Table 1.
Summary of the antiviral roles of galectins against influenza virus infection.
| Galectin | Antiviral Effects | Target Virus | Ref. |
|---|---|---|---|
| Gal-1 directly binds to the envelope glycoproteins of influenza virus and constrain the viral hemagglutination activity and infectivity. | A/WSN/1933(H1N1) | [28] | |
| Galectin-1 | Recombinant Gal-1 (rGal-1) treatment reduced mice fatality via mediating the expression of cytokines and chemokines. | 2009 influenza A H1N1 subtype (H1N1pdm09) | [25] |
| Gal-1 participated in regulation of cytopathic processes by H1N1pdm09 virus to induce an arrest of the cell cycle at the G0/G1 phase. | H1N1pdm09 | [30] | |
| Gal-1 expression was correlated with the differential susceptibility to H7N9 influenza via extracellular matrix (ECM)-receptor interaction and mitogen-activated protein kinase (MAPK) signaling. | Human H7N9 isolates | [31] | |
| IAVs and S. pneumoniae coinfection induced the secretion of Gal-1 to the epithelial cell surface and further modulated the expression of SOCS1 and RIG1 and activate ERK, AKT, or JAK/STAT1 signaling pathways. | H1N1pdm09 | [42] | |
| Galectin-3 | Aloe-emodin treatment ameliorated influenza H1N1 virus infection via up-regulation of Gal-3 expression to further trigger antiviral genes expression | A/Taiwan/CMUH01/2007(H1N1) | [38] |
| Gal-3 enhances effects of H5N1 promoting host inflammatory response by up-regulating IL-1β via NLRP3. | A/Vietnam/1204/03 | [41] | |
| IAVs and S. pneumoniae coinfection induced the secretion of Gal-3 to the epithelial cell surface and further modulated the expression of SOCS1 and RIG1, and activate ERK, AKT, or JAK/STAT1 signaling pathways. | H1N1pdm09 | [42] | |
| Gal-3 preferred binding to desialylated multivalent glycoligands. | A/PuertoRico/08/1934 (H1N1) | [43] | |
| Galectin-9 | Gal-9 inhibited the infection of IAVs via Gal-9 binding to influenza virus particles to inhibit virus attachment. | A/Puerto Rico/8/34 (H1N1); Aichi/2/68 (H3N2); A/Hong Kong/483/97 (H5N1) | [51] |
| Virus-specific CD8 T cells upregulate Tim-3 expression and Gal-9/Tim-3 interaction induce cell apoptosis after IAV infection from in vitro and ex vivo assays. | HK/×31 (H3N2) A/Puerto Rico/8/34 (H1N1)) | [55] | |
| Influenza virus infection induces plasma Gal-9 expression, suggesting Gal-9 as a possible biomarker for influenza. | Seasonal influenza virus | [56] |