The Antigenic Property Of The H5N1 Avian Influenza Viruses And Study On Co-infection Of Mice With Influenza Viruses

In April 2009, a novel influenza A H1N1 virus (2009 H1N1) outbreak in Mexico and soon spread worldwide and developed into the first human influenza pandemic in 21st century. Since 1997, highly pathogenic avian influenza viruses (HPAI) of the H5N1 subtype have caused numerous outbreaks in poultry in Southeast Asia that have led to the death or depopulation of significant numbers of chickens. These outbreaks are accompanied by the occasional transmission of HPAI H5N1 viruses to humans, resulting in a case fatality rate of more than 50%.To comprehend the antigenic property of the H5N1 avian influenza viruses and co-infection of BALB/c mice with H1N1 and H5N1 influenza viruses, we design the main research as follows.1. The Antigenic Property of the H5N1 Avian Influenza VirusesThe antigenic characterizations of the viruses isolated respectively in 2004,2006 and 2007 were investigated in the present study. Hemagglutinin inhibition assay and neutralization assay displayed obviously differential antigenic characteristics of the viruses isolated in two periods. The phylogenisis analysis revealed that HA genes of the viruses located in different branches. Crystal model also displayed that most of amino acid mutations of the viruses investigated in this study located in the globular head of the HA protein, and some of the mutations were even distributed at the epitope sites. The study demonstrated that a major antigenic drift had occurred in the viruses isolated in the two periods. 2. Co-infection of mice with influenza virusesIn present study, mice were infected with H1N1 influenza virus, H5N1 influenza virus and were co-infected with H1N1 and H5N1 virus. virus LN was a human H1N1 influenza virus of strong transmissibility, and HM was a high pathogenicity H5N1 avian influenza virus. The survival rate, mortality rate and MDT, body weight, clinical symptom and pathological findings of the infected mice were detected. The expression of several pro-inflammatory cytokine responses in the lungs of infected mice were detected by ELISA, including IL-1β, IFN-γ, TNF-α. It was found that virus LN didn’t lead to the death of mice. Group HM and co-infected groups all dead in the 6th day,The survival rate of co-infected 48h group decrease most, and the MDT of it is the lowest. Pathological findings of group LN were not obvious except the group HM and co-infected groups, but there were no obvious differences among the co-infected groups. It was also found that mice infected with HM could stimulate higher level of IL-1β, IFN-γ, TNF-αthan group LN. But co-infected groups die faster, and the concentration of IL-1β, IFN-γ, TNF-αof them were high. The study demonstrated that co-infection enhance the pathogenicity of influenza virus to the mice.