tetano
Editor, Senior Moderator
J Gen Virol. 2014 Oct 17. pii: vir.0.071001-0. doi: 10.1099/vir.0.071001-0. [Epub ahead of print]
The C-terminal elongation of NS1 of H9N2 influenza virus induces a high level of inflammatory cytokines and increases transmission.
Kong W1, Liu L1, Wang Y1, He Q1, Wu S1, Qin Z1, Wang J1, Sun H1, Sun Y1, Zhang R1, Pu J1, Liu J2.
Author information
Abstract
H9N2 avian influenza viruses are enzootic around the world, and can infect many different avian and mammalian hosts, including humans. Unlike the H9N2 viruses, which mainly originated in other countries and possess an non-structural protein 1( NS1) of 230 amino acids (aa), 98% of the H9N2 viruses isolated in China lack the 13 aa at the C-terminus of NS1 (217 aa in total). The biological significance of NS1 elongation remains elusive. In the current study, reverse genetics was used to generate a wild-type avian influenza H9N2 virus containing a 217 aa NS1 (H9N2NS1217) and two mutant viruses with elongated NS1s of 230 aa and 237 aa (H9N2NS1230 and H9N2NS1237), in order to examine the effect NS1 C-terminal elongation in the influenza virus. The C-terminal elongation of NS1 did not have significant impact on virus replication in MDCK or DF-1 cells. Although the three variants exhibited similar replicability in mice, the H9N2NS1230 and H9N2NS1237 up-regulated the level of inflammatory cytokines. In addition, both the H9N2NS1230 and H9N2NS1237 viruses increased replication and induced a high level of inflammatory cytokines and transmission in chickens, compared to the wild-type virus. These findings suggest that the NS1 extension conferred a gain of fitness to some extent.
Copyright ? 2014, the Society for General Microbiology.
KEYWORDS:
H9N2 influenza virus; NS1; inflammatory cytokines; transmission
PMID:
25326314
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25326314
The C-terminal elongation of NS1 of H9N2 influenza virus induces a high level of inflammatory cytokines and increases transmission.
Kong W1, Liu L1, Wang Y1, He Q1, Wu S1, Qin Z1, Wang J1, Sun H1, Sun Y1, Zhang R1, Pu J1, Liu J2.
Author information
Abstract
H9N2 avian influenza viruses are enzootic around the world, and can infect many different avian and mammalian hosts, including humans. Unlike the H9N2 viruses, which mainly originated in other countries and possess an non-structural protein 1( NS1) of 230 amino acids (aa), 98% of the H9N2 viruses isolated in China lack the 13 aa at the C-terminus of NS1 (217 aa in total). The biological significance of NS1 elongation remains elusive. In the current study, reverse genetics was used to generate a wild-type avian influenza H9N2 virus containing a 217 aa NS1 (H9N2NS1217) and two mutant viruses with elongated NS1s of 230 aa and 237 aa (H9N2NS1230 and H9N2NS1237), in order to examine the effect NS1 C-terminal elongation in the influenza virus. The C-terminal elongation of NS1 did not have significant impact on virus replication in MDCK or DF-1 cells. Although the three variants exhibited similar replicability in mice, the H9N2NS1230 and H9N2NS1237 up-regulated the level of inflammatory cytokines. In addition, both the H9N2NS1230 and H9N2NS1237 viruses increased replication and induced a high level of inflammatory cytokines and transmission in chickens, compared to the wild-type virus. These findings suggest that the NS1 extension conferred a gain of fitness to some extent.
Copyright ? 2014, the Society for General Microbiology.
KEYWORDS:
H9N2 influenza virus; NS1; inflammatory cytokines; transmission
PMID:
25326314
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25326314