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PubMed1967

Inhibition of host protein synthesis in type 5 adenovirus-infected cells.

The effect of type 5 adenovirus infection on the synthesis of host-cell proteins by suspension cultures of KB cells was investigated. Although total protein synthesis continued at a constant rate for approximately 36 hr, net synthesis of five host enzymes (lactic dehydrogenase, acid phosphatase, deoxyribonuclease, fumarase, and phosphoglucose isomerase) was found to stop 16 to 20 hr after infection. The synthesis of alkaline phosphatase stopped 9 to 12 hr after infection. The inhibition of host protein synthesis occurred shortly after the synthesis of viral antigens had begun, accounting for the continued synthesis of total protein. An investigation of the relationship between synthesis of viral antigens and inhibition of host protein synthesis yielded results which suggest that the two processes are in some way coupled.

Acid Phosphatase↗

PubMed2001

[Latent adenovirus infection in chronic obstructive pulmonary disease].

OBJECTIVE: To study latent adenovirus infection in the stable stage of chronic obstructive pulmonary disease(COPD). METHOD: The bronchial epithelial cells and alveolar macrophages from 12 patients with chronic bronchitis, 10 patients with COPD, 6 patients with asthma and 8 healthy volunteers were obtained by bronchosocpy. The adenoviral DNA was determined in the epithelial cells and macrophages. All patients were in the stable stage. The polymerase chain reaction(PCR) was used for detection of the adenoviral genome E1A. RESULTS: The E1A region of adenovirus was found in the epithelial cells of COPD and chronic bronchitis patients (27%), not found in the patients with asthma and normal volunteers. Furthermore, E1A DNA was much more commonly in the COPD patients (50%) than in the patients with chronic bronchitis (8%) (P < 0.05). CONCLUSIONS: Latent adenoviral infection was present in the stable stage of COPD and may be related to the pathogenesis of the disease.

Adenoviridae↗

PubMed1987

Induced heat shock mRNAs escape the nucleocytoplasmic transport block in adenovirus-infected HeLa cells.

Under conditions in which cytoplasmic accumulation of HeLa cell mRNAs has been blocked by adenovirus infection, hsp70 family mRNAs are transported from the nucleus to the cytoplasm at near normal efficiency subsequent to heat shock. Heat shock does not reverse the general virus-induced block to host cell mRNA transport. The heat shock mRNAs are translated within the cytoplasm of the infected cell but at substantially reduced efficiency compared with that of uninfected cells. Thus, the hsp70 family of mRNAs can escape the transport block but not the translational block instituted late after adenovirus infection. The beta-tubulin gene family is induced by the viral E1A gene after infection, and its mRNAs also accumulate in the cytoplasmic compartment. Given these two examples, it seems likely that the process of transcriptional induction allows the resulting mRNA to escape the viral block of transport.

Adenoviridae↗

PubMedDate not supplied

Adenovirus infection and cytopathic alterations of human cervical epithelial cells in vitro.

The effect of adenovirus infection was studied in monolayer cultures of human ecto- and endocervical epithelial cells. In both types of cultures adenovirus type 1 resulted in a slowly progressing lytic infection with persistent production of infectious virus, viral antigens and of cytopathic alterations in a fraction of cells. The changes were similar in ecto- and endocervical epithelial cells. Although many of the alterations detected may represent unspecific lesions, nuclear changes consisting of lobulated nuclear inclusion bodies seemed to be characteristic. These alterations differ from those observed during infection with the herpes group of viruses and may serve as indicators of cervical adenovirus infection in cytologic screening.

Adenoviruses, Human↗

PubMed2003

Bovine lactoferrin inhibits adenovirus infection by interacting with viral structural polypeptides.

We recently demonstrated that lactoferrin, an antimicrobial glycoprotein, can inhibit adenovirus infection by competing for common glycosaminoglycan receptors. This study further characterizes the antiadenovirus activity of the protein, thus demonstrating that lactoferrin neutralizes infection by binding to adenovirus particles and that its targets are viral III and IIIa structural polypeptides.

