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Open Access Research

Differences in the ability to suppress interferon β production between allele A and allele B NS1 proteins from H10 influenza A viruses

Siamak Zohari12*, Muhammad Munir1, Giorgi Metreveli1, Sándor Belák12 and Mikael Berg1

Author Affiliations

1 Swedish University of Agricultural Sciences (SLU), Department of Biomedical Sciences and Veterinary Public Health, Section of Virology, SLU, Ulls väg 2B, SE-751 89 Uppsala, Sweden

2 Department of Virology, Immunobiology and Parasitology, National Veterinary Institute (SVA), Ulls väg 2B, SE-751 89 Uppsala, Sweden

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Virology Journal 2010, 7:376  doi:10.1186/1743-422X-7-376

Published: 31 December 2010

Abstract

Background

In our previous study concerning the genetic relationship among H10 avian influenza viruses with different pathogenicity in mink (Mustela vison), we found that these differences were related to amino acid variations in the NS1 protein. In this study, we extend our previous work to further investigate the effect of the NS1 from different gene pools on type I IFN promoter activity, the production of IFN-β, as well as the expression of the IFN-β mRNA in response to poly I:C.

Results

Using a model system, we first demonstrated that NS1 from A/mink/Sweden/84 (H10N4) (allele A) could suppress an interferon-stimulated response element (ISRE) reporter system to about 85%. The other NS1 (allele B), from A/chicken/Germany/N/49 (H10N7), was also able to suppress the reporter system, but only to about 20%. The differences in the abilities of the two NS1s from different alleles to suppress the ISRE reporter system were clearly reflected by the protein and mRNA expressions of IFN-β as shown by ELISA and RT-PCR assays.

Conclusions

These studies reveal that different non-structural protein 1 (NS1) of influenza viruses, one from allele A and another from allele B, show different abilities to suppress the type I interferon β expression. It has been hypothesised that some of the differences in the different abilities of the alleles to suppress ISRE were because of the interactions and inhibitions at later stages from the IFN receptor, such as the JAK/STAT pathway. This might reflect the additional effects of the immune evasion potential of different NS1s.