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At least 343 records · Page 19Linked to original sources
PubMed2002

Upregulation of the Golgi protein GP73 by adenovirus infection requires the E1A CtBP interaction domain.

GP73 is a novel type II Golgi transmembrane protein that is expressed at high levels in the hepatocytes of patients with viral hepatitis (R. D. Kladney, G. A. Bulla, L. Guo, A. L. Mason, A. E. Tollefson, D. J. Simon, Z. Koutoubi, and C. J. Fimmel, 2000, Gene 249, 53-65) and is induced in cultured cells by infection with viruses including adenoviruses. Its biological function and the mechanisms by which its expression may be regulated by viral infection are unknown. Here we report that GP73 is induced at the RNA and protein level in human Hep3B hepatoma cells infected by human Ad5 and Ad2. Hep3B cells were infected with wild-type or mutant adenoviruses. GP73 expression was measured by RNase protection assay, immunoblotting, or immunofluorescence microscopy. GP73 RNA and protein levels were strikingly induced following infection. The rise in GP73 expression coincided with the appearance of the adenovirus E1A and DBP proteins and preceded the expression of the fiber protein, a marker of the late phase of infection. Infection did not affect the expression of giantin, GPP130, or golgin-84, three integral Golgi membrane proteins with structural similarities to GP73. Mapping studies using a panel of mutant adenoviruses demonstrated that the E1A C-terminus, specifically its CtBP interaction domain (CID), is required for GP73 expression. Subsequently, Hep3B cells were transiently transfected with plasmids expressing wild-type or mutant E1A proteins. These studies confirmed that E1A induced GP73 expression via the CID. Our studies establish GP73 as a novel adenovirus-induced cellular protein whose expression is regulated through the CID of the E1A protein.

Adenovirus E1A Proteins↗
PubMed2001

Adenovirus infection increases iNOS and peroxynitrite production in the lung.

Host inflammatory and immune responses limit viral gene expression after administration of replication-deficient adenoviruses to the lung. The current study asks whether inducible nitric oxide synthase (iNOS) expression and peroxynitrite generation accompanied the inflammatory response following intratracheal administration of adenovirus. Pulmonary iNOS mRNA and protein were increased 2, 7, and 14 days following administration of 2 x 10(9) plaque-forming units of recombinant adenovirus (Av1Luc1) to BALB/c mice. Adenovirus infection was associated with a marked increase in nitrotyrosine staining. Intense nitrotyrosine staining was observed in alveolar macrophages, respiratory epithelial cells, conducting airways, and alveolar spaces 2 days postinfection. Two weeks after exposure to adenovirus, nitrotyrosine staining was detected within alveolar macrophages, suggesting adenovirus enhanced the nitration of proteins that were subsequently taken up by alveolar macrophages. Western blot analysis using anti-nitrotyrosine antibody did not demonstrate accumulation of nitrated surfactant protein A (SP-A), although a small fraction of aggregated SP-A comigrated with a nitrotyrosine-positive protein. iNOS expression, peroxynitrite, and nitrotyrosine generation accompany and may contribute to inflammatory responses to adenovirus in the lung.

Adenoviridae Infections↗
PubMed1983

Characterization of a phosphoprotein associated with the SS-B/La nuclear antigen in adenovirus-infected and uninfected KB cells.

We have employed sera from patients with autoimmune disease to characterize the nuclear SS-B/La antigen in uninfected and adenovirus-infected KB cells. A 45,000-dalton phosphorylated polypeptide was specifically precipitated with anti-SS-B sera, and the level of phosphorylation was increased after infection. The increased phosphorylation appears to occur at the same amino acid residues phosphorylated in uninfected cells and results from increased phosphorylating activity rather than from altered enzyme specificity. A competition experiment between infected and uninfected cell extracts indicates that the antigen in the infected cell binds more strongly to SS-B/La antibodies. Fragments of adenovirus-induced virus-associated RNA as well as intact molecules complex with SS-B/La antigen and are immune precipitated with autoimmune sera.

Adenoviridae↗
PubMed1969

Experimental adenovirus infection in calves.

Twenty-four dairy calves ranging in age from six to 15 weeks were divided so that 10 were inoculated with bovine adenovirus serotype 1 (BA-1), eight were inoculated with bovine adenovirus serotype 3 (BA-3), and six were inoculated with control tissue culture and fluids.Post-inoculation serum samples from most of the calves presented evidence of adenovirus infection, but none of the animals exhibited signs of respiratory or enteric disease. Histopathological examination of lung tissue was not considered to be specific for adenovirus pneumonia, but was characterized by peribronchial cuffing and slight aspiration pneumonia. BA-1 was not isolated from any of the inoculated calves, and BA-3 was only recovered from the feces of two animals. Reasons for the discrepancy between these results and those of other workers are considered, and the etiology of peribronchial cuffing is briefly discussed.

