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At least 19 recordsLinked to original sources
PubMed1998

Rapid simultaneous diagnosis of infections with respiratory syncytial viruses A and B, influenza viruses A and B, and human parainfluenza virus types 1, 2, and 3 by multiplex quantitative reverse transcription-polymerase chain reaction-enzyme hybridization assay (Hexaplex).

A multiplex quantitative reverse transcription-polymerase chain reaction-enzyme hybridization assay (Hexaplex; Prodesse, Milwaukee) was developed and used to rapidly detect and quantitate RNA of respiratory syncytial viruses A and B, influenza viruses A and B, and human parainfluenza virus types 1, 2, and 3 in nasal wash specimens in a single test. Primers and probes originated from highly conserved regions of each viral genome. Six and a half primer pairs were mixed for the simultaneous detection and quantitation of RNA from seven different respiratory viruses. We tested 109 clinical samples with this assay. Twenty-nine virus culture-positive samples were all positive by Hexaplex. Samples from 40 symptomatic patients were negative by virus culture, but eight of these were positive by Hexaplex. Forty samples from asymptomatic children were negative by both virus culture and Hexaplex. No cross-reactions were noted among 17 different respiratory viruses with use of this assay. Hexaplex was 100% sensitive (95% confidence interval [CI], 0.88-1.0) and 98% specific (95% CI, 0.97-0.99). All eight "false-positive" Hexaplex results (in comparison with negative viral culture results) were for symptomatic patients with low numbers of virus RNA copies. This finding suggests that Hexaplex may be more sensitive than virus culture. Our data demonstrate that Hexaplex is a rapid, sensitive, and specific quantitative test for the diagnosis of infections with these seven common respiratory viruses.

Humans↗
PubMed1994

Activated THP-1 cells depress mitochondrial respiration in Hep G2 cells infected with influenza B virus.

Influenza B virus has been aetiologically linked to Reye Syndrome (RS), but the mechanism(s) by which this pathogen could disrupt liver metabolism and produce the hepatic mitochondrial injury characteristic of the syndrome are unknown. In this study, two mechanisms by which infection of hepatocytes with influenza B virus could disrupt cellular metabolism were investigated. (1) virus-induced increase in pro-oxidant iron with subsequent iron-induced lipid peroxidation (LP) and (2) increased membrane permeability. Hep G2 cells, a well-differentiated continuous human liver cell line derived from a hepatoblastoma, were infected with allantoic-fluid derived influenza B Lee/40 virus (AFDV) at a multiplicity of infection of 10 for 24 h; productive infection was confirmed by both haemagglutination of chick erythrocytes and by plaque assay. Infection of Hep G2 cells preloaded with 59Fe-transferrin resulted in increased release of 59Fe (153 +/- 17% of controls, P < 0.03). However, the iron released did not result in increased LP (assessed by thiobarituric acid reactive substances; TBARS). To confirm that this lack of of increase in TBARS was not due to insensitivity of the cell line to pro-oxidant iron, cells were exposed to 15 microM iron ascorbate for 60 min. Production of TBARS was increased (122 +/- 4% of controls, P < 0.0003). Release of 51Cr from infected cells was also increased (128 +/- 12% of controls, P < 0.05); thus the infected cells exhibited a generalized increase in membrane permeability. However, infection did not depress mitochondrial respiration (as assessed by the formation of MTT-f3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide-formazan. To determine if the combination of viral infection and soluble products of activated macrophages would affect mitochondrial respiration, infected hepatocytes were exposed to the supernatant fluid from THP-1 cells which had previously been incubated with lipopolysaccharide at 100 ng ml-1 for 18 h. This supernate did depress the formation of MTT-f (81 +/- 5% of controls, P < 0.03). We conclude that influenza B virus does productively infect Hep G2 cells, and does increase hepatocyte membrane permeability. This effect does not impair mitochondrial respiration directly. However, infection does act in concert with soluble products of activated macrophages to depress hepatic mitochondrial respiration. Whether this interaction can be explained by virus-induced permeability changes and/or other effects of infection deserves further investigation.

Animals↗
PubMed1982

Role of viral glycoproteins in haemolysis by influenza B virus.

Influenza B virus exhibited haemolytic activity at low pH, but the pH profile for its activity varied from strain to strain. The results of selective heat-inactivation of the enzyme activity of neuraminidase (NA) or elimination from virions of the enzyme-active portion of the NA molecule by trypsin digestion, suggest that proteolytically cleaved haemagglutinin, but not enzyme activity of NA, is essential for haemolysis by influenza B virus.

