ABSTRACT
Over the last 10 years, the antiviral and antimicrobial activities of non-functionalised inorganic nanoparticles against different pathogens were experimentally shown. This effect has attracted the attention of scientists due to the COVID-19 pandemic;however, its mechanism is still unclear. For understanding the mechanism of nanoparticle’s action, it is important to know how this action depends on the parameters of nanoparticles and the properties of a pathogen. In the work, we have studied the action of gold nanoparticles on the viruses outside and inside the cell and compared this action with two sizes of nanoparticles and two types of viruses. The study has been conducted for adenovirus and H1N1 influenza virus, and gold nanoparticles of 5 nm and 20 nm diameter. Virucidal and antiviral actions were observed experimentally for both sizes of nanoparticles against both viruses. It has also been shown with the electron microscopy that the viruses may be destructed in 2 h after adsorption of 5 nm gold nanoparticles on their surface;and that the viruses may change their shape in 2 h after adsorption of 20 nm nanoparticles on their surface. The model of physical adsorption of nanoparticles on the virus surface due to near-field interaction was used to explain observed results.
ABSTRACT
OBJECTIVE: Both COVID-19 and influenza are viral respiratory tract infections and the epidemics of viral respiratory tract infections remain highly prevalent with lethal consequences in susceptible individuals. Expression of ICAM-1 on vascular endothelium recruits leukocytes which initiates inflammation. IL-6 induces ICAM-1. Both ICAM-1 and IL-6 can be enhanced in influenza virus infection and COVID-19 patients. Besides initiation of virus entry host cells, whether HA alone, instead of whole virus, of influenza has the effects on expression of ICAM-1 and IL-6 in vascular endothelium with injury in the lungs, remains to be demonstrated. METHODS: RT-qPCR and Western blot as well as histopathologic examination were used to examine mRNA and protein of ICAM-1 and IL-6 as well as pathological injury in the lung tissues, respectively. RESULTS: After incubation of the Human Umbilical Vein Endothelial Cells (HUVECs) with HA of H1N1 for 24 h, the mRNA and protein of ICAM-1 and IL-6 in HUVECs were increased in group of 5 µg/ml concentration with statistical significance (p < 0.05). Pathological injury in lung tissues of the mice was shown 12 h after tail intravenous injection with 100 µl of HA (50 µg/ml and 100 µg/ml in normal saline), including widened alveolar spaces with angiotelectasis in alveolar wall, alveolar luminal and interstitial inflammatory infiltrates, alveolar luminal erythrocyte effusion. CONCLUSIONS: HA alone, instead of whole H1N1 virus, induced more expression of ICAM-1 and IL-6, two molecules involving in pathological and inflammatory responses, in HUVECs and pathological injury in lung tissues of the mice. This knowledge provides a new HA-targeted potential direction for prevention and treatment of disease related to H1N1 infection.