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At least 991 records · Page 55Linked to original sources
PubMed1974

Beta-glucuronidase response of cells infected with Adenovirus types 5 and 12.

Beta-glucuronidase activity was investigated during a 48-h period in which virus replication and changes in cell morphology occurred. Infection of an established line of chimpanzee liver cells with either nononcogenic adenovirus 5 or highly oncogenic adenovirus 12 under one-step growth conditions produced differing patterns of enzyme activity. There was an increase in total activity and also enhanced leakage of beta-glucuronidase from cells infected with adenovirus 12. In contrast, the enzymatic pattern of cells infected with adenovirus 5 was similar to that of uninfected cells. Hydrocortisone prevented the abnormal release of beta-glucuronidase from adenovirus 12-infected cells. The compound had no effect on total enzyme activity or on virus replication and the development of cytopathology.

Adenoviridae↗
PubMed1983

Acylated simian virus 40-specific proteins in the plasma membrane of HeLa cells infected with adenovirus 2-simian virus 40 hybrid virus Ad2+ND2.

HeLa cells infected with the adenovirus 2-simian virus 40 (Ad2+SV40) hybrid virus Ad2+ND2 were labeled with either [35S]methionine or [3H]palmitate and fractionated into cytoplasmic, nuclear, and plasma membrane fractions. Analysis of these fractions by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that the SV40-specific proteins in the plasma membrane fraction were specificially acylated.

Adenoviridae↗
PubMed1979

Microcentrifuge technique and its application for visualizing the simultaneous replication and transcription of an adenovirus DNA.

Miller's technique (microcentrifuge method) of visualizing transcriptional events at the molecular level is introduced with a review on the work that applied this technique, and followed by presentation of an article describing one such application in which the modes of replication and transcription are electronmicroscopically demonstrated in an adenovirus-infected cell nucleus. Adenovirus is chosen owing to its character of multiplying in a mammalian cell nucleus. Recently, there have been many important discoveries on the modes of DNA replication and RNA transcription through biochemical probes. It is confirmed by Miller's technique that large primary precursor messenger RNA is first transcribed at a late stage in a cell nucleus productively infected with adenovirus. Evidence is shown that a replicating viral DNA molecule can be simultaneously transcribed.

Adenoviridae↗
PubMed2004

[Nosocomial infections due to adenovirus in a paediatric unit].

OBJECTIVE: We carried out a retrospective analysis of an outbreak of adenovirus (AdV) infections in a paediatric unit. The aim of the study was to analyse cases, determine the route of transmission and to evaluate the efficacy of the prevention measures. PATIENTS AND METHODS: The study was performed by recollection of AdV infection cases during a period of 1 year and the results were compared with the list of clinical cases recorded during the epidemic. The clinical files of children with a positive specimen were retrospectively analysed. During that period, five members of the medical staff showed clinical signs and symptoms of AdV infection. A throat swab was collected from a subset of the staff. RESULTS: Among nine patients with positive AdV detection, six were infected with an Adv type 2. Six were nosocomially-acquired, the other two were only probable nosocomial infections. The index case was a child presenting a febrile diarrhoea 48 h prior to being admitted to the hospital. Nosocomial transmission was associated with the prolonged shedding of the virus with faeces of the infected cases. The specimens collected from the staff remained negative. The outcome was favourable for all children. CONCLUSIONS: Prevention measures, implemented when the epidemic was characterised, allowed the control of the nosocomial outbreak.

Adenovirus Infections, Human↗
PubMed1993

Structurally related class I and class II receptor protein tyrosine kinases are down-regulated by the same E3 protein coded for by human group C adenoviruses.

Receptor tyrosine kinases (RTKs) are grouped into subcategories based on shared sequence and structural features. Human group C adenoviruses down-regulate EGF receptors, which are members of the class I family of RTKs, during the early stages of infection. Adenovirus appears to utilize a nonsaturable intracellular pathway since it causes EGF-R down-regulation even in cells that significantly overexpress EGF-R. Adenovirus-induced down-regulation is mediated by a small hydrophobic molecule coded for by the E3 early transcription region that has recently been localized to plasma membrane. Here we examine intracellular trafficking of other RTKs in adenovirus-infected cells, to better understand the molecular basis for the action of the E3 protein. Although p185c-neu, which is a class I RTK closely related to the EGF receptor, is down-regulated in cells expressing physiological concentrations of this molecule, it is not down-regulated in tumor cell lines that significantly overexpress p185c-neu. Cell surface receptors for insulin and IGF1, which are class II RTKs, are also reduced in cells expressing the E3 protein, although to a slightly lesser extent than the EGF receptor. Moreover, whereas EGF receptors are degraded between 3- and 9-h postinfection, insulin and IGF1 receptors are degraded between 6- and 12-h postinfection under identical conditions. In contrast to the class I and class II RTKs, there is no difference in the expression of the class III receptors for PDGF and aFGF in cells infected with a virus with an intact E3 region versus a virus mutant with an internal deletion in the relevant E3 gene. These results suggest that the E3 protein provides an internalization and degradative sorting signal for some class I and class II RTKs, although down-regulation of class II RTKs is somewhat less efficient. Molecular recognition of class I and class II RTKs during adenovirus infection may not be due strictly to amino acid structure, however, since EGF-R but not p185c-neu is down-regulated in cells where it is significantly overexpressed.