Animals↗
PubMed1996

Differential diagnoses of influenza A virus, influenza B virus, and respiratory syncytial virus infections by direct immunofluorescence using mixtures of monoclonal antibodies of different isotypes.

Differences between isotypes of monoclonal antibodies were employed to detect influenza A and B viruses and respiratory syncytial virus by direct immunofluorescence using fluorescein isothiocyanate or Texas Red conjugates. Examination of 56 specimens for influenza A and B viruses and 112 specimens for influenza A virus and respiratory syncytial virus showed the mixed-isotype test to be comparable to the conventional procedure.

Antibodies, Monoclonal↗
PubMed1994

Reinfection with influenza B virus in children: analysis of the reinfection influenza B viruses.

Influenza B virus reinfection in Japanese children was studied epidemiologically during 1979-91 and virologically during 1985-91. During this investigation, there were four epidemics caused by influenza B viruses, each of which accompanied antigenic drift. Between the epidemics in 1987/88 and 1989/90, the viruses changed drastically, both genetically and antigenically. The minimum rate of reinfection with influenza B virus during the whole period was 3-25% depending on the influenza seasons. The antigens of primary and reinfection strains of influenza B virus isolated from 18 children during 1985-90, which covered three epidemic periods, were studied by haemagglutination inhibition tests. The results showed that the viruses isolated in the 1984/85 and 1987/88 influenza seasons, which belonged to the same lineage, were antigenically close, and reinfection occurred with these viruses. The results of amino-acid analysis of the HA1 polypeptide of these viruses corresponded with those of antigenic analysis. There were no specific amino-acid changes shared by the primary infection and reinfection influenza B viruses; the patients were infected with the viruses epidemic at that time.

Adolescent↗
PubMedDate not supplied

[Biological characteristics of influenza B viruses isolated during influenza B epidemics in 1976-1977].

Comparative studies of the antigenic structure of influenza B viruses isolated in 1976-1977 and in previous years demonstrated one-way relationship of the hemagglutinin of B/76 viruses with that of B/72 viruses. Antisera to new B/76 strains neutralized the hemagglutinating activity of all known reference influenza B virus strains beginning from 1972. Influenza B/76 viruses were divided into two groups depending on complete or partial neutralization by antiserum B/Hong Kong/7/75. The study of the antigenic structure of neuraminidase showed no significant differences between influenza B/76 and B/72 virus neuraminidase. All the influenza B viruses from different years under study had marked interferon-inducing properties and were sensitive to interferon. Unlike the Yamagata/1/73 strain, all the influenza B/76 viruses under study were resistant to thermostable inhibitors of normal horse, guinea pig, and rabbit sera.

Animals↗
PubMed2006

Rapid identification of small interfering RNA that can effectively inhibit the replication of multiple influenza B virus strains.

Influenza B virus is a cause of substantial morbidity and mortality in humans and current vaccination strategies and antiviral drugs only provide limited protection. Here, we report the evaluation of small interfering RNA (siRNA) for repression of viral replication in cultured cells as well as in chicken embryos. Several siRNAs targeting conserved regions of the virus (in chemically synthesized or plasmid-encoded forms) were found to effectively block the replication of the influenza B virus. The siRNAs were found to offer broad protection over several strains of influenza B virus (B/Beijing/76/98, B/Beijing/37/99 and B/Jiangsu/10/03) that differ substantially in their genetic content. The antiviral effects of 500 ng siRNA-encoding plasmids or 60 nmoles synthetic siRNA were found to be comparable to that of 3.6 microg ribavirin. These results indicated that RNA interference warrants further study for management of influenza B virus infections.

Animals↗
PubMed2004

Homology model of the structure of influenza B virus HA1.

Influenza B virus is one of two types of influenza virus that cause substantial morbidity and mortality in humans, the other being influenza A virus. The inability to provide lasting protection to humans against influenza B virus infection is due, in part, to antigenic drift of the viral surface glycoprotein, haemagglutinin (HA). Studies of the antigenicity of the HA of influenza B virus have been hampered by lack of knowledge of its structure. To address this gap, two possible models have been inferred for this structure, based on two known structures of the homologous HA of the influenza A virus (subtypes H3 and H9). Statistical, structural and functional analyses of these models suggested that they matched important details of experimental observations and did not differ from each other in any substantive way. These models were used to investigate two HA sites at which viral variants appeared to carry a selective advantage. It was found that each of these sites coevolved with nearby sites to compensate for either size or charge changes.

