Inhibition of the replication of H9N2 influenza virus in vivo by short-term repeated oral administration of chicken interferon α.
- Author:
Meng WANG
1
;
Jie SONG
1
;
Wenhui FAN
1
;
Lirong LIU
1
;
Zhuoran HUANG
2
;
Chengcheng YANG
2
;
Hao WU
2
;
Wenjun LIU
1
;
Jing LI
1
Author Information
- Publication Type:Journal Article
- Keywords: H9N2 influenza viruses; chicken interferon α; oral administration; short-term repeated
- MeSH: Administration, Oral; Animals; Chickens; Humans; Influenza A Virus, H9N2 Subtype; Interferon-alpha; Virus Replication
- From: Chinese Journal of Biotechnology 2019;35(6):1029-1040
- CountryChina
- Language:Chinese
- Abstract: To evaluate the optimal administration frequency for interferon-α (IFN-α) and the effect of its combined use with inactive virus on chicken flocks, the prokaryotic expression plasmid pET-22b-ChIFN-α was constructed and transferred into Escherichia coli BL21(DE3) host bacteria to induce the expression of chicken IFN-α and to harvest recombinant proteins inclusion bodies. The expression of recombinant chicken IFN-α was confirmed by SDS-PAGE, and the results demonstrated that the chicken IFN-α (20 kDa) was highly expressed using the prokaryotic expression vector with a concentration of 0.2 mg/mL in the medium. Chicken IFN-α was diluted to 2.5×10⁴ U/fowls and administered to immunized specific-pathogen-free chickens orally in combination with inactivated H9N2 subtype influenza virus. Chicken that received chicken IFN-α were safe after three repeated immunizations (96 h). In addition, chicken IFN-α could induce higher levels of antiviral-related inducible genes in peripheral blood, spleen, and thymus of chicken flocks. The results of a challenge assay revealed that the lowest detoxification rates of chicken IFN-α ranged from three to five days, suggesting a higher capacity to resist H9N2 subtype avian influenza virus. The present study obtained the optimal immune frequency and immunization period for chicken IFN-α to provide theoretical support for the optimal clinical application of IFN-α.