Thus releasing nucleocapsids to allow trafficking into the cell nucleus where the expression of baculoviral genes takes place

Under physiological conditions and they are capable of absorbing water, which is essential for optimal wound healing. The previously reported strong photobactericidal effect of O2-producing nanofiber materials led us to test a similar approach for the photoinactivation of viruses. We used polyomaviruses as models for non-enveloped viruses and baculoviruses as models for enveloped viruses. The capsid proteins of non-enveloped viruses and the envelope glycoproteins encoded by enveloped viruses enable the viruses to cross plasma membranes into cells and deliver their genetic material to the cell nucleus, resulting in viral gene expression. These proteins are responsible for cell surface receptor recognition and for subsequent interactions with cellular structures, leading to the disassembly of virus particles and the release of genetic information. Therefore, oxidative damage to virion surface proteins via photooxidation of readily oxidizable amino acids by O2 may be an effective way to prevent infection. Polyomaviruses, small tumorogenic non-enveloped DNA viruses, have a wide range of hosts, including humans. Two human polyomaviruses, JCV and BKV, which were discovered in 1971, cause progressive multifocal leukoencephalopathy and nephropathy, respectively, in immunosuppressed patients. Since 2007, six new human polyomaviruses have been identified. Merkel cell polyomavirus, which was described in 2008, is suspected to cause the majority of the cases of Merkel cell carcinoma, a rare but aggressive form of human skin cancer. Baculoviruses, which are large enveloped DNA viruses, are insect pathogens that have been widely used to produce recombinant proteins in cultured insect cells. Baculovirus envelope proteins are also able to mediate entry into human and other mammalian cells and, thus, facilitate the expression of recombinant genes under the transcriptional control of a mammalian promoter. The Autographa californica multiple nuclear polyhedrosis virus, which was used in our experiments, enters cells via a low pH-dependent CPI-613 endocytic pathway. During endocytosis, the major envelope glycoprotein GP64 mediates low pH-triggered membrane fusion. Singlet oxygen generated in close proximity to living eukaryotic or bacterial cells has been shown to have strong cytotoxic effects. It is well established that the main targets of O2 are cytoplasmic membrane proteins. Integrated proteins that cross the lipid bilayer and peripheral proteins associated with the cell surface have important, often indispensable physiological functions, and damaging these proteins quickly leads to cell death. Exposure of proteins to O2 can result in oxidation of side-chains, formation of crosslinked/aggregated species, protein unfolding or conformational changes. Aromatic amino acids and sulphur-containing amino acids are direct targets of O2. Other O2 targets include unsaturated lipids in the cytoplasmic membrane, which can be oxidized to form lipid hydroperoxides. Oxidation of cholesterol by O2 results in the formation of a number of readily distinguishable oxidation products, especially hydroperoxides. Enveloped viruses possess a lipid bilayer envelope derived from cellular membranes and embedded with viral proteins. These viral surface proteins are often glycosylated and play a crucial role in cell receptor recognition and viral entry into host cells. Therefore, enveloped viruses might be affected by O2 in a manner similar to bacterial and animal cells. Indeed, we showed that the baculoviruses, as representative enveloped viruses, were efficiently inactivated when applied to the surface of the nanofiber textiles doped with 1% TPP and exposed to visible light for 30 minutes. Similar effects may also be expected for other enveloped viruses.

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