Disease relevance of Influenza B Virus

• An influenza A virus containing influenza B virus 5' and 3' noncoding regions on the neuraminidase gene is attenuated in mice [1].
• Inhibition of fatty acid beta oxidation by influenza B virus and salicylic acid in mice: implications for Reye's syndrome [2].
• Although evolutionary rates of the HA, NP, M, and NS genes of influenza B viruses were estimated to be generally lower than those of human influenza A viruses, genes of influenza B viruses demonstrated complex phylogenetic patterns, indicating alternative mechanisms for generation of virus variability [3].
• The roles of the 3'- and 5'-terminal nucleotides and the panhandle structure of influenza B virus virion RNA were analyzed in vitro by transcription of model RNA templates with influenza B virus RNA polymerase [4].
• The neuraminidase of the reassortant viruses is most closely related to that of B/Victoria/2/87-like viruses currently circulating in Nanchang, China. A pattern of insertions and deletions in the hemagglutinin and the neuraminidase of different strains of influenza B viruses is observed [5].

High impact information on Influenza B Virus

• Retrospective analyses of sera collected from 971 seals showed a prevalence of antibodies to influenza B virus in 2% of the animals after 1995 and in none before 1995 [6].
• Ribavirin aerosol treatment of influenza B virus infection [7].
• The identical motif was found on the M1 matrix protein of influenza B viruses, and affinity-purified human anti-ERKRR autoantibodies recognized this epitope also in the viral amino acid sequence context [8].
• Human anti-p68 autoantibodies recognize a common epitope of U1 RNA containing small nuclear ribonucleoprotein and influenza B virus [8].
• Influenza B virus NS1 protein inhibits conjugation of the interferon (IFN)-induced ubiquitin-like ISG15 protein [9].

Chemical compound and disease context of Influenza B Virus

• A previously unrecognized influenza B virus glycoprotein from a bicistronic mRNA that also encodes the viral neuraminidase [10].
• Three randomized, double-blind, placebo-controlled, parallel-group studies evaluated oral oseltamivir for early treatment (75 or 150 mg twice daily for 5 days) or prevention (75 mg once or twice daily for 7 days) of experimental influenza B virus infection in healthy susceptible adults [11].
• However, influenza B virus infection appears to interfere with ASA metabolism [12].
• We adapted the technique for engineering influenza B virus and generated a mutant bearing an amino acid change E116G in the viral neuraminidase which was resistant in vitro to the neuraminidase inhibitor zanamivir [13].
• The cytoplasmic tail (CT) of hemagglutinin (HA) of influenza B virus (BHA) contains at positions 578 and 581 two highly conserved cysteine residues (Cys578 and Cys581) that are modified with palmitic acid (PA) through a thioester linkage [14].

Biological context of Influenza B Virus

• Eukaryotic coupled translation of tandem cistrons: identification of the influenza B virus BM2 polypeptide [15].
• Complete nucleotide sequence of the neuraminidase gene of influenza B virus [16].
• RNA segment 6 of the influenza B virus genome codes for a previously unidentified polypeptide designated NB [10].
• Determination of the orientation of an integral membrane protein and sites of glycosylation by oligonucleotide-directed mutagenesis: influenza B virus NB glycoprotein lacks a cleavable signal sequence and has an extracellular NH2-terminal region [17].
• Influence of acylation sites of influenza B virus hemagglutinin on fusion pore formation and dilation [14].

Anatomical context of Influenza B Virus

• The BM2 protein of influenza B virus functions as an ion channel, which is suggested to be important for virus uncoating in endosomes of virus-infected cells [18].
• However, a much lesser hyperpolarization (approximately -130 mV) was able to evoke a similar current from oocytes that expressed the cellular proteins IsK and phospholemman, the synthetic protein SYN-C, and the NB protein of influenza B virus [19].
• Treatment with ribavirin was instituted in 12 allogeneic and one autologous bone marrow transplant (BMT) recipients with proven respiratory syncytial virus (RSV), influenza B virus or parainfluenza virus infections [20].
• Influence of additional acylation site(s) of influenza B virus hemagglutinin on syncytium formation [21].
• The influence of cyclic 3'5'-adenosine monophosphate (cAMP), adrenalin and theophylline on interferon synthesis induced by influenza B virus (Lee strain) in chick embryo cell cultures was studied [22].

Gene context of Influenza B Virus

• A bicistronic mRNA transcribed from the influenza B virus RNA segment 7 encodes two viral proteins, matrix protein M1 and uncharacterized small protein BM2 [23].
• Our results support the hypothesis that the NS1 protein of influenza B virus plays an important role in antagonizing the IRF-3- and IFN-induced antiviral host responses to virus infection [24].
• Expression of the full-length B/NS1 protein (281 amino acids), as well as either its N-terminal RNA-binding domain (amino acids 1 to 93) or C-terminal domain (amino acids 94 to 281), in the absence of any other influenza B virus proteins resulted in the inhibition of IRF-3 nuclear translocation and IFN-beta promoter activation [24].
• Comparison with the only other known sequence of an influenza B virus nucleoprotein gene (B/Singapore/222/79) indicates striking homology [25].
• Differences in the phylogenetic pathways of three polymerase genes were not only a reflection of genetic reassortment between co-circulating influenza B viruses, but also an indication that the polymerase genes were not co-evolving as a unit [26].

Analytical, diagnostic and therapeutic context of Influenza B Virus

• Sequence analysis indicated that the hemagglutinin of Vero cell-derived influenza B viruses was identical to that of MDCK-grown counterparts but differed from that of egg-grown viruses at amino acid positions 196 to 198 [27].
• A specific glycosylation site at the distal tip of the HA of influenza B virus grown exclusively in mammalian cell culture is lost or altered during egg adaptation [28].
• Hemagglutination inhibition (HI) and neutralization tests were used to determine antibody responses to egg-derived and Madin-Darby canine kidney (MDCK)-derived influenza B virus (B/England/222/82) in paired sera from persons naturally infected with influenza B and in persons vaccinated with standard egg-derived inactivated influenza vaccine [29].
• The sensitivity of an enzyme-linked immunosorbent assay (ELISA) for the detection of antibody to influenza B virus was compared with that of the hemagglutination inhibition test on acute- and convalescence-phase sera obtained from adults and children infected with influenza B virus [30].
• Among 51 additional persons with known or presumed influenza B virus infections early in 1982, ET B/Singapore/222/79 was also more sensitive than WV for serodiagnosis (69 versus 49%), but eight persons with both WV and ET B/Singapore/222/79 HI responses also had an HI titer rise to WV A/Brazil/11/78 (H1N1) antigen [31].

References