Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q17RS7 (Gen)
 130,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genetic compositions of four antigenic variants of A/Memphis/1/71 (H3N2) influenza virus, which were selected by growth in the presence of monoclonal antibodies against the haemagglutinin, were compared. The results indicate that the mutant haemagglutinin genes can be differentiated by polyacrylamide gel electrophoresis of the double stranded RNA hybrids formed between virion RNA and transcripts isolated from infected cells.
J Gen Virol 1979 Oct
PMID:Differentiation of the haemagglutinin genes of variant influenza viruses by RNA-RNA hybridization. 52 5

Polyadenylated transcripts synthesized in vitro by detergent-disrupted influenza virus resemble virus mRNAs in that they possess the complement of the 3' terminus of the genome RNAs but lack sequences corresponding to the same 5' terminal region, including the homologous sequence of nucleotides 1 to 22. Transcription is initiated at the 3' terminus by both ApG and GpG as well as in the absence of added primer.
J Gen Virol 1979 Sep
PMID:Characterization of influenza virus RNA transcripts synthesized in vitro. 52 78

Several influenza A strains and recombinants of fowl plague virus (FPV) with a known gene constellation were tested for amantadine sensitivity under two different experimental conditions. In a haemagglutinin yield analysis of a single growth cycle experiment FPV was found to be highly sensitive to amantadine, while in the plaque reduction and inhibition test it was highly resistant. With the A3 Hong Kong and equi 2 strains the opposite observation was made. The A2 Singapore strain was sensitive while Ao PR8 was resistant in both tests. In the haemagglutinin yield analysis of a single growth cycle all recombinants carrying segment 4 (HA) of the resistant strain were resistent against amantadine, independent of the derivation of the other genes. In the plaque reduction and inhibition test recombinants carrying the haemagglutinin of the sensitive strain were either resistant or sensitive depending on the gene constellation. Drug sensitivity was transferred by the combination of segments 5 (NP) and 6 (NA). Segment 7 (M) of certain sensitive strains seems to counteract this effect. The results are compatible with the concept that amantadine resistance or sensitivity is not confined to a single gene product or a single mechanism.
J Gen Virol 1979 Sep
PMID:Amantadine-resistant and -sensitive influenza A strains and recombinants. 52 83

Chicken fibroblasts and MDCK cells were infected with influenza virus labelled with either 3H-uridine or 14C-amino acids, and the location in infected cells and properties of input virus-labelled structures were studied. Input virus RNA and protein were found in the cytoplasm of nuclei 1 h p.i. A part of the intranuclear parental structures was associated with chromatin while the other part could be extracted from nucleoplasm by 0.16 M-NaCl and represented free ribonucleoprotein (RNP) particles. These RNPs sedimented in glycerol velocity gradients at 40 to 70S, very similar to cytoplasmic RNPs, but differed distinctly from them in buoyant density. The bulk of cytoplasmic RNPs after fixation with formaldehyde banded in CsCl at 1.34 g/ml while nucleoplasmic RNPs banded at 1.39 or 1.41 g/ml. RNPs isolated from virions and infected cells contained the NP polypeptide which was revealed by SDS-PAGE analysis as a double band. The ratio of the two bands varied in cytoplasmic and nucleoplasmic RNPs, the lower band being dominant in cytoplasmic but not in nucleoplasmic RNPs. In addition, cytoplasmic RNPs were phosphorylated. The possible significance of intracellular RNP modifications for virus replication is discussed.
J Gen Virol 1979 Dec
PMID:Cytoplasmic and nuclear input virus RNPs in influenza virus-infected cells. 54 71

Structural and virus-induced infected cell polypeptides of several strains of influenza B virus were examined by high resolution polyacrylamide gel electrophoresis and shown to be directly analogous to those of the influenza A viruses. Eight structural polypeptides, P1, P2, P3, HA1, HA2, NA, NP and M were observed in purified virus and at least two additional polypeptides, HA and NS could be detected in infected MDCK cells. The three P proteins plus NP were shown to be associated with RNA-dependent RNA polymerase activity and HA, HA1, HA2 and NA were shown to be glycosylated. Like the influenza A viruses, migrational differences of some of the infected cell polypeptides could be observed between different B strains. Investigation of a time course of virus replication failed to show any temporal control of protein synthesis in the infected cell.
J Gen Virol 1979 Dec
PMID:The structural and infected cell polypeptides of influenza B virus. 54 75

All the girls at a boarding school who presented with symptoms of influenza were interviewed and examined. Their symptoms and signs were recorded and related to age, date of last menstrual period, and previous influenza immunization.The age of the girls had no influence on the incidence of disease, nor did the number of girls in each form. However, the attack rate among those not immunized was 61 per cent and those not immunized 71 per cent. There was a highly significant variation in the incidence of influenza in relation to the menstrual cycle.
J R Coll Gen Pract 1979 Mar
PMID:'Red'flu': a study of an epidemic in a girls' boarding school in February 1978. 54 88

Lectins of different specificities do not interfere with the maturation of myxo-viruses; their inhibitory effect on virus replication is mainly due to prevention of the detachment of infectious virus particles from the host cell. In chick embryo fibroblasts infected with an influenza virus and treated with concanavalin A, budding occurs into intracytoplasmic vacuoles, but this phenomenon is not observed with a parainfluenza virus and with different cells.
J Gen Virol 1977 Mar
PMID:Studies on the inhibitory effect of lectins on myxo-virus release. 55 81

The infection of eggs, cell cultures or mice with a mixture of amantadine-resistant and amantadine-sensitive strains of influenza virus resulted in the transfer of amantadine-resistance or sensitivity between strains. The response of a recombinant virus to amantadine was not related to either of its surface antigens. Resistance to amantadine was transferred as an all-or-none character. It is concluded that amantadine-resistance is a useful genetic marker for influenza viruses.
J Gen Virol 1977 Aug
PMID:Amantadine-resistance as a genetic marker for influenza viruses. 56 Nov 63

Cells were cultured from the breast muscle of 11- to 12-day-old chick embryos and were grown under conditions optimal for the development of the cells into terminally differentiated, fused myotubes. Myotubes were infected with influenza virus A/Ann Arbor/6/60(H2N2) at high multiplicity, and synthesis of virus-specific proteins and RNAs was detected by haemadsorption, fluorescence microscopy and/or isotope labelling and electrophoresis techniques. Provided that myotubes were maintained at temperatures below 39 degrees C after infection, production of virus components and yield of infectious virus in these cells was similar to those observed in infected chick kidney cells. However, if cells were maintained at temperatures of 39 degrees to 40 degrees C after infection, virus nucleoprotein was prominent in the nuclei, and synthesis of virus-specific polypeptides and of plus-strand RNA was reduced about fourfold to 20-fold compared to that detected at lower temperatures. Moreover, infectious virus was not produced when temperatures of 39 to 40 degrees C were used during virus replication. The results demonstrate that under suitable conditions avian myotubes formed in culture resemble epithelioid cells in their ability to support the productive replication of influenza virus.
J Gen Virol 1977 Oct
PMID:Replication of animal viruses in differentiating muscle cells: influenza virus A. 56 89

During the propagation of A (H3N2) influenza virus in chick embryos, incorporation of 3H-thymidine into virions takes place, whereas no such incorporation occurs with Newcastle disease virus. Incorporation of 3H-thymidine is a result of DNA synthesis. This virion-associated DNA is present in cores obtained after treatment of virions with bromelain.
J Gen Virol 1978 Nov
PMID:DNA sequences in influenza virions. 56 83


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