Adenoviridae↗

PubMed1991

The use of adenovirus-infected HeLa cells for the detection of low titer autoantibodies.

Following infection of HeLa cells with adenovirus type 5 the cellular La protein becomes predominantly associated with the virally encoded RNA polymerase III products VAI, and VAII, while most of the host RNA polymerase II (e.g. U1, U2, U4, U5 and mRNA) and RNA polymerase III transcription (e.g. U6 and pre-tRNAs) ceases. Other RNA polymerase III products such as the cellular Ro RNAs continue to be transcribed and assembled into ribonucleoprotein complexes containing the Ro (SS-A) antigens. Using a 32P-pulse chase-labeled, adenovirus-infected HeLa cellular extract as a source of antigen, anti-La (SS-B) and anti-Ro (SS-A) antibodies can be detected simultaneously using an immunoprecipitation assay. In the present study this method was found to be more sensitive in detecting anti-La antibodies then counter immunoelectrophoresis and immunoblotting. In studies of sera from patients suffering from rheumatic diseases the percentage positive for anti-La antibody was significantly elevated using this method, especially in patients with systemic lupus erythematosus.

Adenoviruses, Human↗

PubMed1985

Reye's syndrome associated with adenovirus infections in infants.

The isolation of adenovirus from the liver of an infant with Reye's syndrome prompted a retrospective review to determine the role of this group of viruses in the cause of Reye's syndrome. A total of 34 patients with Reye's syndrome who were admitted to Vanderbilt University, Nashville, Tenn, during a ten-year period were identified. Six of the patients were younger than 1 year, and positive adenoviral cultures and increased serological responses were obtained in three of these children. The clinical and pathologic data from these three children suggest that adenovirus may be an important agent in initiating Reye's syndrome in the very young child. Further, the mitochondrial abnormalities present in the livers of the patients with adenovirus-associated disease tended to be mild in spite of severe clinical disease.

Adenoviridae Infections↗

PubMed1983

Effects of adenovirus infection on rRNA synthesis and maturation in HeLa cells.

The production of cytoplasmic and nucleolar rRNA species was examined in HeLa cells infected with high multiplicities of adenovirus type 5. Both 28S and 18S rRNA newly synthesized in infected cells ceased to enter the cytoplasm as reported previously (N. Ledinko, Virology 49: 79-89, 1972; H. J. Raskas, D. C. Thomas, and M. Green, Virology 40: 893-902, 1970). However, the effects on 28S cytoplasmic rRNA were observed considerably earlier in the infectious cycle than those on 18S rRNA. The inhibition of cellular protein synthesis and of the appearance in the cytoplasm of labeled cellular mRNA sequences (G. A. Beltz and S. J. Flint, J. Mol. Biol. 131: 353-373, 1979) were also monitored in infected cultures. During the later periods of an infectious cycle, from 18 h after infection, nucleolar rRNA synthesis and processing and exit of 18S rRNA from the nucleus were inhibited, probably reflecting the failure of infected cells to synthesize normal quantities of ribosomal proteins. The earliest responses of cellular RNA metabolism to adenovirus infection were, however, the rapid and apparently coordinate reductions in the levels of newly synthesized 28S rRNA and cellular mRNA sequences entering the cytoplasm.

Adenoviridae Infections↗

PubMed1995

Immunocytochemistry, autoradiography, in situ hybridization, selective stains: complementary tools for ultrastructural study of structure-function relationships in the nucleus. Applications to adenovirus-infected cells.

