In late 2019, the emergence of a novel coronavirus led to its identification as SARS-CoV-2, precipitating the onset of the COVID-19 pandemic. Many experimental and computational studies were performed on SARS-CoV-2 to understand its behavior and patterns. In this research, Molecular Dynamic (MD) simulation is utilized to compare the behaviors of SARS-CoV-2 and its Variants of Concern (VOC)-Alpha, Beta, Gamma, Delta, and Omicron-with the hACE2 protein. Protein structures from the Protein Data Bank (PDB) were aligned and trimmed for consistency using Chimera, focusing on the receptor-binding domain (RBD) responsible for ACE2 interaction. MD simulations were performed using Visual Molecular Dynamics (VMD) and Nanoscale Molecular Dynamics (NAMD2), and salt bridges and hydrogen bond data were extracted from the results of these simulations. The data extracted from the last 5 ns of the 10 ns simulations were visualized, providing insights into the comparative stability of each variant’s interaction with ACE2. Moreover, electrostatics and hydrophobic protein surfaces were calculated, visualized, and analyzed. Our comprehensive computational results are helpful for drug discovery and future vaccine designs as they provide information regarding the vital amino acids in protein-protein interactions (PPIs). Our analysis reveals that the Original and Omicron variants are the two most structurally similar proteins. The Gamma variant forms the strongest interaction with hACE2 through hydrogen bonds, while Alpha and Delta form the most stable salt bridges; the Omicron is dominated by positive potential in the binding site, which makes it easy to attract the hACE2 receptor; meanwhile, the Original, Beta, Delta, and Omicron variants show varying levels of interaction stability through both hydrogen bonds and salt bridges, indicating that targeted therapeutic agents can disrupt these critical interactions to prevent SARS-CoV-2 infection.

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impairments in social interaction and communication. According to recent research, neuroinflammation may play a role in the pathogenesis of ASD. Curcumin, the active compound in turmeric, has been demonstrated to exhibit neuroprotective, antioxidant, and anti-inflammatory properties. This review summarizes the potential mechanisms by which curcumin may influence the inflammatory pathways implicated in ASD. Curcumin can suppress nuclear factor kappa-light-chain-enhancer of activated B-cell activation, thereby reducing the levels of pro-inflammatory cytokines. In addition, it can protect mitochondrial function, upregulate antioxidant enzymes, scavenge reactive oxygen and nitrogen species, and modulate the gut–brain axis. Animal studies have shown that curcumin can improve sociability, repetitive behaviors, and enhance cognitive function in ASD models. The beneficial effects of curcumin supplementation on autism symptoms have also been documented in several small clinical trials involving children with ASD. Overall, curcumin is a natural compound with the potential to modulate neuroinflammatory pathways implicated in ASD; however, its therapeutic role remains under investigation.