Adenoviridae↗
PubMed1985

Resistance to adenovirus infection after administration of Bordetella pertussis vaccine in mice.

Treatment of mice with Bordetella pertussis vaccine rendered mice resistant to mouse adenovirus infection. The resistant state took at least 5 days to develop, and susceptibility returned to a portion of the test population 35 days after treatment. Transient resistance developed in congenitally athymic mice also. Treatment with a dose of 25 micrograms (dry weight) of B. pertussis vaccine protected approximately 50% of the test population. Vaccines prepared from several different strains of B. pertussis were capable of inducing resistance, and the induction of resistance was not dependent on the mouse strain used for testing. Cross-reacting antibodies capable of neutralizing the virus or protecting against a challenging infection were not induced by treatment with B. pertussis vaccine.

Adenoviridae Infections↗
PubMed1995

Upregulation of class I major histocompatibility complex antigens by interferon gamma is necessary for T-cell-mediated elimination of recombinant adenovirus-infected hepatocytes in vivo.

Recombinant adenoviruses are attractive vehicles for liver-directed gene therapy because of the high efficiency with which they transfer genes to hepatocytes in vivo. First generation recombinant adenoviruses deleted of E1 sequences also express recombinant and early and late viral genes, which lead to development of destructive cellular immune responses. Previous studies indicated that class I major histocompatibility complex (MHC)-restricted cytotoxic T lymphocytes (CTLs) play a major role in eliminating virus-infected cells. The present studies utilize mouse models to evaluate the role of T-helper cells in the primary response to adenovirus-mediated gene transfer to the liver. In vivo ablation of CD4+ cells or interferon gamma (IFN-gamma) was sufficient to prevent the elimination of adenovirus-transduced hepatocytes, despite the induction of a measurable CTL response. Mobilization of an effective TH1 response as measured by in vitro proliferation assays was associated with substantial upregulation of MHC class I expression, an effect that was prevented in IFN-gamma-deficient animals. These results suggest that elimination of virus-infected hepatocytes in a primary exposure to recombinant adenovirus requires both induction of antigen-specific CTLs as well as sensitization of the target cell by TH1-mediated activation of MHC class I expression.

Adenoviruses, Human↗
PubMed1988

Recent respiratory and enteric adenovirus infection in children in the Manchester area.

Seventy-three group B adenoviruses (29 type 3 and 44 type 7) identified in a recent community outbreak were analysed with restriction endonucleases. Considerable genetic heterogeneity was identified, particularly amongst the type 3 isolates, but this genome variation could not be correlated with either clinical or epidemiological findings. Group F adenoviruses were found in 132 (4.1%) of 3202 stool specimens from children with gastroenteritis and, after rotaviruses, they were the most common viruses identified. Unlike rotaviruses, these enteric adenoviruses were endemic throughout the 3-year study period and the greatest proportion of infections (47.6%) were found in babies under 6 months old.

Adenoviridae Infections↗
PubMed1985

Adenovirus infections in patients undergoing bone-marrow transplantation.

Viral infection is commonly observed after bone-marrow transplantation. We isolated adenovirus from 51 of 1051 patients undergoing marrow transplantation between 1976 and 1982. Of the 46 isolates available for typing, 13 (27.7 per cent) were of the closely related species 11, 34, or 35 (subgenus B). All 13 of the patients with these species had positive urine cultures. The species have previously been associated with the acquired immunodeficiency syndrome or with renal transplantation but are not commonly found in community surveys. Invasive infection was confirmed by biopsy or autopsy in 10 of 51 patients. Seven of the 10 had virus isolated from lung, and 4 died from pneumonia attributed to adenovirus. Two of the five patients with renal isolates had evidence of virally induced renal impairment, and both patients with liver isolates had adenovirus hepatitis. There was no common source that accounted for these adenovirus infections, and the most likely source of infection appeared to be endogenous viral reactivation. The only identifiable risk factor for the development of infection and for severe disease was the presence of moderate to severe graft versus host disease.

Adenoviridae Infections↗
PubMed1984

Replication and recombination in adenovirus-infected cells are temporally and functionally related.

