Animals ; Birds ; China ; epidemiology ; Humans ; Influenza A Virus, H5N1 Subtype ; physiology ; Influenza A Virus, H7N7 Subtype ; physiology ; Influenza A Virus, H9N2 Subtype ; physiology ; Influenza A virus ; physiology ; Influenza, Human ; epidemiology ; prevention & control

Animals ; Cytokines ; physiology ; Humans ; Influenza A virus ; immunology ; Influenza B virus ; immunology ; Influenza Vaccines ; Influenza, Human ; immunology ; prevention & control ; Vaccines, DNA

OBJECTIVETo study the apoptotic effects of influenza A virus on the Raji cell line.

METHODSCultured Raji cells were infected with influenza A virus at a multiplicity of infection (m.o.i) of 20 and the effects of apoptosis were detected at different time points post infection using the following methods: electron microscope, DNA agarose gel electrophoresis, PI stained flow cytometry (FCM) and Annexin-V FITC/PI stained FCM.

RESULTSRaji cells infected with influenza A virus showed changes of morphology apoptosis, DNA agarose electrophoresis also demonstrated a ladder-like pattern of DNA fragments in a time-dependent manner. PI stained FCM showed "apoptosis peak" and FITC/PI stained FCM showed apoptotic cells. Quantitative analysis indicated that the percentage of apoptotic Raji cells increased after infection, and cycloheximide (CHX), an eukaryotic transcription inhibitor, could effectively inhibit the apoptotic effects of influenza A virus in vitro.

CONCLUSIONSInfluenza A virus can induce apoptosis in Raji cell line suggesting that it may lead to a potential method for tumor therapy.

Apoptosis ; physiology ; Humans ; Influenza A virus ; physiology ; Tumor Cells, Cultured

Disease Outbreaks ; Humans ; Influenza A Virus, H1N1 Subtype ; physiology ; Influenza A Virus, H5N1 Subtype ; physiology ; Influenza, Human ; epidemiology ; prevention & control ; transmission ; virology

To investigate the susceptibility of Chukars to duck avian influenza virus H9N2 and explore their role in interspecies transmission of influenza viruses. Chukars were inoculated with duck avian influenza viruses H9N2. The present study demonstrated that inflammatory lesions and virus antigen were present in the trachea, bronchus, and parabronchus, and the viruses could be isolated from throat swabs and lung tissue homogenate supernatants. At 14 d post virus inoculation, anti-H9 influenza virus antibody in the serum was detected. The results indicated that Chukars are susceptible to duck avian influenza virus and serve as an intermediate host, thereby facilitating viral gene evolution and supporting the need for continued surveillance of epidemiology and evolution of the influenza virus in Chukars.
Animals ; Galliformes ; Influenza A Virus, H9N2 Subtype ; pathogenicity ; physiology ; Influenza in Birds ; virology ; Respiratory System ; pathology ; virology ; Virus Replication ; physiology

Adult ; Female ; Humans ; Influenza A Virus, H5N1 Subtype ; physiology ; Influenza, Human ; diagnostic imaging ; virology ; Male ; Radiography

OBJECTIVETo identify genes in human cells infected with high pathogenic avian influenza viruses H5N1.

METHODSThe lung carcinoma cells line A549 was infected with H5N1 and H1N1, respectively. We harvested the infected cells at the different time points after infection and screened the genes with differential expression via microarray technology. The candidate genes were selected and confirmed by quantitative real-time PCR.

RESULTSThe spectrum of genes with the differential expression in the cells infected with H5N1 was obtained and 16 candidate genes were identified in the cellular apoptosis pathway, mTOR pathway, and the cellular immunity as well.

CONCLUSIONSOur results suggest that H5N1 exert a stronger impact on eliciting apoptosis of infected cells than the common influenza virus H1N1.

