Disease relevance of Influenza A Virus

• Rapid interferon gamma-dependent clearance of influenza A virus and protection from consolidating pneumonitis in nitric oxide synthase 2-deficient mice [1].
• Unlike amantadine and rimantadine that target the M2 protein of influenza A viruses, these drugs inhibit replication of both influenza A and B viruses [2].
• In this study, we show that an influenza A virus polymerase transcribes and replicates a chloramphenicol acetyltransferase (CAT) gene flanked by the nontranslated sequences of an influenza B virus gene [3].
• A JAK3 -/- SCID mouse model for the human disease has been used to test whether transplant with retrovirally transduced bone marrow (BM) cells (JAK3 BMT) could restore immunity to an influenza A virus [4].
• Effect of priming polymorphonuclear leukocytes with cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF] and G-CSF) on the host resistance to Streptococcus pneumoniae in chinchillas infected with influenza A virus [5].

High impact information on Influenza A Virus

• Emergence and apparent transmission of rimantadine-resistant influenza A virus in families [6].
• Rimantadine-resistant strains of influenza A virus (H3N2 subtype) with mutations consisting of single amino acid changes in the M2 protein (residue 27, 30, or 31) were recovered from eight index patients and five contacts treated with rimantadine [6].
• Ten NH2-terminal residues are conserved in all strains of influenza A virus for which sequences are available [7].
• We use this approach to investigate the T-helper cell response of 42 asymptomatic HIV-seropositive patients to four synthetic gp160 peptides and to influenza A virus, an antigen requiring intact CD4 T-helper cell function [8].
• Variation in influenza A viruses was examined by comparison of nucleotide sequences of the NS gene (890 bases) of 15 human viruses isolated over 53 years (1933 to 1985) [9].

Chemical compound and disease context of Influenza A Virus

• Human mannose-binding protein functions as an opsonin for influenza A viruses [10].
• The influenza A virus hemagglutinin (HA) glycoprotein contains a cytoplasmic tail which consists of 10-11 amino acids, of which five residues re conserved in all subtypes of influenza A virus [11].
• We have investigated the ability of antisense phosphorothioate oligonucleotides to enhance the survival of mice infected with influenza A virus [12].
• CONCLUSIONS: Intranasal immunization with live attenuated influenza A virus vaccine provided additional protection against influenza A when added to parenteral trivalent inactivated influenza vaccine among elderly nursing home residents [13].
• L and H2 mutants of the A/NJ/11/76 H1N1 strain of swine influenza virus differ by having either a lysine or a glutamic acid at position 153 of the hemagglutinin glycoprotein of the virus [14].

Biological context of Influenza A Virus

• Inhibition of the nuclear export of poly(A)-containing mRNAs caused by the influenza A virus NS1 protein requires its effector domain [15].
• Secondary effector T-cell populations generated by cross-priming with heterologous influenza A viruses operate only in H-2K or H-2D compatible situations, when assayed on SV40-transformed target cells infected with a range of influenza A viruses [16].
• Crystal structure of the M1 protein-binding domain of the influenza A virus nuclear export protein (NEP/NS2) [17].
• RNA segment 8 of the influenza A virus genome codes for two nonstructural proteins, NS1 and NS2, for which the functions are unknown [18].
• This unique, global countermeasure against the early, IFN-alpha/beta-independent antiviral response of cells may be an important factor in the pathogenicity of influenza A virus infection [19].

Anatomical context of Influenza A Virus

• This paper shows that most murine (C57BL/6) influenza A virus-specific memory cytotoxic T lymphocyte (CTL) clones tested in limiting dilution did not react with the influenza A virus surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA) [20].
• The present study examined the effect of various unopsonized strains of influenza A virus on release of myeloperoxidase (MPO) and acid phosphatase in polymorphonuclear leukocytes (PMNL) [21].
• T cell-dependent production of IFN-gamma by NK cells in response to influenza A virus [22].
• We have previously shown that infection of macrophages by influenza A virus is capable of priming for a high TNF-alpha production in response to LPS [23].
• Human peripheral blood lymphocytes from an HLA-Dw1,3 individual were primed in vitro with influenza A virus (A/Texas/1-77/x-49) and subsequently cloned by limiting dilution in TCGF [24].

Gene context of Influenza A Virus

• Influenza A virus employs a different strategy: its NS1 protein does not bind the ISG15 protein, but little or no ISG15 protein is produced during infection [25].
• A protein analogous to NB has not been found with influenza A virus, and this represents a major difference between the two virus types [26].
• Infection by influenza A virus has previously been shown to prime macrophages for a high TNF-alpha production [27].
• Influenza A virus infection also induced a double band of IL-1 beta and IL-6 mRNA [27].
• Expression of TLR3 was positively regulated by the influenza A virus and by dsRNA but not by other inflammatory mediators, including bacterial lipopolysaccharide, the cytokines tumor necrosis factor-alpha and interleukin (IL)-1beta, and the protein kinase C activator phorbol 12-myristate 13-acetate [28].

Analytical, diagnostic and therapeutic context of Influenza A Virus

• To characterize the sites and nature of binding of influenza A virus matrix protein (M1) to ribonucleoprotein (RNP), M1 of A/WSN/33 was altered by deletion or site-directed mutagenesis, expressed in vitro, and allowed to attach to RNP under a variety of conditions [29].
• The effect of small-particle aerosol therapy with amantadine was assessed in a randomized, double-blind study of 20 patients with naturally acquired influenza A virus infection [30].
• Chemoprophylaxis of influenza A virus infections, with single doses of zanamivir, demonstrates that zanamivir is cleared slowly from the respiratory tract [31].
• Despite comparable renal allograft function, cyclosporine-treated patients had a significantly lower immune response against influenza A viruses than azathioprine-treated patients, whether mean antibody levels, fourfold titer rise, or seroconversion to protective titers was analyzed [32].
• Utility of reverse transcriptase PCR for rapid diagnosis of influenza a virus infection and detection of amantadine-resistant influenza a virus isolates [33].

References