ABSTRACT
The adsorption of viruses from aqueous solution is frequently performed to detect viruses. Charged filtration materials capture viruses via electrostatic interactions, but lack the specificity of biological virus-binding substances like heparin. Herein, we present three methods to immobilize heparin-mimicking, virus-binding polymers to a filter material. Two mussel-inspired approaches are used, based on dopamine or mussel-inspired dendritic polyglycerol, and post-functionalized with a block-copolymer consisting of linear polyglycerol sulfate and amino groups as anchor (lPGS-b-NH2). As third method, a polymer coating based on lPGS with benzophenone anchor groups is tested (lPGS-b-BPh). All three methods yield dense and stable coatings. A positively charged dye serves as a tool to quantitatively analyze the sulfate content on coated fleece. Especially lPGS-b-BPh is shown to be a dense polymer brush coating with about 0.1 polymer chains per nm2. Proteins adsorb to the lPGS coated materials depending on their charge, as shown for lysozyme and human serum albumin. Finally, herpes simplex virus type 1 (HSV-1) and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) can be removed from solution upon incubation with coated fleece materials by about 90% and 45%, respectively. In summary, the presented techniques may be a useful tool to collect viruses from aqueous environments. © 2022 The Authors. Journal of Applied Polymer Science published by Wiley Periodicals LLC.
ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a highly contagious respiratory disease referred to as COVID-19. However, emerging evidence indicates that a small but growing number of COVID-19 patients also manifest neurological symptoms, suggesting that SARS-CoV-2 may infect the nervous system under some circumstances. SARS-CoV-2 primarily enters the body through the epithelial lining of the respiratory and gastrointestinal tracts, but under certain conditions this pleiotropic virus may also infect peripheral nerves and gain entry into the central nervous system (CNS). The brain is shielded by various anatomical and physiological barriers, most notably the blood-brain barrier (BBB) which functions to prevent harmful substances, including pathogens and pro-inflammatory mediators, from entering the brain. The BBB is composed of highly specialized endothelial cells, pericytes, mast cells and astrocytes that form the neurovascular unit, which regulates BBB permeability and maintains the integrity of the CNS. In this review, potential routes of viral entry and the possible mechanisms utilized by SARS-CoV-2 to penetrate the CNS, either by disrupting the BBB or infecting the peripheral nerves and using the neuronal network to initiate neuroinflammation, are briefly discussed. Furthermore, the long-term effects of SARS-CoV-2 infection on the brain and in the progression of neurodegenerative diseases known to be associated with other human coronaviruses are considered. Although the mechanisms of SARS-CoV-2 entry into the CNS and neurovirulence are currently unknown, the potential pathways described here might pave the way for future research in this area and enable the development of better therapeutic strategies.