Amino Acid Sequence↗
PubMed1998

Evolutionary characteristics of influenza B virus since its first isolation in 1940: dynamic circulation of deletion and insertion mechanism.

New antigenic variants of B/Yamagata/16/88-like lineage which appeared in the season of 1997 as a minor strain tended to predominate in the following season. Also, we could observe for the first time, three peaks of activity caused by H3N2 virus and two variants of B influenza virus. Antigenic and phylogenetic analyses revealed that B/Victoria/2/87-like variants appeared again in Japan in 1997 after a nine-year absence. Influenza B viruses evolved into three major lineages, including the earliest strain (I), B/Yamagata/16/88-like variants (II), which comprised of three sublineages (II-(i), II-(ii), II-(iii)), and B/Victoria/2/87-like variants (III). Evolution of influenza B virus hemagglutinin was apparently distinguishable from that of influenza A virus, showing a systematic mechanism of nucleotide deletion and insertion. This phenomenon was observed to be closely related to evolutionary pathways of I, II-(i), II-(ii), II-(iii) and III lineages. It was noteworthy to reveal that the nucleotide deletion and insertion mechanism of influenza B virus completed one cycle over a fifty-year period, and that a three nucleotide deletion was again observed in 1997 strains belonging to lineage II-(iii). It was evident that amino acid substitutions accompanying nucleotide insertions were highly conserved.

Antigens, Viral↗
PubMed1995

2,3-didehydro-2,4-dideoxy-4-guanidino-N-acetyl-D-neuraminic acid (4-guanidino-Neu5Ac2en) is a slow-binding inhibitor of sialidase from both influenza A virus and influenza B virus.

The effect of 2,3-didehydro-2,4-dideoxy-4-guanidino-N-acetyl-D-neuraminic acid (4-guanidino-Neu5Ac2en) on the sialidases from influenza virus reassortant X31 (which contains the sialidase from A/Aichi/2/68) and influenza virus B/Beijing/1/87 has been investigated. We find that 4-guanidino-Neu5Ac2en is a slow-binding inhibitor of both influenza A and influenza B virus sialidase, and that association and dissociation rate constants are almost identical for both enzymes. Furthermore, values for these rate constants are independent of whether purified enzyme or detergent-treated virus is used in the assays.

Dose-Response Relationship, Drug↗
PubMed1988

Sequence analysis of the hemagglutinin of B/Ann Arbor/1/86, an epidemiologically significant variant of influenza B virus.

Influenza B/Ann Arbor/1/86 is representative of antigenic variants responsible for the most important influenza epidemics during the 1985/1986 season. The nucleotide sequence of the hemagglutinin HA1 region and the deduced amino acid sequence are presented. Compared to the previous winter's vaccine strain B/USSR/100/83, B/AA/1/86 possesses 18 amino acid substitutions and 2 amino acid insertions, 50% of which are distributed within the vicinity of the reported single immunodominant antigenic site.

Amino Acid Sequence↗
PubMed1992

Influenza B virus infection associated with non-bacterial septic shock-like illness.

We report the details of four children aged between 6 months and 5.5 years who had underlying chronic disease and who developed life-threatening illness in association with influenza virus B infection. Influenza has received relatively little attention, yet its morbidity and mortality in children can be considerable. This report emphasises the need to vaccinate the population groups at high risk, such as children with cardiovascular disorders, chronic bronchopulmonary, metabolic and renal disease and chronic neurological disorders.

Child, Preschool↗
PubMed1992

Comparison of the HA genes of type B influenza viruses in herald waves and later epidemic seasons.

From January 1985 to May 1991, herald strains of influenza B virus were isolated in 1987 and 1989 in Japan. In both cases, influenza epidemics caused by the same type followed in the next winter season. The HA gene sequences of the influenza B viruses isolated in Japan from 1987-91, which covers two herald waves of influenza B viruses, were analysed and located on the phylogenetic tree for influenza B viruses after the B/Singapore/64 strain. Co-circulation of at least two evolutionary lineages of the HA genes existed for influenza B viruses in Japan during the period of this study. The herald viruses in one wave (1987) were genetically close to the winter isolates and were considered to be the parental viruses for the following influenza season, while in the other wave (1989) winter isolates belonged to another lineage on which one of the herald viruses was located, but they were genetically and antigenically different from the herald viruses.