Adenovirus E3 Proteins↗
PubMed2005

Phylogenetic analysis of the hexon loop 1 region of an adenovirus from psittacine birds supports the existence of a new psittacine adenovirus (PsAdV).

Adenovirus infections in psittacine birds have been well known. Most of these infections were caused by fowl adenoviruses (FAdV). In this study, liver samples showing typical histological signs of an adenovirus infection were collected from Poicephalus spp. with acute disease. A PCR amplifying the variable loop 1 region of the hexon gene was developed using primers located in two conserved pedestal regions. A PCR product of approximately 590 bp in size was amplified and sequenced. The sequence obtained grouped outside of the FAdV reference strains of the 12 serotypes as well as egg drop syndrome virus and turkey adenovirus 3 indicating that a new avian adenovirus was detected. In comparison to the FAdV reference strains, the percentage of identical nucleotides ranged between 60.3 and 67.0 and that of identical amino acids (aa) between 51.3 and 61.0. Furthermore, 37 unique aa exchanges were observed; out of these, 27 are located in the 4 hypervariable regions of loop 1, which encode the serotype-specific epitopes. The g/c content, the isoelectric point and the charge of the amplified fragment, however, are in the range as those of group I avian adenoviruses. It was proposed, therefore, to designate this new adenovirus as psittacine adenovirus (PsAdV).

Adenoviridae↗
PubMed2001

Diagnostic assessment of haemorrhagic rash and fever.

AIMS: To establish criteria for early distinction between meningococcal disease and other conditions with similar clinical features, and to identify other causes for haemorrhagic rashes accompanied by fever. METHODS: In a prospective study, 264 infants and children hospitalised with fever and skin haemorrhages were studied. RESULTS: We identified an aetiological agent in 28%: 15% had meningococcal disease, 2% another invasive bacterial infection, 7% enterovirus infection, and 4% adenovirus infection. Five clinical variables distinguished between meningococcal disease and other conditions on admission: (1) skin haemorrhages of characteristic appearance; (2) universal distribution of skin haemorrhages; (3) maximum diameter of one or more skin haemorrhages greater than 2 mm; (4) poor general condition (using a standardised observation scheme); and (5) nuchal rigidity. If any two or more of these clinical variables were present, the probability of identifying a patient with meningococcal disease was 97% and the false positive rate was only 12%. This diagnostic algorithm did not identify children in whom septicaemia was caused by other bacterial species.

Adenovirus Infections, Human↗
PubMed2006

[Expression of B7 molecules and TLR-9 on corneal epithelial cells infected with adenovirus: clinico-pathological implications in viral keratoconjunctivitis].

PURPOSE: B7 molecules are a family of proteins that co-stimulate T cells during immune activation. Normally the corneal epithelial cells (CEC) do not express these molecules on their cell surface. Toll-like receptors play an important role in the innate immune response to invading pathogens and recently have been demonstrated to be expressed on mice cornea. The objective of this study was to determine whether adenoviral infection induces B7 molecules and TLR9 on human CEC. METHODS: CEC were isolated from human corneas treated with dispase-II, and grown in the presence of supplemented hormonal epithelial medium until confluence. Then CEC were then infected with adenovirus 5 (Ad5) and cultured for different times. The CEC were then recovered and stained against human CD80, CD86, TLR-9 and cytokeratin. All cells were analyzed by flow cytometry. RESULTS: Ad5 infection of CEC induced the expression of B7 molecules and TLR-9 after 24 hours in culture, rising to maximum levels at 72 hours. B7 expression at 72 hours was as follows: CD80 expression on infected CEC was 62% (standard error [SE] 2.6) versus 3% (SE 1.2) on non-infected CEC (p<0.001); CD86 expression on infected CEC was 95% (SE 2.1) versus 5% (SE 1.2) on non-infected CEC (p<0.001). TLR-9 expression at 72 hours was 80% (SE 1.2) on infected CEC versus 5% (SE 1) on non-infected CEC (p<0.001). CONCLUSIONS: Ad5 infection induced the expression of B7 molecules and TLR-9 on CEC.

Adenovirus Infections, Human↗
PubMed1999

Induction of apoptosis after switch-on of the hepatitis B virus X gene mediated by the Cre/loxP recombination system.

