Park, Su-Jin
Kumar, Mukesh
Kwon, Hyeok-il
Seong, Rak-Kyun
Han, Kyudong
Song, Jae-min
Kim, Chul-Joong
Choi, Young-Ki
Shin, Ok Sarah
Article History
Received: 1 June 2015
Accepted: 12 October 2015
First Online: 18 November 2015
Change Date: 29 January 2016
Change Type: Update
Change Details: A correction has been published and is appended to both the HTML and PDF versions of this paper. The error has not been fixed in the paper.
Change Date: 29 January 2016
Change Type: Erratum
Change Details: Emerging outbreaks of newly found, highly pathogenic avian influenza (HPAI) A(H5N8) viruses have been reported globally. Previous studies have indicated that H5N8 pathogenicity in mice is relatively moderate compared with H5N1 pathogenicity. However, detailed mechanisms underlying avian influenza pathogenicity are still undetermined. We used a high-throughput RNA-seq method to analyse host and pathogen transcriptomes in the lungs of mice infected with A/MD/Korea/W452/2014 (H5N8) and A/EM/Korea/W149/2006 (H5N1) viruses. Sequenced numbers of viral transcripts and expression levels of host immune-related genes at 1 day post infection (dpi) were higher in H5N8-infected than H5N1-infected mice. Dual sequencing of viral transcripts revealed that in contrast to the observations at 1 dpi, higher number of H5N1 genes than H5N8 genes was sequenced at 3 and 7 dpi, which is consistent with higher viral titres and virulence observed in infected lungs <i>in vivo</i>. Ingenuity pathway analysis revealed a more significant upregulation of death receptor signalling, driven by H5N1 than with H5N8 infection at 3 and 7 dpi. Early induction of immune response-related genes may elicit protection in H5N8-infected mice, which correlates with moderate pathogenicity <i>in vivo</i>. Collectively, our data provide new insight into the underlying mechanisms of the differential pathogenicity of avian influenza viruses.
Competing interests
: The authors declare no competing financial interests.