A significant amount of new information on structure-function relationships in nuclei of adenovirus-infected cells has accumulated during the last decade as a result of the combined use of several new cytochemical techniques. Localization of viral DNA on ultrathin sections of infected cells has been investigated at the ultrastructural level by using specific DNA staining and immunocytochemistry with monoclonal anti-DNA antibodies. Both techniques, however, concomitantly visualize cellular and viral DNA. The specific stain for DNA reveals the configuration of the DNA molecules in the different nuclear substructures, whatever their synthetic activities. The immunodetection of DNA reveals that specific antibodies strongly bind to DNA of condensed host chromatin and to both encapsidated and nonencapsidated inactive viral genomes. However, the observation of an abnormally low level of labeling over the substructures in which synthetic activities of viral genomes are known to be intense demonstrates a serious limitation of this technique for the detection of active DNA. Postembedding in situ hybridization is the most useful method for identifying with certainty the structures containing defined nucleic acid sequences. By using a biotinylated viral DNA probe, in situ hybridization provides specific identification of structures containing either viral DNA or viral RNA molecules. In addition, with appropriate pretreatment of the sections, it is possible to reveal either all the viral DNA--that is, both double- and single-stranded DNA molecules (dsDNA, ssDNA)--or more specific species such as only ssDNA or only dsDNA molecules. The replicative and transcriptional activities of viral genomes are determined by high-resolution autoradiography. Autoradiography after a short pulse incorporation of appropriate radioactive precursors by infected cells reveals the sites of cellular and viral DNA replication or transcription. A short pulse followed by chase periods of different durations reveals the progressive migration of the cellular and viral synthesized products. The in situ distribution of the viral 72 kDa DNA-binding protein, a highly phosphorylated protein which protects the viral ssDNA, is revealed either by immunocytochemistry with specific antibodies or by the bismuth staining method which stains all highly phosphorylated proteins, including both cellular and viral proteins. The combined results of all these cytochemical procedures reveal the composition and functions of some of the structures induced by adenovirus infection. They demonstrate that viral genomes engaged in replication lead to the formation of the replicative foci in which two compartments rapidly develop, one of which results from the aggregation of single strands of viral DNA and their accompanying 72 kDa protein.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenoviruses, Human↗

PubMed1993

Alterations of fibrillarin distribution and nucleolar ultrastructure induced by adenovirus infection.

Nucleolar modifications induced by adenovirus type 5 (Ad5) have been examined in HeLa cells by bismuth staining and immunogold labeling of fibrillarin, both of which visualize the dense fibrillar component (DFC) of nucleoli. A progressive increase in the compaction of the nucleolus is accompanied both by a migration of strands of DFC towards the border of the nucleolar body and by a decrease in the amount of fibrillarin within the bismuth stained DFC. In addition, the bismuth-stained extranucleolar fibrillar spots induced by Ad5 infection often were intensely labeled with monoclonal anti-fibrillarin antibody. Previously reported defects in ribosomal RNA expression during adenovirus infection could result from the migration and accumulation of nucleolar proteins implicated in ribosomal biogenesis into virus-induced extranucleolar structures.

Adenovirus Infections, Human↗

PubMed1964

Control of aspartate transcarbamylase activity in type 5 adenovirus-infected HeLa cells.

Consigli, Richard A. (University of Pennsylvania, Philadelphia), and Harold S. Ginsberg. Control of aspartate transcarbamylase activity in type 5 adenovirus-infected HeLa cells. J. Bacteriol. 87:1027-1033. 1964.-Type 5 adenovirus infection induces increased aspartate transcarbamylase (ATCase) activity during the period of magnified nucleic acid biosynthesis. Increased activity can be prevented by addition of pyrimidines to the culture medium. ATCase in HeLa cells is regulated by feedback inhibition, and purified enzyme can be inhibited in vitro by cytidine triphosphate (CTP). The enzyme from infected cells has a pH optimum, maximal velocity, and K(m) for aspartate distinctly different from ATCase from control cells. However, heating of ATCase from uninfected cells converts the enzyme so that its characteristics are identical with enzyme from infected cells. Conversely, addition of CTP to ATCase from infected cells changes the characteristics of the enzyme so that they are the same as those of enzyme from uninfected cells. The evidence presented suggests that increased nucleic acid biosynthesis in infected cells initiates a release from feedback inhibition and increases ATCase activity by reducing the concentration of pyrimidines and purines in the acid-soluble pool.

Adenoviridae↗

PubMedDate not supplied

[Irreversible generalized pulmonary emphysema resulting from destructive bronchitis and bronchiolitis following adenovirus infection].