Antigens, Viral↗
PubMed1991

An influenza A virus containing influenza B virus 5' and 3' noncoding regions on the neuraminidase gene is attenuated in mice.

Influenza A and B viruses have not been shown to form reassortants. It had been assumed that the lack of genotypic mixing between influenza virus types reflected differences in polymerase and packaging specificity. 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. Although the transcription level of this CAT gene was several times lower than that of a CAT gene flanked by the homologous nontranslated sequences of an influenza A virus, we proceeded to construct a chimeric type A/B influenza virus. Using recombinant DNA techniques, a chimeric neuraminidase gene was introduced into the genome of influenza A/WSN/33 virus. The hybrid influenza A/B virus gene contained the coding region of the A/WSN neuraminidase and the 3' and 5' nontranslated sequences of the nonstructural gene of influenza B/Lee virus. The resulting chimeric virus formed plaques in Madin-Darby bovine kidney cells but replicated more slowly and achieved lower titers than wild-type influenza A/WSN/33 virus. The chimeric virus was attenuated for mice as indicated by a 400-fold increase in its LD50. Interestingly, the virus was greatly restricted in replication in the upper respiratory tract and partially restricted in the lungs. Animals infected with the transfectant virus were highly resistant to influenza virus challenge. It appears that this chimeric virus has many of the properties desirable for a live attenuated virus vaccine.

Animals↗
PubMedDate not supplied

[Antigenic heterogeneity of influenza virus B neuraminidases].

Antigenic relationships among neuraminidases of influenza B viruses isolated in 1940-1980 were studied by means of the neuraminidase activity inhibition test using hypoimmune sera from rats and roosters. Cross-reactions between influenza B virus enzymes showed their antigenic heterogeneity. The results permit conclusion that among influenza B virus strains both the drift and shift variants may be distinguished by the antigenic composition of the neuraminidase component.

Animals↗
PubMed1998

Identification of new influenza B virus variants by multiplex reverse transcription-PCR and the heteroduplex mobility assay.

A quick genetic approach for the screening of influenza virus variants was developed in this laboratory (S. Zou, J. Clin. Microbiol. 35:2623-2627, 1997). It uses multiplex reverse transcription and multiplex PCR to amplify and differentiate the variable region of the hemagglutinin genes of different types and subtypes of influenza viruses. Variants within the same type or subtype are then identified by the heteroduplex mobility shift assay of the amplicons. The method was used to screen influenza virus isolates received from provincial laboratories during the 1996-1997 season and was able to identify new influenza B virus variants. Sequencing of the amplicons derived from the hemagglutinin gene of the identified variants and comparison with the vaccine strain B/Harbin/7/94 showed substitution rates of 2.26 to 2.55% at the nucleotide level and 4.26 to 4.68% at the amino acid level. The result further demonstrated that the approach provides a quick, sensitive, and reliable screening for influenza virus variants. It also suggested the necessity of close monitoring of influenza B virus isolates in the 1997-1998 season and critical evaluation of the reference strain for the type B influenza virus.

Base Sequence↗
PubMed2006

[Antigenic and genetic study of influenza virus B circulated in China in 2004-2005].

BACKGROUND: To analyze the genetic and antigenic characteristics of hemagglutinin (HA) gene of human influenza B virus isolated from the mainland of China since 2004-2005. METHODS: The single-way hemagglutinin inhibition (HI) tests were used to test the antigenic characteristics, and the HA1 gene was sequenced based on the antigenic results. RESULTS: The Yamagata-like and Victoria-like viruses co-circulated in 2004-2005. For the Yamagata-like virus, the single-way HI results showed that 3.7% and 4.5% of the viruses had 4-fold greater HI titer difference compared with B/Shanghai/361/02 in 2004 and 2005, respectively. The HA1 sequence data showed that the virus had amino acid mutation, and there was one more glycosylation site at 196th site. For the Victoria-like virus, the single-way HI results showed that 8.5% and 20.6% of the viruses had 4-fold greater HI titer difference compared with B/Hong kong/330/01 in 2004 and 2005, respectively. The HA1 sequence data showed that the virus had replacement of 9 amino acids, and there was one more glycosylation site at 197th site. CONCLUSION: The results showed that influenza B viruses had changed antigenic and genetic characteristics compared with B/Shanghai/361/02, B/Hong kong/330/01 in 2004-2005.

Antigens, Viral↗