The HBx protein of hepatitis B virus is a multifunctional protein that is implicated in the pathogenesis of hepatocellular carcinoma by regulating gene transcription, causing cell proliferation and, as shown recently, inducing cell death. However, analysis of the effects of HBx in stable cultured cell clones has been hampered because only cell lines that adapted to the effects of HBx were selected during the establishment of cell clones. Here, we describe a system in which transcription of the X gene of hepatitis B virus is switched on by the use of the site-specific Cre recombinase. Two human liver cell lines, HLF and HepG2, were used, the former with a mutant p53 allele and the latter with wild-type p53. The stable cell clones isolated, which carried the X gene in a transcriptionally silent state, were infected with recombinant adenovirus carrying Cre recombinase. Ninety-six hours after adenovirus infection, cell clones that expressed HBx had undergone TUNEL-positive cell death with characteristics of apoptosis. Apoptosis was induced despite concomitant inactivation of the p53 protein as a result of its cytoplasmic translocation by HBx. In contrast, neither the X gene-carrying cells infected with wild-type adenovirus nor various control cells infected with Cre-expressing adenovirus exhibited apoptosis. These results indicate that the expression of HBx protein leads to liver cell apoptosis independently of the p53 pathway. The significance of HBx-induced apoptosis in natural infection is unclear, but it may contribute to the development of hepatitis and serve to spread progeny virus to neighbouring cells while evading the host immune responses.

Adenoviridae↗
PubMed1987

Study of avian adenovirus DNA infectivity in chick embryos.

Inoculation of CELO adenovirus deproteinized DNA into the allantoic cavity of 9-day-old chick embryos (CE) induced the synthesis of infectious viral particles. The produced virions appeared to be identical with CELO adenovirions in terms of morphology, electrophoretic and immunochemical properties of hexon major capsid protein and also of DNA dot-hybridization. High infectivity of CELO DNA (minimal infective dose equaled 40 ng) may be also related, at least in part, to the absence of deoxyribonuclease activity in the allantoic fluid (AF).

Adenoviridae↗
PubMed1997

Adenovirus vector-infected cells can escape adenovirus antigen-specific cytotoxic T-lymphocyte killing in vivo.

The recent findings that prolonged expression of certain adenovirus (Ad) vector-encoded proteins, including human alpha1-antitrypsin (huAAT), mouse erythropoietin (EPO), and human factor IX, can be achieved in animals that do not mount an immune response to the reporter protein were obtained with mouse strains which have been shown to be capable of mounting a cellular immune response against Ad vector antigens. This suggests either that Ad vectors expressing nonimmunogenic transgenes fail to elicit a cellular immune response or that an Ad-specific cellular immune response does develop but is ineffective against cells expressing nonimmunogenic transgenes. Here we demonstrate that an Ad vector expressing huAAT administered by intravenous injection does stimulate an Ad-specific cellular immune response but that this response fails to abolish vector-directed gene expression in vivo. Moreover, expression of huAAT remained stable in animals stimulated by concurrent and multiple administrations of different Ad vectors or viruses. We also demonstrate prolonged expression of huAAT in CD1 mice transgenic for the huAAT gene, indicating that long-term expression is not restricted to C57BL/6 mice. These results demonstrate that under some circumstances, an Ad vector can direct prolonged expression of a nonimmunogenic transgene despite the presence of a robust Ad-specific cellular immune response.

Adenoviridae↗
PubMed2001

Characterization of adenovirus-induced inverted terminal repeat-independent amplification of integrated adeno-associated virus rep-cap sequences.

Stable packaging cell lines expressing the rep and cap genes for recombinant adeno-associated virus type 2 (rAAV-2) assembly constitute an attractive alternative to transient transfection protocols. We recently characterized a stable HeLa rep-cap cell clone (HeRC32) and demonstrated that upon vector transfection and adenovirus infection, efficient rAAV assembly correlated with a 100-fold amplification of the integrated rep-cap sequence with the inverted terminal repeats (ITRs) deleted. We now report a more detailed analysis of this phenomenon and highlight the key cellular and viral factors involved. Determination of the rep-cap copy number of HeRC32 cells indicated that maximum rep-cap amplification occurred between 24 and 48 h following adenovirus infection. Analysis by pulsed-field gel electrophoresis of adenovirus-infected HeRC32 cells indicated that amplified rep-cap sequences were found in an extrachromosomal form. Amplification of the rep-cap sequence with the ITRs deleted was not dependent on adenovirus replication and still occurred when the highly specific adenovirus polymerase was inactivated. In contrast, amplification was inhibited in the presence of aphidicolin, indicating that cellular polymerases were needed. Our study also documented that among the adenovirus gene products, the DNA-binding protein (DBP) was essential, since rep-cap amplification was severely abrogated when HeRC32 cells were infected at a nonpermissive temperature with an adenovirus mutant encoding a thermosensitive DBP. Furthermore, expression of DBP alone in HeRC32 cells was sufficient to induce a sustained level of rep-cap amplification. Finally, immunofluorescence analysis showed that HeRC32 cells expressing the DBP also simultaneously expressed the Rep proteins, suggesting a possible involvement of the latter in rep-cap amplification. Indeed, the lack of detectable amplification in an adenovirus-infected stable rep-cap HeLa cell clone unable to produce Rep proteins further supported that, among the viral gene products, both the DBP and Rep proteins are necessary to induce the targeted amplification of the integrated rep-cap sequences in the absence of the AAV ITRs.

Adenoviridae↗