Report of an 1 1/2 year old boy with the typical features of Williams-Campbell syndrome: chest deformity (thorax piriformis), pulmonary hyperinflation, ballooning of the segmental and subsegmental bronchi during inspiration and collapse with expiration. Atelectasis of the left upper lobe after bronchiolitis obliterans. The literature reports 23 patients with Williams-Campbell syndrome. There is every reason to believe that the extensive bronchiectasis are not due primarily to developmental deficiency of the bronchial cartilage, as the most authors assume, but result from destructive changes after inflammation. In our case very likely an adenovirus infection was the cause. The clinical features of the syndrome look like a severe therapy resistant asthma bronchiale.

Adenoviridae Infections↗

PubMed1981

Antibody to human adenovirus early antigens during acute adenovirus infections.

The antibody (Ab) response to human adenovirus (AV) early antigens (EA) in acute AV infections was studied by the immunoperoxidase antibody technique for determining virus-specific immunoglobulin G (IPA-IgG). AV-EA-Ab appeared about 5 days after the onset of clinical symptoms, reached a peak 15 to 30 days later, and declined in titer after a few months. The staining pattern in the IPA-IgG reaction was usually nuclear; however, in most primary infections sera obtained 2 to 3 weeks after the onset of infection also showed cytoplasmic staining. According to the recent deoxyribonucleic acid homology classification of human AV in five groups (A, B, C, D, and E), the EA-Ab response in primary human infections was found to be group specific for groups A to D, with consistent cross-reactions with group E. In AV type 4 (group E) infections, EA-Ab appeared to be directed against all groups, although at different titers. Comparable results were obtained using AV type-specific animal antisera. Thus, it was concluded that group E shares EA with all the other groups. Furthermore, in each individual with remote AV infections, the current infection elicited an anamnestic EA-Ab response to all AV groups responsible for previous infections. In diagnostic virology these findings can be applied to the rapid diagnosis of a current for recent) AV infection on a single serum sample and to the rapid group identification of clinical isolates by using type-specific animal antisera containing EA-Ab (one for each group) or sera from patients with primary AV infections.

Acute Disease↗

PubMed1998

Adenovirus infection in the lung results in graft failure after lung transplantation.

OBJECTIVES: Our goal was to examine the relationship between viral pneumonia and outcome in pediatric patients undergoing lung or heart-lung transplantation. METHODS: Prospective surveillance for common respiratory viruses of childhood was performed in all patients undergoing lung or heart-lung transplantation. Specimens were examined for the presence of replicating virus (by culture), viral genome (by polymerase chain reaction), and viral antigen (by immunofluorescence and immunohistochemical staining). The relationship between viral infection and outcome was examined. RESULTS: Sixteen patients underwent 19 transplants during the study period, with follow-up of 1 to 26 months. Virus was identified in the transplanted lung in 29 instances; adenovirus was identified most commonly (8/16 patients) and had the greatest impact on outcome. In 2 patients with early, fulminant infection, adenovirus was also identified in the donor. Adenovirus was significantly associated with respiratory failure leading to death or graft loss and with the histologic diagnosis of obliterative bronchiolitis (P < or = .002 in each case). CONCLUSIONS: Adenovirus infection in the transplanted lung is significantly associated with graft failure, histologic obliterative bronchiolitis, and death. Health care personnel and families must be vigilant in preventing exposure of transplant recipients to this virus. Availability of a rapid and reliable test for adenovirus in donors and recipients would have an impact on management and could improve outcome for pediatric lung recipients.

Adenovirus Infections, Human↗

PubMed1993

Nuclear organization of splicing small nuclear ribonucleoproteins in adenovirus-infected cells.