We have studied the temporal and functional relationships between DNA replication and recombination in adenovirus-infected cells by using Southern blot hybridization to detect recombinant products among intracellular viral genomes. The data show that recombination can be detected soon after DNA replication has commenced and that the proportion of recombinant products increases thereafter. To determine the functional relationship between DNA replication and recombination, replication was blocked with the protein synthesis inhibitor anisomycin, the replication inhibitor cytosine arabinoside, and conditionally lethal mutations in either the virus-specified DNA-binding protein or the DNA polymerase. All treatments that directly or indirectly blocked DNA replication caused a delay in the appearance of recombinant products and a marked decline in their abundance relative to products of parental genotype. These data strongly suggest that DNA replication and recombination are interrelated, either because both processes share functions or because DNA structures produced by replication are suitable substrates for recombination. In addition, we have shown that some recombination function(s) is intrinsically thermolabile at 40.9 degrees C, even in wild-type crosses, since the appearance of recombinant products is delayed and their extent is reduced compared with that from crosses performed at 39.9 degrees C.

Adenoviruses, Human↗
PubMed1999

Significant increase of adenovirus infectivity in glioma cell lines by extracellular domain of hCAR.

Recombinant adenoviruses are highly advantageous as vectors for transferring genes into mammalian cells, but the transfer is not efficient in all types of cells. We investigated the effects of four adenoviral receptors [integrinalphav, integrinbeta3, integrinbeta5, and human coxsackievirus and adenovirus receptor (hCAR)] on adenovirus-mediated transfer of exogenous cDNA into each of 10 glioma cell lines. Transfection efficiency varied widely from one cell line to another (0-100%) when we measured it by infection with AdLacZ, a vector designed to express beta-galactosidase. Levels of integrinalphav and integrinbeta5 expression were similar among the 10 cell lines, but expression of hCAR and integrinbeta3 varied significantly. As these observations indicated a possible correlation between expression of hCAR and the efficiency of gene transfer, we induced the hCAR gene into three glioma cell lines (T98G, U118MG, and U138MG) that expressed hCAR at very low levels and had also revealed low efficiencies of adenoviral gene transfer. In U118MG- and U138MG-derived cells that had regained the ability to express hCAR in stable fashion, adenovirus-mediated gene transfer became highly efficient. Moreover, addition of the peptide corresponding to the extracellular domain of hCAR (ECD-hCAR) by preincubation significantly increased the adenovirus infectivity to these adenovirus-tolerant cells. These results suggest that hCAR could be one of important determinants of the infectivity of adenovirus, and that the ECD-hCAR might be a novel useful tool for improvement of adenovirus-mediated gene therapy against the adenovirus-tolerant cancer cells.

Adenoviridae↗
PubMed1975

Polyamines in type 5 adenovirus-infected cells and virions.

The incorporation of l-[(14)C]ornithine and [(14)C]putrescine into putrescine, spermidine, and spermine in type 5 adenovirus-infected KB cells was identical to that in uninfected control cells early in infection, but incorporation into putrescine stopped after 8 to 12 h and the rate of incorporation into spermidine was reduced between 12 and 20 h after infection. The amount of polyamines found associated with purified virus could neutralize a maximum of 3 to 4% of the virus DNA, but the small quantities of polyamines detected could not be distinguished from nonspecific binding of polyamines to virions. These data suggest that polyamines are probably not integral components of adenovirus particles.

Journal Article↗
PubMed1986

Hemorrhagic cystitis associated with adenovirus infection in bone marrow transplantation.

A retrospective study of bone marrow transplant recipients shedding adenovirus type 11 in the urine was carried out to determine the association between viral shedding and hemorrhagic cystitis in this population. Weekly urine virology surveillance cultures were obtained during the first 100 days following transplantation. Adenovirus type 11 was cultured from five of 502 bone marrow transplant recipients from 1977 through 1984. In four of these five patients there was associated hemorrhagic cystitis. This contrasts with an overall incidence of hemorrhagic cystitis of 20% in this bone marrow transplant population. A case of hemorrhagic cystitis occurred in a patient following bone marrow transplantation. Recognition of a viral origin of hemorrhagic cystitis may explain the occurrence of late hemorrhagic cystitis in patients despite interventions designed to prevent cyclophosphamide-induced hemorrhagic cystitis. Hemorrhagic cystitis may be the presenting sign of a lethal adenoviral infection.

Adenoviridae Infections↗
PubMed2002

Incidence of Norwalk-like viruses, rotavirus and adenovirus infection in patients with acute gastroenteritis in Jakarta, Indonesia.

