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Results for “ADENOVIRUS INFECTIONS”

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At least 577 records · Page 32Linked to original sources
PubMed2001

Rapid assessment of adenovirus serum neutralizing antibody titer based on quantitative, morphometric evaluation of capsid binding and intracellular trafficking: population analysis of adenovirus capsid association with cells is predictive of adenovirus infectivity.

Neutralizing antiviral antibodies are typically detected on the basis of inhibition of viral function, such as propagation of a viral infection or inhibition of viral gene expression. Evidence is presented that anti-adenovirus neutralizing antibodies can be evaluated by analysis of cell-associated capsids or by analysis of intracellular trafficking of the capsids within 1 h after infection. Quantitative analyses of these morphologic parameters represent rapid, broadly applicable, functional assays for the detection of anti-adenovirus neutralizing antibodies.

Adenoviridae↗
PubMed1982

Defective parvoviruses acquired via the transplacental route protect mice against lethal adenovirus infection.

Adeno-associated virus type 1 (AAV-1) interfered with the replication of its murine adenovirus (MAV) helper in primary mouse kidney cells and in 1-day-old ICR mice. Mice carrying AAV-1 acquired via the transplacental route were protected against lethal infection with MAV. The replication of AAV-1 in these mice could be triggered by multiple challenges with MAV, and antibodies to AAV-1 were subsequently detected.

Adenoviridae↗
PubMed1958

Characterization of a factor formed in the course of adenovirus infection of tissue cultures causing detachment of cells from glass.

Infectious tissue culture fluids of the majority of serotypes of adenovirus at low dilutions detach HeLa or KB cells from glass surfaces within a few hours after inoculation. A reproducible method for testing cell detachment was devised. The factor present in infectious tissue culture fluids and responsible for cell detachment is trypsin-sensitive and non-dialyzable; it is smaller and more resistant to the effect of heat or ultraviolet light than the infectious virus particle. Cell detachment activity was found to be temperature-dependent, and the cell-detaching titer of infectious tissue culture fluids was not affected by repeated exposure to HeLa cells. Inhibition of cell detachment by human or rabbit sera was observed only when other antibodies to adenovirus antigens were also present, but the antibody inhibiting cell detachment could not be correlated quantitatively with complement-fixing or homologous neutralizing antibody.

Adenoviridae↗
PubMedDate not supplied

Increased MHC H-2K gene transcription in cultured mouse embryo cells after adenovirus infection.

The class I major histocompatibility complex (MHC) antigens are highly polymorphic cell-surface proteins whose expression is essential for the cellular immune response against virus-infected, abnormal and foreign cells. Transformation of primary rat cell cultures by the oncogenic adenovirus 12 (Ad12) results in suppression of the transplantation antigens, thus enabling the transformed cells to escape the immune response and efficiently form tumours in vivo. In contrast, transformation of the same cells with the non-oncogenic adenovirus 5 (Ad5) does not suppress the transplantation antigens and, consequently, they elicit an effective (MHC-restricted) immune response. Here, however, we show that infection of mouse embryo cells with both viruses initially increases the level of transcripts from the H-2Kb transplantation antigen gene. Both the adenovirus E1a (12S RNA) and E1b genes are required for activation of the H-2K gene and measurement of the relative rate of transcription indicates that the increase in the level of H-2K messenger RNA following infection is at least in part due to a gene-specific transcriptional activation. The newly transcribed H-2Kb mRNA is then properly transported to the cytoplasm.

Adenoviruses, Human↗
PubMed1989

Relationship between organization of the actin cytoskeleton and the cell cycle in normal and adenovirus-infected rat cells.

Flow cytometry and staining with 7-nitrobenz-2-oxa-1,3-diazole-phallacidin were used to investigate organization of the actin cytoskeleton in rat embryo cells at different stages of normal and adenovirus E1A-induced cell cycles. In uninfected cells in G0-G1 and S phases, actin was predominantly in the form of stress fibers. In G2, this organization changed to peripheral rings of thin filaments, while during mitosis, actin had a diffuse distribution. Infection of quiescent rat cells by adenovirus caused them to enter the cell cycle and replicate DNA and also caused disruption of stress fibers. Rapid disappearance of stress fibers and the appearance of peripheral rings of actin filaments began from 13 h after infection and closely followed synthesis of the E1A proteins. Infected cells began S phase at about 24 h after infection, and cells in G2 and mitosis were seen from 30 to 50 h. Thus, disruption of the actin cytoskeleton is an early effect of E1A and not an indirect consequence of the entry of infected cells into the cell cycle.

Actins↗
PubMed1978

Subclinical pneumonia associated with an experimental adenovirus infection in the domestic fowl and the effect of concurrent infectious laryngotracheitis virus.

A CELO-type adenovirus (AV) isolated from fowls with respiratory disease was inoculated experimentally into the tracheas of young birds. No symptoms referable to respiratory infection were evident. Post mortem examination between days 2 and 5 after inoculation revealed pneumonia involving up to 30 per cent of the surface of the lungs. Histologically, a focal to diffuse interstitial lymphocytic infiltration and bronchiolar degeneration were present. Concurrent infections with a mild strain of infectious laryngotracheitis virus (ILT) failed to enhance the pathogenicity of either the AV or ILT infections.

Adenoviridae Infections↗
PubMed2005

Ionizing radiation-induced adenovirus infection is mediated by Dynamin 2.

