Expression of importin-α isoforms in human nasal mucosa: implication for adaptation of avian influenza A viruses to human host. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Ninpan, Khwansiri; Suptawiwat, Ornpreya; Boonarkart, Chompunuch; Phuangphung, Peerayuht; Sathirareuangchai, Sakda; Uiprasertkul, Mongkol; Auewarakul, Prasert
• Is Part Of: Virology journal. Volume 13:Issue 1(2016)
• Page Start: 1
• Page End: 4
• Publication Date: 2016-12
• Subjects: Influenza A virus -- Importin-α1 isoform -- Importin-α3 isoform -- Importin-α7 isoform -- Human nasal mucosa -- Human lung cells -- Human respiratory tract -- Interspecies barrier; Virology -- Periodicals; 579.2
• DOI: 10.1186/s12985-016-0546-y
• Languages: English
• ISSNs: 1743-422X

Abstract

Abstract Background Transportation into the host cell nucleus is crucial for replication and transcription of influenza virus. The classical nuclear import is regulated by specific cellular factor, importin-α. Seven isoforms of importin-α have been identified in human. The preference of importin-α3 of avian influenza virus and -α7 isoform of human strains during replication in human cells was previously identified. In addition, both avian and human influenza viruses were shown to use importin-α1 isoform for their replication. Finding The mRNA levels of importin-α1, −α3, and –α7 isoforms in human respiratory tract was determined by real-time RT-PCR. The results indicate that mRNA level of importin-α7 was significantly higher than that of importin-α1 (p -value < 0.0001) and importin-α3 (p -value < 0.0001) isoforms in human nasal mucosa while importin-α1 was detected as the highest expression importin-α isoform in lung tissues. Conclusions These results may explain the preference of importin-α7 isoforms in seasonal influenza viruses in human upper respiratory tract and may suggest a selective pressure toward importin-α7 in human respiratory tract infection of an avian virus.