Newly identified beta-coronavirus i.e. the 2019 novel coronavirus is associated with a contagious transmittable respiratory disease called COVID-19. This disease has been declared as a “pandemic” by the World Health Organization (WHO). The entry of coronavirus in the human respiratory epithelial cells depends upon the interaction between host cell receptor ACE2 and viral S-glycoprotein. However, this type of molecular recognition in between cell surface receptors and envelope glycoproteins are mediated by specific glycan epitopes and attribute to viral entry through membrane fusion. Glycans are essential biomolecules made by all living organisms, have roles in serving structure, energy storage, and system regulatory purposes. The glycan shield plays a crucial role in concealing the surface S protein from molecular recognition. The immunomodulatory properties of Glycan-binding proteins (GBPs) like Lectins, build them as an attractive candidates for vaccine adjuvant. Investigations involving the complement system activation by the lectin pathway in COVID-19 and diseases are in need of the hour. The innate immune response involving complement system could have varied biological effects against an array of microbial infections. The advances in glycoprotein style methods especially immunomodulatory action of some lectins are necessary to boost the effectiveness of treatment of COVID-19 and other pandemics.
Part of the book: Biotechnology to Combat COVID-19
In the COVID-19 pandemic, neurological complications have emerged as a significant cause of morbidity and mortality. A wide range of neurological manifestations ranging from cognitive or memory disturbances, headache, loss of smell or taste, confusion, and disabling strokes have been reported during and post COVID conditions. The COVID-19 virus can utilize two possible pathways for invasion into the brain, either through retrograde axonal transport (olfactory route) or by crossing the blood-brain barrier (BBB). Furthermore, the production of SARS-CoV-2-associated cytokines, such as interleukin (IL)-6, IL-17, IL-1b, and tumor necrosis factor (TNF), is able to disrupt the BBB. The neuroinvasive nature of SARS-CoV-2 has a more severe impact on patients with preexisting neurological manifestations such as Parkinson’s disease (PD). Pathological features of PD include selective loss of dopaminergic neurons in the substantia nigra pars compacta and aggregation of α-syn proteins present in neurons. Interaction between SARS-COV-2 infection and α-synuclein might have long-term implications on the onset of Parkinsonism by the formation of toxic protein clumps called amyloid fibrils—a hallmark of Parkinson’s. Molecular modeling is an emerging tool to predict potential inhibitors against the enzyme α-synuclein in neurodegenerative diseases by using plant bioactive molecules.
Part of the book: COVID-19 Pandemic, Mental Health and Neuroscience