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Query: UNIPROT:Q17RS7 (
Gen
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130,125
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Infection
of human embryonic kidney cells with adenovirus type 5 (Ad5) induces aberrations (gaps and breaks) in the cell chromosomes. We have conducted a study utilizing a large number of Ad5 mutants to identify the viral functions that are responsible for the occurrence of cytogenetic damage. The results of our investigation have indicated that expression of the gene products of the Ad5 early region 1A (E1A) is necessary for the induction of chromosomal aberrations and that other early viral gene products do not appear to contribute to this phenotype. We have also shown that expression of both the major E1A gene products, the 243 amino acid and the 289 amino acid proteins, is required for induction of damage at wild-type levels, although the 289 amino acid protein appears to retain detectable activity on its own. Lastly, we have observed that deletions in the amino-terminal region of the E1A proteins and in the transactivating domain of the 289 amino acid protein prevent the occurrence of cytogenetic damage, whereas mutations elsewhere in the proteins do not affect this process.
J
Gen
Virol 1990 Apr
PMID:Definition of adenovirus type 5 functions involved in the induction of chromosomal aberrations in human cells. 213 7
Pulmonary A2 strain respiratory syncytial virus infection of BALB/c laboratory mice persisted for up to 7 days after initial infection with peak virus titres being recovered on day 4. Virus antigen within the lungs was found to be restricted essentially to the alveolar regions. Similarly, pulmonary histopathological changes remained confined to the peri-alveolar regions being consistent with mild pneumonia.
Infection
was found to elicit a pulmonary major histocompatibility complex-restricted cytotoxic T lymphocyte (CTL) response which was first detectable 6 days after infection and optimal 7 to 9 days after infection. This local CTL response was preceded by a rapid transient virus-specific lymphocyte transformation response which was detectable only 3 days after intranasal infection. In addition, infection induced rapid interferon production within the lungs which was accompanied by an equally rapid rise in pulmonary natural killer (NK) cell cytotoxic activity. Enhanced NK cell cytotoxicity could be detected after only 1 day post-infection and continued to rise to maximum levels on day 3. This response like the acute CTL response was found to be restricted to the lower respiratory tract. IgG was the first class of virus-specific immunoglobulin to be detected in the lungs of infected animals after experimental infection. However, IgG was not detected until day 10 post-infection, 5 days after the initial decline of virus shedding. Virus-specific IgA although detectable did not appear in the lung until day 24.
J
Gen
Virol 1990 Jul
PMID:Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection. 219 71
Infection
of tissue culture cells with vaccinia virus results in the specific secretion of several polypeptides into the medium. Previous studies identified a protein of approximate Mr 35,000 (35K) which was secreted in large amounts at both early and late times after infection with the Evans strain. We now show that a related protein is secreted by the Lister strain but not by WR, Wyeth nor Tian Tan. The gene encoding the Lister strain 35K protein was mapped within the inverted terminal repeats of the genome. The DNA sequence of this region showed that the ends of this gene are very similar to previously published sequences flanking a gene of WR which encodes a protein of approximate Mr 7,500 (7.5K). Our results suggest that the 7.5K polypeptide of WR may have arisen as a result of a deletion event and is a truncated form of the 35K Lister protein. Site-directed mutagenesis demonstrated that the 35K secreted protein encoded by Lister is not essential for growth in tissue culture.
J
Gen
Virol 1990 Sep
PMID:DNA sequence of the gene encoding a major secreted protein of vaccinia virus, strain Lister. 221 91
The coding region of the gene for the nucleocapsid protein of Lassa virus has been inserted into the genome of Autographa californica nuclear polyhedrosis virus (AcNPV) using the transfer vector pAcYM1, so that expression of the foreign DNA is under the control of the promoter of the AcNPV polyhedrin gene.
Infection
of cultured Spodoptera frugiperda cells with recombinant virus resulted in the synthesis of high levels of a protein that was indistinguishable from the authentic Lassa virus protein by SDS gel electrophoresis and immunoblotting with a variety of specific immune sera and monoclonal antibodies (MAbs). The kinetics of appearance of the protein were comparable to those of polyhedrin production in wild-type AcNPV-infected cells. The recombinant material was antigenic when used in ELISA for Lassa virus-specific antibodies, reacting well with MAbs specific for the nucleocapsid protein and with sera from experimentally infected guinea-pigs. The recombinant ELISA was able to clearly distinguish sera from human cases of Lassa fever against a panel of known negative sera of African origin. Recombinant-infected insect cells were an effective substitute for mammalian cells infected with Lassa virus itself in the immunofluorescence assay for Lassa virus-specific antibodies. This system offers attractive alternatives to the use of Lassa virus-infected materials as reagents in diagnostic procedures.
J
Gen
Virol 1990 Jan
PMID:Expression of the Lassa virus nucleocapsid protein in insect cells infected with a recombinant baculovirus: application to diagnostic assays for Lassa virus infection. 240 67
Infection
by a human spumavirus of human foetal diploid lung (HFDL) cells was found to be productive with virus titres ranging from 10(3) to 10(5) p.f.u./ml. In contrast, infection of recovered amnion (RA) aneuploid cells resulted in a persistent infection with less than 100 p.f.u./ml infectious virus produced. The decreased sensitivity of RA cells to the spumavirus was not due to the failure of virus to penetrate into the cell since infectious virus was not produced even after transfection of infectious proviral DNA. The effect of 5-azacytidine, an inhibitor of DNA methylation, on virus replication was examined. Whereas virus production in HFDL cells was not affected, there was a 100-fold increase in virus yield in RA cells treated with the drug for at least 48 h and maximum virus yields were obtained 4 days post-infection.