Animals ; Apoptosis ; Cell Line, Tumor ; Gene Expression Profiling ; Humans ; Influenza A Virus, H1N1 Subtype ; physiology ; Influenza A Virus, H5N1 Subtype ; physiology ; Influenza, Human ; genetics ; metabolism ; virology ; Oligonucleotide Array Sequence Analysis

Seasonal influenza epidemics and influenza pandemics caused by influenza A virus (IAV) has resulted in millions of deaths in the world. The development of anti-IAV vaccines and therapeutics is urgently needed for prevention and treatment of IAV infection and for controlling future influenza pandemics. Hemagglutinin (HA) of IAV plays a critical role in viral binding, fusion and entry, and contains the major neutralizing epitopes. Therefore, HA is an attractive target for developing anti-IAV drugs and vaccines. Here we have reviewed the recent progress in study of conformational changes of HA during viral fusion process and development of HA-based antiviral therapeutics and vaccines.
Antiviral Agents ; therapeutic use ; Epidemics ; Hemagglutinins ; physiology ; Humans ; Influenza A virus ; immunology ; Influenza Vaccines ; immunology ; Influenza, Human ; immunology ; therapy ; Pandemics

IFIT family genes are a kind of interferon stimulated genes (ISGs), and play important roles in antiviral sector and immunity regulation. To study the regulatory effect of IFIT family genes during influenza A virus (IAV) infection, we used RNA-sequencing analysis (RNA-Seq) technique and found that when 293T cells were infected by A/WSN/33 (WSN), the concentration of IFIT family genes were increased. Further study reveals that overexpression of IFIT2 or IFIT3 could inhibit IAV replication and transcription, and cause the dose-dependent inhibition of polymerase activity of vRNP. In addition, IFIT2 and IFIT3 encoding protein could colocalize with NS1 in 293T cells infected by WSN, indicating that they might interact with each other. The results suggest that IFIT family genes can inhibit the replication and transcription of IAV, which contributes to our understanding of the regulatory effect of host factors during influenza virus infection.
HEK293 Cells ; Humans ; Influenza A virus ; physiology ; Influenza, Human ; genetics ; Intracellular Signaling Peptides and Proteins ; genetics ; Proteins ; genetics ; Virus Replication

Two H5N1 avian influenza viruses (AIV), A/mallard/Huadong/S/2005 (S, IVPI = 2.65, in mallard) and A/mallard/Huadong/Y/2003 (Y, IVPI = 0, in mallard), were capable of distinct in pathogenicity to non-immunized mallards (Anas platyrhynchos). There were two amino acid residues difference in the HA cleavage site between two viruses, 322 (S, Leu; Y, Gln) and 329 (S, deletion; Y, Lys). Based on the variation, a series of recombinant viruses carrying HA gene either from S or Y virus with mutation at 322 and/or 329 were constructed via reverse genetics system to explore the influence of the two amino acid residues on viral pathogenicity in mallards. Recombinant viruses with S virus backbone were completely attenuated in terms of their virulence to ducks when position 322 (L322Q) and/or position 329 (-329K) of HA gene had been mutated. The critical role that L322 and -329 of HA protein from S virus play in the high virulence to ducks were influenced by the entire background of that protein because the recombinant virus with HA gene from Y and other seven genes from S were completely attenuated even if Q322L and K329- mutations of HA gene had been achieved. Recombinant viruses with Y virus backbone significantly increased their virulence to ducks when position 322 (Q322L) and/or position 329 (K329-) of HA gene had been mutated. All recombinant viruses carrying HA gene from Y with Q322L and/or K329-mutations and other seven genes from S were completely attenuated in terms of virulence to ducks whereas all recombinant viruses carrying HA gene from Y with same mutations and other seven genes from Y gained significant virulence. It seems that the compatibility among eight genes might be an important factor for HA to exert its functions. Results indicated that the mutation at amino acid position 322 and deletion at 329 in HA cleavage site significantly influence the pathogenicity of S and Y viruses in mallard, the compatibility among eight genes also contribute to the pathogenicity of both viruses in mallard.
Animals ; Birds ; Hemagglutinin Glycoproteins, Influenza Virus ; chemistry ; genetics ; physiology ; Influenza A Virus, H5N1 Subtype ; genetics ; pathogenicity ; Structure-Activity Relationship ; Virulence