Beta-sitosterol (BS) is a phytosterol, widely distributed throughout the plant kingdom and known to be involved in the stabilization of cell membranes. To compile the sources, physical and chemical properties, spectral and chromatographic analytical methods, synthesis, systemic effects, pharmacokinetics, therapeutic potentials, toxicity, drug delivery and finally, to suggest future research with BS, classical as well as on-line literature were studied. Classical literature includes classical books on ethnomedicine and phytochemistry, and the electronic search included Pubmed, SciFinder, Scopus, the Web of Science, Google Scholar, and others. BS could be obtained from different plants, but the total biosynthetic pathway, as well as its exact physiological and structural function in plants, have not been fully understood. Different pharmacological effects have been studied, but most of the mechanisms of action have not been studied in detail. Clinical trials with BS have shown beneficial effects in different diseases, but long-term study results are not available. These have contributed to its current status as an “orphan phytosterol”. Therefore, extensive research regarding its effect at cellular and molecular level in humans as well as addressing the claims made by commercial manufacturers such as the cholesterol lowering ability, immunological activity etc. are highly recommended.

SummaryActivation of the alpha7 receptor (a7nAChR) has been shown to be important in inflammation and immune regulation, and is also essential in the neural cholinergic anti-inflammatory pathway. The aim of this study was to investigate the role of a7nAChR in the development of experimental arthritis and immune activation. Mice lacking the a7nAChR were immunized with collagen II and the development of arthritis was assessed. Another group of a7nAChR-deficient mice was immunized with ovalbumin, spleen and lymph node cells were isolated and the proliferative responses to restimulation with ovalbumin or concanavalin A were investigated. We could demonstrate significantly milder arthritis and less cartilage destruction, together with a decrease of T cell content in lymph nodes in mice lacking the a7nAChR compared to wild-type controls. In addition, mice lacking the a7nAChR had a deficient proliferative response to concanavalin A, whereas antigen presentation-dependent proliferation was not affected. These results indicate important roles for a7nAChR in arthritis development as well as in regulation of T cell-dependent immunological mechanisms. In addition, the data implicate a7nAChR as a therapeutic target for modulation of adaptive immune responses.

Nipah virus (NiV) is highly pathogenic single-stranded negative sense RNA virus. It can cause severe encephalitis and respiratory disease in humans. In addition, NiV infects a large range of host including mammals. As a result of its higher zoonotic potential and pathogenicity for human, it has been rated as an alert in recent days. A therapeutic treatment or vaccines has become elusive to fight against this virus. In this study, the attachment (G) and fusion (F) glycoproteins of NiV, responsible for the viral attachment and entry to the host cell, were selected to develop epitope-based vaccine against Nipah virus. Epitopes were identified from the conserved region of G and F protein of NiV. Both B-cell and T-cell immunity were checked to affirm it that these epitopes will be able to induce humoral and cellular immunity. A total of 6 T-cell epitopes and 19 significant HLA-epitope interactions were identified. Eventually it has shown an acceptable percentage in population coverage (46.45 %) and efficient binding with HLA molecule by molecular docking study.

A major challenge in evaluating the success of HIV eradication approaches is the need for accurate measurement of persistent HIV during effective antiretroviral therapy (ART). Previous studies have reported that the anti-HIV antibody assay “luciferase immuno-precipitation systems (LIPS)” can distinguish HIV-infected individuals harboring different sizes of the viral reservoirs. We performed antibody profiling of HIV-1 proteomes using LIPS in viremic progressors (n = 38), elite controllers (ECs; n = 19) and patients with fully suppressive long-term antiretroviral therapy (ART) (n = 19) (mean 17 years). IgG was quantified against six HIV-1 fusion proteins: p24, gp41, RT, Tat, integrase and protease. Lower antibody levels to all six-fusion proteins were observed in long-term ART patients compared to viremics (p < 0.05). In contrast ECs had lower antibody levels only against Tat and Integrase (p < 0.05). Principal component analysis and cluster-network analysis identified that 68% (13/19) of the long-term ART patients clustered together with 26% (5/19) ECs. The remaining ECs clustered together with the viremics indicating non-homogeneity among the ECs. The low anti-HIV levels in the long-term treated patients may indicate a restricted remaining viral replication. In contrast, the higher levels in ECs suggest a continuous viral expression with a limited concomitant release of extracellular virus.