Background: Newcastle disease virus (NDV) is a highly contagious and economically devastating pathogen affecting poultry worldwide, leading to significant losses in the poultry industry. Despite existing vaccines, outbreaks continue to occur, highlighting the need for more effective vaccination strategies. Developing a multi-epitopic peptide vaccine offers a promising approach to enhance protection against NDV. Objectives: Here, we aimed to design and evaluate a multi-epitopic vaccine against NDV using molecular dynamics (MD) simulation. Methodology: We retrieved NDV sequences for the fusion (F) protein and hemagglutinin–neuraminidase (HN) protein. Subsequently, B-cell and T-cell epitopes were predicted. The top potential epitopes were utilized to design the vaccine construct, which was subsequently docked against chicken TLR4 and MHC1 receptors to assess the immunological response. The resulting docked complex underwent a 1 microsecond (1000 ns) MD simulation. For experimental evaluation, the vaccine’s efficacy was assessed in mice and chickens using a controlled study design, where animals were randomly divided into groups receiving either a local ND vaccine or the peptide vaccine or a control treatment. Results: The 40 amino acid peptide vaccine demonstrated strong binding affinity and stability within the TLR4 and MHC1 receptor–peptide complexes. The root mean square deviation of peptide vaccine and TLR4 receptor showed rapid stabilization after an initial repositioning. The root mean square fluctuation revealed relatively low fluctuations (below 3 Å) for the TLR4 receptor, while the peptide exhibited higher fluctuations. The overall binding energy of the peptide vaccine with TLR4 and MHC1 receptors amounted to −15.7 kcal·mol⁻¹ and −36.8 kcal·mol⁻¹, respectively. For experimental evaluations in mice and chicken, the peptide vaccine was synthesized using services of GeneScript Biotech^® (Singapore) PTE Limited. Experimental evaluations showed a significant immune response in both mice and chickens, with the vaccine eliciting robust antibody production, as evidenced by increasing HI titers over time. Statistical analysis was performed using an independent t-test with Type-II error to compare the groups, calculating the p-values to determine the significance of the immune response between different groups. Conclusions: Multi-epitopic peptide vaccine has demonstrated a good immunological response in natural hosts.

Introduction: Tuberculosis is a chronic debilitating infectious disease causing a severe challenge to public health, especially in developing countries. The aim of this study was to examine genetic diversity in Mycobacterium tuberculosis strains circulating in the Balochistan region of Pakistan. Methodology: One hundred isolates collected from patients visiting the Fatima Jinnah TB Hospital in Quetta were subjected to genotype analysis by spoligotyping. Results: Three main genotypes were identified: Central Asian Strain 1 (CAS1) (n = 89), East African Indian (EAI) strain (n = 7) and Latin American Mediterranean (LAM) strain (n = 3). The CAS1 clade (ST 26) had high genetic diversity represented by seven different spoligopatterns, of which one had major predominace (n = 75). Conclusions: This is the first insight into the genotype of M. tuberculosis strains in the Balochistan region that might serve as a base line study for control of tuberculosis in the community.

Rheumatoid arthritis (RA) is a chronic inflammatory disorder affecting joints, characterized by pain, stiffness, and limited mobility. Through a meticulous evaluation of recent studies, this review explores emerging molecular and cellular mechanisms underlying RA pathogenesis. Although RA is idiopathic, several factors such as environmental influences, diet, the microbiome, gut microbiota, and genetic variations play a significant role in its pathogenesis. The involvement of various genetic factors, including HLA alleles and specific SNPs in genes such as PADI4, REL, RUNX1, FCGR2A, and CD40, has been identified in RA susceptibility. Additionally, the dysregulation of various genetic molecules, such as lncRNAs and miRNAs and proteins including IL-1 and CD28 contributes to inflammation and disease progression. Understanding the disease causing molecular and cellular mechanisms helps to identify therapeutic targets and guide personalized treatment strategies for RA.