Table 1.
Effects of changes of amino acid sites in NS1 on biological characteristics.
| IAV | NS1 Amino Acid Residue | Biological effects | Impact on infection | Experiment method | Reference |
|---|---|---|---|---|---|
| A/chicken/China/B1-6/2006(H9N2) | X35R X46R |
Losing its RNA silencing suppression activity. | Unreported | In vitro | (Jing et al., 2015) |
| A/swine/Shanghai/3/2014(H1N1) | S42 | Regulating the host IFN response by blocking the activation of IRF3 | Facilitating virus replication | In vitro | (Cheng et al., 2018) |
| A/Duck/Guangxi/12/03(H5N1) | P42S | Preventing the dsRNA-mediated activation of the NF-κB pathway and the IRF-3 pathway | Attenuating virus replication | In vitro | (Jiao et al., 2008) |
| A/chicken/Hunan/1/2009 (H5N1) | K55E/K66E/C133F | Restoring the ability to bind CPSF30 and reduced interferon response activity. | Increasing virus titer and replication efficiency | In vitro | (Li et al., 2018) |
| Recombined A/Puerto Rico/8/34 (H1N1) | I64T | Decreasing general inhibition of host protein synthesis by decreasing its interaction with CPSF30 | Exhibiting an attenuated phenotype | In vivo | (DeDiego et al., 2016) |
| A/Duck/Hubei/2004/L-1(H5N1) | Y84F | Abolishing NS1-mediated downregulation of IFN-inducible STAT phosphorylation, and surface IFNAR1 expression | Reducing lung viral titers and increased lung ISG expression | In vivo | (Wang et al., 2017) |
| A/Hong Kong/156/97(H5N1) | D92E | Activating phosphorylation of NS1 | Unreported | In silico | (Li and Wang, 2007) |
| A/quail/Hong Kong/G1/97(H9N2) | L103F/I106M/P114/G125D/N139D | Restoring CPSF30 binding capacity and inhibiting host gene expression | Unreported | In vitro | (Rodriguez et al., 2018) |
| A/Hong Kong/156/1997(H5N1) | F103L M106I |
Increasing the ability of IFN antagonism, altering RIG-I and CPSF30 host factor binding ability | Increasing viral replication in mouse lungs | In vivo | (Dankar et al., 2013) |
| A/Hong Kong/1/68(H3N2) | F103L M106I |
Increasing tropism and virulence in mouse lungs | In vivo | (Dankar et al., 2011) | |
| Recombined A/Shanghai/1/2013 (H7N9) | I106M | Restoring the ability of CPSF30 binding and that of block host gene expression | Showing enhanced replication and virulence | In vivo | (Ayllon et al., 2014) |
| Recombined A/Puerto Rico/8/34 (H1N1) | A171Y | Decreasing expression of IFN and ISGs | Unknown | In vitro | (Plant et al., 2017) |
| A/Udorn/72(H1N1) | G184R | An unknown mechanism independent of overactivation of the host IFN response or to enhanced sensitivity of these viruses to the antiviral effect of PKR | Remarkable attenuation of virulence | In vivo | (Steidle et al., 2010) |
| A/canine/NY/dog23/2009(H3N8) | K186E | Introducing both the NS1-CPSF30 interaction and ISGs gene expression inhibition | Unreported | In vitro | (Nogales et al., 2017) (Chauché et al., 2018) |
| Recombined A/Puerto Rico/8/34 (H1N1) | D189N | Impairing the ability of the NS1 protein to inhibit general gene expression | Attenuating virulence |
In vitro
In vivo |
(Nogales et al., 2017) |
| V194I | Demonstrating a temperature-sensitive phenotype | Attenuating virulence more than D189N |