Norwalk-like viruses (NLVs), rotavirus and adenovirus are reportedly responsible from 4 to 42% of non-bacterial acute sporadic gastroenteritis. The incidence of NLVs, adenovirus and rotavirus infections in Indonesia is unclear. A total of 402 symptomatic cases from Indonesian patients with acute gastroenteritis and 102 asymptomatic controls that tested negative for bacteria and parasites were screened for the presence of NLVs, rotavirus and adenovirus using the reverse transcriptase-polymerase chain reaction (RT-PCR), Rotaclone kits and Adenoclone kits. Specific prototype probes were used to ascertain which NLV prototypes were present in the area. NLVs were detected in 45/218 (21%), rotavirus was detected in 170/402 (42%) and adenovirus was detected in 11/273 (4%) samples examined. Genetic analysis of the RT-PCR products using specific prototype probes for NLVs indicated that the prototypes were 42% Taunton agent and 58% Hawaii/Snow Mountain agent. Comparative data on patients showed that the incidence of rotavirus infections was two times greater than the NLVs infections, and that adenovirus infections were the least prevalent. All of the control samples tested were negative for NLVs and adenoviruses, however 8/70 (11%) of the samples were positive for rotaviruses. The high incidence of enteric viral-related infections is a threat among acute diarrheic patients in Jakarta, Indonesia.

Acute Disease↗
PubMed2002

Latent adenovirus infection in COPD.

We have concentrated on the adenovirus as the source of the heightened inflammatory response of the lungs of patients with COPD. We have concentrated in particular on the responses to agents such as lipopolysaccharides and environmental particulates that contaminate the air we breathe, and we have accumulated evidence that the E1A gene of this virus could be the key player in this process. As other intracellular pathogens such as Chlamydia pneumoniae have recently been implicated in the pathogenesis of COPD, our studies on the adenovirus E1A could serve as the model for investigating the interaction between host and extrinsic factors in the chronic progression of this debilitating lung disease.

Adenoviridae↗
PubMed1994

Adenovirus infection enhances in vitro adherence of Streptococcus pneumoniae.

Viruses are thought to facilitate bacterial infections of the respiratory tract, but the mechanisms are poorly understood. The present study analyzed the effect of adenovirus on bacterial adherence to human respiratory tract epithelial cells. The human lung carcinoma cell line A549 was infected with adenovirus of types 1, 2, 3, 4, 5, and 9. At a multiplicity of infection of 75 particles per cell, cytopathic effects occurred in 75 to 100% of the cells within 48 h. The virus-infected cells were harvested at various times after infection and analyzed for the ability to bind strains of Haemophilus influenzae and Streptococcus pneumoniae. Adenovirus (types 1, 2, 3, and 5) commonly causing respiratory tract infections increased the binding of adherent S. pneumoniae strains to the cells. This effect was not seen for other adenovirus types. Adenovirus infection did not change the adherence of cells of poorly adhering strains of S. pneumoniae or H. influenzae. The increase in adherence of S. pneumoniae could be inhibited by the DNA synthesis inhibitor cytosine arabinofuranoside, which is known to block the late phase of the adenovirus infection. When electron microscopy was used, there was no evidence that virus particles bound directly to bacteria. Adherence was not affected by pretreatment of the cells with virus particles or viral proteins. This suggested that adenovirus infection upregulated receptors for S. pneumoniae. The increased attachment may be one mechanism by which viruses precondition the respiratory mucosa for bacterial infection.

Adenoviridae↗
PubMed2002

Adenovirus infection targets the cellular protein kinase CK2 and RNA-activated protein kinase (PKR) into viral inclusions of the cell nucleus.

The effects of the adenovirus infection on the distribution of the cellular protein kinase CK2 and double-stranded RNA-activated protein kinase (PKR) were examined at the ultrastructural level. Immunogold labeling revealed the redistribution of CK2 subunits and PKR to morphologically distinct structures of the cell nucleus. The electron-clear amorphous structures, designated pIX nuclear bodies in our previous work (Rosa-Calatrava et al., 2001), contained CK2 alpha and PKR. The protein crystals, which result from the regular assembly of hexon, penton base, and fiber proteins [Boulanger et al. (1970) J Gen Virol 6:329-332], contained CK2 beta and PKR. Both viral structures were devoid of viral RNA, including the PKR-inhibitor VA1 RNA generated by the RNA polymerase III. Instead, VA1 RNA accumulated in PKR-free viral compact rings in which the viral RNA generated by the RNA polymerase II was excluded.

Adenoviruses, Human↗
PubMed1989

Is a persistent adenovirus infection involved in coeliac disease?

Recent evidence has implicated adenovirus 12 in the aetiology of coeliac disease so that persistent infection by this virus must be considered. We have undertaken a search for adenovirus DNA in duodenal biopsy samples from a total of 26 coeliac and non-coeliac patients. We could find no evidence of persistent virus DNA by Southern blot techniques even under conditions which approach a sensitivity of one copy of virus genome per cell, and use either adenovirus 12 or 41 DNA.

Adenoviridae Infections↗