OPN had an AUC of 0.997, sensitivity of 96% and specificity of 100% in predicting fibrosis in patients with CHB, and 0.974, 96.5% and 100% in predicting fibrosis in patients with CHC. In conclusion, BGN and OPN could be considered non-invasive markers for liver fibrosis assessment.

The aim of this study is to assess the level of myeloid-derived suppressor cells (MDSCs) and the expression of costimulatory molecules CD80 and CD86 on monocytes and their ligands (CD28) on T-lymphocytes in children with allergic rhinitis (AR). Methods: The study included 60 children with AR and 50 controls. Flow cytometry was performed to analyze MDSCs and the expression of costimulatory molecules CD80 and CD86 on monocytes and their ligands (CD28) on T-lymphocytes. Results: The percentages of total and monocytic MDSCs and the expression of costimulatory molecule CD86 on monocytes were significantly higher in children with AR than in healthy controls. In addition, the expressions of CD28 on CD4 + and CD8 + were significantly elevated in AR patients. Conclusion: The present study demonstrated that the percentages of MDSCs were significantly elevated in AR children. Moreover, the expressions of CD28 on CD4 + and CD8 + were significantly higher in children with AR.

Background Alopecia areata (AA) is a common inflammatory disorder targeting the hair follicles leading to non-scaring hair loss. The pathogenesis of AA is still unclear, despite the accumulating evidence of the immune-mediated nature of this disease. So, in this study, we aimed to assess the level of CD4 T cells, CD8 T cells and natural killer (NK) cells in the peripheral blood of patients with active AA and control subjects, and to evaluate the association between the level of those cells and the duration of disease in different subtypes of AA. Results Fifty female patients and 50 age- and sex-matched healthy controls were enrolled in this case control study. CBC analysis and the level of CD4, CD8 T cells and NK cells were evaluated during the active stage of the disease. We found that CD4, CD8 T cells and NK cells proportion was significantly lower (P < 0.05) in patients with active stage AA compared with healthy subjects, however, the ratio of CD4:CD8 T cells was significantly higher in patients than control subjects. The level of CD4, CD8 T cells CD56 bright CD16− % NK cells were positively correlated with the disease duration. Conclusion Active stage of AA disease is associated with a reduction of the circulating CD4, CD8 T cells and NK cells and an increase in CD4/CD8 T cells ratio, however, the level of those cells were higher with prolonged disease duration. Our findings confirm that immune mechanisms are involved in the pathogenesis of AA.