Nipah virus (NiV) is an emerging zoonotic pathogen, reported for the recent severe outbreaks of encephalitis and respiratory illness in humans and animals, respectively. Many antiviral drugs have been discovered to inhibit this pathogen, but none of them were that much efficient. To overcome the complications associated with this severe pathogenic virus, we have designed a multi-epitope subunit vaccine using computational immunology strategies. Identification of structural and nonstructural proteins of Nipah virus assisted in the vaccine designing. The selected proteins are known to be involved in the survival of the virus. The antigenic binders (B-cell, HTL, and CTL) from the selected proteins were prognosticated. These antigenic binders will be able to generate the humoral as well as cell-mediated immunity. All the epitopes were united with the help of suitable linkers and with an adjuvant at the N-terminal of the vaccine, for the enhancement of immunogenicity. The physiological characterization, along with antigenicity and allergenicity of the designed vaccine candidates, was estimated. The 3D structure prediction and its validation were performed. The validated vaccine model was then docked and simulated with the TLR-3 receptor to check the stability of the docked complex. This next-generation approach will provide a new vision for the development of a high immunogenic vaccine against the NiV.

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In medical mycology, epigenetic mechanisms are emerging as key regulators of multiple aspects of fungal biology ranging from development, phenotypic and morphological plasticity to antifungal drug resistance. Emerging resistance to the limited therapeutic options for the treatment of invasive fungal infections is a growing concern. Human fungal pathogens develop drug resistance via multiple mechanisms, with recent studies highlighting the role of epigenetic changes involving the acetylation and methylation of histones, remodeling of chromatin and heterochromatin-based gene silencing, in the acquisition of antifungal resistance. A comprehensive understanding of how pathogens acquire drug resistance will aid the development of new antifungal therapies as well as increase the efficacy of current antifungals by blocking common drug-resistance mechanisms. In this article, we describe the epigenetic mechanisms that affect resistance towards widely used systemic antifungal drugs: azoles, echinocandins and polyenes. Additionally, we review the literature on the possible links between DNA mismatch repair, gene silencing and drug-resistance mechanisms.

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Type 2 Diabetic retinopath (T2DR) remains the leading cause of vision loss and preventable blindness in adults aged 20–74 years, particularly in middle-income and high-income countries. The pathogenesis of T2DR is a predominant cause of visual impairment and a range of hyperglycemia linked pathways have been implicated in the initiation and progression of this condition. Apparently in the past T2DR was solely considered a vascular disease as opposed to the present time where it is recognised as a neuro-vascular disease. Some pro-survival neurotrophins such as brain derived neurotrophic factor (BDNF) are considered to guard retinal ganglion and amacrine cells from degenerative. Significant reduction in the levels of BDNF have been witnessed in diabetic patients as well as animal models. miRNAs are a group of 21-23 nucleotide long, highly conserved sequences of endogenous RNAs that do not encode for any protein. Researches carried out over the last decade gives plenty of proof about the miR-15a importance in T2DR. Henceforth, miR15a could be used for the experimental purposes. miRNAs can be considered as an efficient biomarker as they maintain their stability and utility over rigorous processing phases and the presence of quantitative detection boosts their therapeutical significance. Keywords: Type 2 Diabetic Retinopathy, Neurodegeneration, BDNF, Prognosis, Biomarker, miR-15a, Bioinformatics