4.7 Article

Inactivation of influenza A virus via exposure to silver nanoparticle-decorated silica hybrid composites

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 25, Issue 27, Pages 27021-27030

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-018-2620-z

Keywords

Silver nanoparticle; Silica hybrid composite; Influenza A virus; Antiviral agent; Disinfection; Virus inactivation

Funding

  1. National Research Foundation of Korea (NRF) grant - Korean government (MSIP) [2013-069335]
  2. Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, Forestry, and Fisheries (IPET) through a High Value-added Food Technology Development Program - Ministry of Agriculture, Food, and Rural Affair (MAFRA) [315067-3]

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Influenza A virus (IFV-A) is one of the main cause of seasonal flu and can infect various of host species via the reassortment of segmented RNA genomes. Silver nanoparticles (AgNPs) have been known as excellent antiviral agent against IFV. However, the use of free AgNPs has several major drawbacks, including the inherent aggregation among AgNPs and unwanted cytotoxic or genotoxic damages for human body via inhalation or ingestion. In this study, we assessed the efficacy of our novel 30-nm-diameter AgNP-decorated silica hybrid composite (Ag30-SiO2; 400 nm in diameter) for IFV-A inactivation. Ag30-SiO2 particles can inhibit IFV-A effectively in a clear dose-dependent manner. However, when real-time RT-PCR assay was used, merely 0.5-log(10) reduction of IFV-A was observed at both 5 and 20 A degrees C. Moreover, even after 1 h of exposure to Ag30-SiO2 particles, more than 80% of hemagglutinin (HA) damage and 20% of neuraminidase (NA) activities had occurred, and the infection of Madin-Darby Canine Kidney (MDCK) cells by IFV-A was reduced. The results suggested that the major antiviral mechanism of Ag30-SiO2 particles is the interaction with viral components located at the membrane. Therefore, Ag30-SiO2 particles can cause nonspecific damage to various IFV-A components and be used as an effective method for inactivating IFV-A.

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