Disease relevance of Influenza in Birds

• The fowl plague virus hemagglutinin was also cleaved after coexpression with human furin from cDNA by vaccinia virus vectors [1].
• Interestingly, the amino acid at position 627 in every avian influenza A virus PB2 protein analyzed to date is glutamic acid, and in every human influenza A virus PB2 protein, it is lysine [2].
• The hemagglutinin of influenza (fowl plague) virus was expressed in larvae of Heliothis virescens by using recombinant Autographa californica nuclear polyhedrosis virus (AcNPV) as a vector [3].
• Cells preinfected with fowl plague virus followed by treatment with actinomycin D are a suitable system for studying early protein synthesis in cells infected with Semliki forest virus [4].
• The biological role of these oligosaccharides has been investigated by mutational analysis of HA of fowl plague virus that was expressed from a simian virus 40 vector in the presence of ammonium chloride for protection from acid denaturation in the trans-Golgi network [5].

High impact information on Influenza in Birds

• We have recently found that the enzyme activating the haemagglutinin of fowl plague virus (FPV), an avian influenza virus, is furin [6].
• In L-929 cells abortively infected with fowl plague virus, matrix (M) protein synthesis is specifically inhibited, whereas the envelope glycoproteins, hemagglutinin and neuraminidase, are synthesized and incorporated into the plasma membrane [7].
• Coexpression of furin with the fowl plague virus hemagglutinin in the presence of brefeldin A and monensin reveals that furin has to enter the Golgi region to gain substrate cleaving activity [8].
• The proteases responsible for cleavage of the hemagglutinin of fowl plague virus, a prototype of these glycoproteins, has now been isolated from Madin-Darby bovine kidney cells [1].
• A cDNA sequence of the influenza (fowl plague) virus haemagglutinin gene has been inserted into the BamHI site of the pAc373 polyhedrin vector [9].

Chemical compound and disease context of Influenza in Birds

• At calcium-specific ionophore A23187 concentrations of approximately 0.25 microM [which still allow assembly and release of fowl plague virus (FPV) particles] post-translational proteolytic cleavage of the viral hemagglutinin precursor HA into the fragments HA1 and HA2 is inhibited [10].
• The infectivity of fowl plague virus is increased by 80-fold when 4% dimethyl sulfoxide is added to culture medium immediately after infection [11].
• The genomic RNA of the avian influenza A virus, fowl plague, was fractionated into eight species by electrophoresis in polyacrylamide-agarose gels containing 6 M urea [12].
• In addition, the probable sites of initiation of translation of fowl plague virus mRNA are indicated along with the corresponding NH2-terminal amino acid sequences of the virus polypeptides [13].
• To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains [14].
• There was no direct correlation between the IFN-beta induction and replication of avian influenza viruses in human A549 cells [15].

Biological context of Influenza in Birds

• The virulence of avian influenza viruses correlates with the sensitivity of their hemagglutinin (HA) to cellular proteases [16].
• We have previously shown that retroviral vector particles derived from Moloney murine leukemia virus (Mo-MuLV) can efficiently incorporate influenza hemagglutinin (HA) glycoproteins from fowl plague virus (FPV), thus conferring a broad tropism to the vectors [17].
• In this study we used nucleotide sequence analysis to evaluate the genetic stability of the attenuating M and NP genes of the avian influenza A/Mallard/NY/6750/78 attenuated donor virus during the in vitro generation and subsequent in vivo replication of avian-human (AH) influenza A reassortant vaccine viruses in monkeys and humans [18].
• However, unlike previous poultry outbreaks of highly pathogenic avian influenza due to H5 that were controlled by depopulation with or without vaccination, the presently circulating A/H5N1 genotype Z virus has since been spreading from Southern China to other parts of the world [19].
• A multiplex real-time reverse transcriptase-polymerase chain reaction (RRT-PCR) assay for the simultaneous detection of the H5 and H7 avian influenza hemagglutinin (HA) subtypes was developed with hydrolysis type probes labeled with the FAM (H5 probe) and ROX (H7 probe) reporter dyes [20].

Anatomical context of Influenza in Birds

• To test whether NA could also facilitate virus entry into cell, we infected cultures of human airway epithelium with human and avian influenza viruses in the presence of the NA inhibitor oseltamivir carboxylate [21].
• Efficient expression of the tumor-associated antigen MAGE-3 in human dendritic cells, using an avian influenza virus vector [22].
• In chick embryo cells infected with fowl plague virus the CDP-choline pool increases because of an inhibition of the choline phosphotransferase activity [23].
• Fetuin bound latex spheres do not adhere to the membranes of non-infected cells but adhere to those of cells productively infected by fowl plague virus (FPV Dobson strain) [24].
• The total amount and the relative proportions of labeled phospholipids were studied in chorioallantoic membrane cells (CAM), chick embryo cells (CEC) and L cells which were either infected with Newcastle disease virus (NDV), fowl plague virus (FPV) and mouse encephalomyocarditis (EMC) virus or treated with cycloheximide [25].

Gene context of Influenza in Birds

• p38 mitogen-activated protein kinase-dependent hyperinduction of tumor necrosis factor alpha expression in response to avian influenza virus H5N1 [26].
• These data suggest that PC6, as well as furin, can activate virulent avian influenza viruses in vivo, implying the presence of multiple HA cleavage enzymes in animals [27].
• Mice carrying the gene Mx were resistant to the lethal action of a hepatotropic line of avian influenza A virus [28].
• Recent outbreaks of SARS, avian influenza, and others highlight emerging zoonotic diseases as one of the key threats to global health [29].
• Using M-TUR, a macrophage-adapted avian influenza A virus (Hav1, Nav3), antiviral resistance of peritoneal macrophages obtained from specifically or nonspecifically immunized mice towards in vitro infection was assessed [30].

Analytical, diagnostic and therapeutic context of Influenza in Birds

• Sequence analysis of fowl plague virus mutant ts47 reveals a nonsense mutation in the NS1 gene [31].
• Centrifugation on sucrose density gradients and immune precipitation with conformation-specific antibodies were used to compare trimerization of the hemagglutinin in insect cells and in fowl plague virus-infected MDCK cells [32].
• Sera from pigs infected with avian viruses showed high titres of antibodies in ELISA and neutralization tests, but did not inhibit haemagglutination of homologous viruses, cautioning against the use of haemagglutination-inhibition tests to identify pigs infected with avian influenza viruses [33].
• Nucleic acid sequence-based amplification with electrochemiluminescent detection (NASBA/ECL) of avian influenza virus was compared with viral culture in embryonated chicken eggs [34].
• Differences of nucleoproteins of human and avian influenza A virus strains shown by polyacrylamide gel electrophoresis and by the peptide mapping technique [35].

References