J
Gen
Virol 1987 Apr
PMID:Enhanced production of a human spumavirus (Retroviridae) in semi-permissive cell cultures after treatment with 5-azacytidine. 243 43
We have constructed an IPTG-inducible plasmid which overexpresses oop RNA sequences in Escherichia coli.
Infection
of these transformed E. coli cells (SB221/pOOP5) with lambda+ phage produced clear plaques, whereas lambda+ infection of cells transformed with the plasmid vector (SB221/pJDC406) or the plasmid expressing the oop RNA transcript in the other orientation (SB221/pOOP9) gave rise to turbid plaques characteristic of lambda+. Calculations of the percentage of infected cells forming lysogens show a 6-fold decrease in the absence of isopropyl beta-D-thiogalactoside (IPTG) and a 20-fold decrease in the presence of IPTG for SB221/pOOP5 as compared to both SB221/pJDC406 and SB221/pOOP9. We have thus shown that the overexpression of oop RNA favors the lytic mode of lambda development.
Mol
Gen
Genet 1987 Nov
PMID:Overproduction of an antisense RNA containing the oop RNA sequence of bacteriophage lambda induces clear plaque formation. 244 89
Infection
of three calves with a highly plaque-purified strain of bluetongue virus (BTV) resulted in prolonged infections, during which virus and neutralizing antibodies co-circulated in peripheral blood. Oligonucleotide fingerprint analyses of the original challenge virus and of the final virus isolate obtained from each calf demonstrated the BTV genome to remain stable throughout prolonged infection as no differences in fingerprint patterns were detected. Six neutralizing monoclonal antibodies (MAbs), and a polyclonal rabbit antiserum, were produced against the challenge virus. This panel of MAbs recognized at least two distinct neutralizing epitopes as demonstrated by immune precipitation. Neutralizing epitopes remained stable through the prolonged infections, as all MAbs and the polyclonal rabbit antiserum neutralized the challenge virus and the final calf isolates to equivalent titres. These results suggest that antigenic drift is not the mechanism by which BTV is able to persist in cattle in spite of a strong humoral immune response.
J
Gen
Virol 1988 Oct
PMID:Bluetongue virus genome remains stable throughout prolonged infection of cattle. 245 3
Infection
with the bacteriophage mutant Mu c+ gemts2 at 42 degrees C induces synchrony in cell division in cultures of Escherichia coli K12. This synchrony may last for several cycles and is not only due to selection since synchronization is observed even when bacterial survival to the infection is over 80% as in lysogens for Mu c+ gemts2. The mechanism by which synchrony is induced is not known, but since the product of Mu gene gem (previously called lig) has been shown to interact with the enzymatic system in the bacteria controlling the degree of DNA supercoiling, the phenomenon could be a consequence of this interaction.
Mol
Gen
Genet 1989 Jul
PMID:Synchronous division induced in Escherichia coli K12 by gemts mutants of phage Mu. 252 78
Infection
of the lymphoblastoid CEM cell line with herpes simplex virus (HSV) type 1 results in a persistent infection with production of infectious virus. Evidence suggests that the persistent infection was not maintained by interferon or non-interferon-soluble antiviral inhibitors. Treatment of persistently infected cells with anti-HSV serum (termed CEMACR cells) or elevated temperature (39 degrees C) for 14 days (termed CEMTCR cells) resulted in loss of evidence of virus. HSV DNA was not detected in CEMACR or CEMTCR cells by Southern blot or in situ hybridization. The CEMACR or CEMTCR cells, however, were resistant to reinfection with homologous, parental virus (HSV0), but were susceptible to heterologous virus (vesicular stomatitis virus). Resistance to reinfection with HSV was not absolute; CEMACR or CEMTCR cells were less permissive to virus isolated from persistently infected cultures at times early in the course of infection, but were more permissive for HSV isolated at later times. Virus isolated later during persistent infection also displayed progressively increased virulence for the parental CEM cells. These results suggest that persistent infection of a human T lymphoblastoid cell line, CEM, with HSV-1 is maintained by a genetically determined cell-virus equilibrium, in which the resistance of cells and virulence of virus increase during persistence.
J
Gen
Virol 1989 Jan
PMID:Coevolution of virulent virus and resistant cells as a mechanism of persistence of herpes simplex virus type 1 in a human T lymphoblastoid cell line. 254 40
Infection
by Thogoto (THO) virus, a tick-borne virus related to the orthomyxoviruses, has been compared in vertebrate cell culture and in Rhipicephalus appendiculatus ticks using infectivity titrations, immunofluorescence, and immune electron microscopy with colloidal gold markers to detect cell surface and intracellular antigens. Morphogenesis of THO virus in cell culture was similar to that of influenza virus, with polymorphic virus particles budding at the plasma membrane. In the tick, THO viral infection caused no obvious pathology; virions or budding profiles were not observed in electron micrographs, although replication, trans-stadial persistence and transmission to a susceptible host occur. THO virus was not detected in the salivary glands of trans-stadially infected ticks until about 7 days after the commencement of feeding on a host. The synganglion (brain) appears to be the major organ involved in trans-stadial persistence of the virus; viral antigens were detected in the neural cortex (cell bodies) but not in nerve fibres and axons. The detection of THO viral antigen in basement membranes and connective tissue, but its absence from nerve fibres, suggests that dissemination occurs via the haemolymph rather than a neural route.
J
Gen
Virol 1989 May
PMID:Anatomical basis of Thogoto virus infection in BHK cell culture and in the ixodid tick vector, Rhipicephalus appendiculatus. 254 69
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