Because of the high mutation rates of the viral genome, vaccines and drugs
initially directed against the virus often become ineffective [3, 4]. Therefore, measures are urgently needed to prevent and treat influenza virus infections, especially for high-risk groups and in the event of another pandemic. Certain host cell factors involved in the viral infection cycle have attracted interest as therapeutic targets because these are crucial for viral infections. Targeting these HDAC inhibitor factors might inhibit infection, and there is the added advantage that they are less prone to mutations [5–7]. Sialic acid (SA) molecules, found at the non-reducing terminal position of glycoproteins or glycolipids on the surface of cells, are binding targets for influenza A virus (IAV) hemagglutinin (HAs) . The HAs of human IAVs preferentially bind to α-2,6 linked SA, which is abundantly expressed in the human respiratory tract. The HA proteins of avian IAVs prefer α-2,3 linked SA as a receptor, as it HSP990 is predominant in the avian enteric tract . The binding of HA to its appropriate receptor is crucial for the initiation of infection and therefore serves as a potential therapeutic target. The novel sialidase fusion protein, DAS181 (Fludase), enzymatically removes SAs from the respiratory epithelium and exhibits potent antiviral see more activity against influenza A and B viruses
. Sialyltransferases Tenoxicam are key enzymes that regulate the biosynthesis of sialylated oligosaccharide sequences . Weinstein et al. concluded that one enzyme, βgalactoside α2,6sialyltransferase I (ST6Gal I), encoded by ST6GAL1, was responsible for the addition of α-2,6 SAs to the Galβ1-4GlcNAc disaccharide found on the glycans of N-linked and some O-linked glycoproteins . Lin et al.
found that antisense-oligodeoxynucleotides targeting ST6GAL1 mRNAs could inhibit the enzymatic activity of ST6Gal I, and reduced 2,6-sialylation at the cell surface [13, 14]. Numerous studies involving small interfering RNAs (siRNAs) in the treatment of viral infections have been conducted [15–17], including our successful application of siRNAs to treat severe acute respiratory syndrome (SARS)-infected rhesus macaques . Qe et al. used siRNAs specific for conserved regions of the influenza virus genome; these proved to be potent inhibitors of influenza virus replication in vitro and in vivo[19, 20]. However, siRNAs solely targeting the genes of influenza viruses are unlikely to be sufficient in eliminating infection because there is a high possibility of generating resistant mutants. Therefore siRNAs targeting host cellular determinants crucial for viral entry and/or replication could be a more efficacious antiviral therapy. Our study was designed to evaluate siRNAs targeting ST6GAL1 in airway epithelial cells.