Specific viral targeting into intrahepatic tumors remains critical for adenovirus gene therapy in liver cancer. We previously showed that ionizing radiation increases adenovirus uptake and transgene expression in cells and colon cancer xenografts. Here, we tested whether radiation induces viral uptake through virus-cell membrane interaction. We found that radiation (8 Gy) induced adenoviral gene transfer in rat hepatocytes (WB) and human colon carcinoma cells (LoVo). This induction (24.4- and 6.5-fold, respectively) and viral uptake were significantly diminished by preincubation with antibody for Dynamin 2 but not for Coxsackie adenovirus receptor or for integrin alpha(v). Radiation-induced Dynamin 2 expression was detected by immunohistochemical staining and by increased mRNA levels for Dynamin 2 in WB (1.5-fold) and LoVo (2.2-fold) cells. Specific small interference RNA (siRNA) transfection significantly inhibited Dynamin 2 expression in various tumor cell lines (LoVo, D54, and MCF-7) and abolished the radiation induction of Dynamin 2. Likewise, radiation-induced viral gene transfer in these cells (6.5-, 5.5-, and 9.0-fold, respectively) was significantly reduced in siRNA-transfected cells (2.7-, 3.7-, and 5.0-fold, respectively). Moreover, viral uptake in LoVo tumor xenografts was significantly increased in s.c. tumors (10.9-fold) when adenovirus was given i.v. at 24 hours after tumor irradiation, coincident with an elevated Dynamin 2 expression in irradiated tumors. These data suggest that ionizing radiation induces adenovirus gene transfer in cells and tumor xenografts by regulating viral uptake, potentially through interaction with cellular Dynamin 2 and thus should provide insight into improving adenovirus targeting in tumors.

Adenoviridae↗
PubMed1998

Differential susceptibility of primary and established human glioma cells to adenovirus infection: targeting via the epidermal growth factor receptor achieves fiber receptor-independent gene transfer.

Adenovirus (Ad) vectors are promising for gene therapy of glioma due to their ability to achieve efficient gene transfer upon intratumoral administration. Yet in this context, Ad mediates widespread gene transfer to both tumor and surrounding parenchyma. Ad entry is dependent upon the expression of fiber receptors, such as coxsackie/adenovirus receptor, and alpha(v) integrins on the target cells for binding and internalization, respectively. We hypothesized that the susceptibility of human gliomas to Ad would likely be heterogeneous due to variable expression of these receptors. It was found that established human glioma cell lines exhibited differential susceptibility to Ad-mediated gene transfer, which correlated directly with the level of radiolabeled Ad binding and with the expression of coxsackie/adenovirus receptor but not with the expression of alpha(v) integrins. To circumvent the lack of fiber receptors and to target Ad gene transfer specifically to tumor cells, we used a bispecific antibody conjugate to ablate Ad binding to fiber receptors and retarget binding to the epidermal growth factor receptor (EGFR), a tumor-associated marker negligibly expressed in normal, mitotically quiescent neural tissues. The results demonstrate that EGFR-targeted Ad gene transfer was EGFR specific and independent of fiber-fiber receptor interactions. Furthermore, EGFR targeting significantly enhanced Ad gene delivery to 7 of 12 established glioma cell lines and to 6 of 8 cultured primary gliomas. Interestingly, EGFR-targeted Ad gene transfer did not correlate with EGFR expression across cell lines, suggesting the importance of other factors. This study establishes that fiber receptor expression limits the utility of Ad vectors for gene transfer to glioma cells and suggests that targeting Ad via EGFR may prove valuable for tumor-specific gene transfer to high-grade gliomas. These findings have key relevance in the context of Ad vector-based approaches for glioma gene therapy.

Adenoviruses, Human↗
PubMed2003

Corneal IL-8 expression following adenovirus infection is mediated by c-Src activation in human corneal fibroblasts.

Emerging evidence indicates that intracellular signaling cascades mediate entry of pathogenic adenoviruses into target host cells as well as some of the undesirable inflammatory responses to adenoviral gene vectors. We found that Ad19 infection of cultured human corneal fibroblasts induced IL-8 gene transcription independently of IL-1beta, TNF-alpha, and viral gene expression, suggesting that intracellular signaling events might mediate early inflammatory events in adenovirus keratitis. Heat but not UV light inactivation of the virus abrogated the effect of infection on IL-8 mRNA and protein levels, consistent with a viral binding-mediated mechanism. The tyrosine kinase inhibitor herbimycin blocked Ad19-induced IL-8 expression. Western blot analysis revealed tyrosine phosphorylation of the functionally related kinases c-Src and extracellular signal-regulated kinase (ERK) 1/2 in corneal fibroblasts within 15 min after infection. Respective inhibitors of these kinases, PP2 and PD98059, also blocked Ad19-induced IL-8 mRNA and protein expression. Application of inhibitors to Src and ERK kinase assays suggested an upstream relationship of c-Src to ERK. Finally, DNA microarray studies performed 1 h after Ad19 or mock infection of corneal fibroblasts in the presence or absence of the Src-specific inhibitor PP2 confirmed a relationship between c-Src and IL-8 expression in Ad19-infected corneal cells. c-Src may act as a global regulator of early proinflammatory host responses to Ad19 infection of the human cornea.

Adenoviruses, Human↗