We have studied the effect of adenovirus infection on the nuclear organization of splicing small nuclear ribonucleoproteins (snRNPs) in HeLa cells. In uninfected HeLa cells, snRNPs are widespread throughout the nucleoplasm but also are concentrated in specific nuclear structures, including coiled bodies, interchromatin granules, and perichromatin fibrils. We have used immunofluorescence microscopy to study the localization of splicing snRNPs relative to centers of viral DNA synthesis and accumulation identified with antiserum against the viral 72,000-molecular-weight single-stranded DNA-binding protein (72K protein). Splicing snRNPs were independently detected with both monoclonal and polyclonal antibodies specific for common snRNP antigens, snRNP-specific proteins, and the snRNA-specific 2,2,7-trimethylguanosine 5' cap structure. We have examined infected cells 2 to 24 h after infection, and, in the majority of these cells, we observed no colocalization of the snRNP and 72K-protein staining patterns. In the late phase, snRNPs were found to markedly concentrate in discrete clusters that were distinct from the centers of viral DNA synthesis and accumulation identified with anti-72K protein. We have treated cells with hydroxyurea at various times after infection to inhibit aspects of the virus infectious program. We have found that the accumulation of snRNP clusters is correlated with late gene expression rather than with DNA synthesis or early gene expression. Finally, we show that the late-phase snRNP clusters colocalize with a monoclonal antibody that primarily stains interchromatin granules. These results suggest that the centers of snRNP concentration in late-phase infected cells are likely to correspond to interchromatin granule clusters.

Adenoviruses, Human↗

PubMed1986

Partition of E1A proteins between soluble and structural fractions of adenovirus-infected and -transformed cells.

The partition of E1A proteins between soluble and structural framework fractions of human cells infected or transformed by subgroup C adenoviruses was investigated by using gentle cell fractionation conditions. A polyclonal antibody raised against a trpE-E1A fusion protein (K.R. Spindler, D.S.E. Rosser, and A. J. Berk, J. Virol. 132-141, 1984) synthesized in Escherichia coli was used to measure the steady-state levels of E1A proteins recovered in the various fractions by immunoblotting. The relative concentration of E1A proteins recovered in the soluble fraction of adenovirus type 2-infected cells was at least fivefold greater than the relative concentration in the corresponding fraction of transformed 293 cells. The observed distribution of E1A proteins was not altered by the sulfhydryl-blocking reagent N-ethylmaleimide. E1A proteins were recovered in nuclear matrix, chromatin, and cytoskeleton fractions after further fractionation of the structural framework fraction. However, the E1A protein species that could be identified by one-dimensional gel electrophoresis were not uniformly distributed among the subcellular fractions examined. The results obtained when fractionation was performed in the presence of the oxidation catalysts Cu2+ or (ortho-phenanthroline)2 Cu2+ indicate that E1A proteins can be efficiently cross-linked, via disulfide bonds, to the structural framework of both adenovirus-infected and adenovirus-transformed cells.

Adenoviridae Infections↗

PubMed1979

[Histopathological pattern of adenovirus infection in the calf].

Pneumo-enteritis is the clinical manifestation of adenovirus infection in calf. Proliferative alveolitis, endobronchitis, and peribronchitis with intranuclear inclusions in the epithelial cells, histiocytes, and macrophages were histologically recorded. Proliferative changes with minor pleomorphism of cells were recorded from lymph nodes and lymph follicles of spleen and intestines. The epithelial cells of the renal tubules and liver exhibited degenerative changes, while the endothelium of the capillaries was activated. Five Serotype-1 adenoviruses were isolated from the lung, liver, and kidneys of the foetuses. IE were recordable from the epithelial cells of kidneys and lung. Other calves were examined following natural infection with adenovirus and virus of the mucosa disease. Dystrophic and necrotic changes were recorded from their digestive organs, lymphocytolysis from spleen and lymph nodes (a characteristic change related to mucosa disease), and nephrosis with adenovirus inclusions from the epithelial cells of the renal tubules.

Adenoviridae↗

PubMed2006

Adenovirus infections in transplant recipients.

Adenoviruses are increasingly recognized as contributors to morbidity and mortality among stem cell and solid-organ transplant recipients. Clinical presentations range from asymptomatic viremia to respiratory and gastrointestinal disease, hemorrhagic cystitis, and severe disseminated illness. The limited clinical data available support the use of cidofovir for many of these illnesses. Prospective studies are needed to better understand the pathogenesis of and therapeutic options for adenoviral infections in this patient population.

Adenoviridae↗