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PubMed1978

Preparation of sera for typing of adenovirus infections by immunofluorescence.

The conditions for preparation of adenovirus antisera with group, subgroup and type-specific reactivity to be used in the immunofluorescence technique have been evaluated. Group-specific antibodies were prepared by passing an antiserum against virions or hexons of one serotype through an immunosorbent column containing soluble viral components of an adenovirus type belonging to a different subgroup. The group-specific antibodies were recovered from the solid phase by elution at pH 2.8. Reagents specific for subgroup I and II were obtained by passing anti-dodecon sera through an immunosorbent column containing soluble viral components from heterologous subgroups. In this case antibodies not attaching to the absorbent were recovered. Sera against fibers of subgroup III members could be used as subgroupspecific sera without absorption. Type-specific antibodies were prepared by removal of antibodies of other specificities by passing anti-virion or anti-hexon sera through immunosorbent columns containing soluble viral components of an adenovirus type belonging to the same subgroup. Reagents specific for seven adenovirus types representing Rosen's three subgroups were prepared according to the outlined procedures.

Adenoviridae Infections↗

PubMed2000

Relevance of commercial diagnostic tests to detection of enteric adenovirus infections in South Africa.

The prevalence of enteric adenoviruses detected by an in-house enzyme-linked immunosorbent assay (the RIVM-ELISA) ranged from 13 to 38%, and subgroup F adenoviruses comprised 86%. All subgroup F adenoviruses reacted with both RIVM anti-adenovirus type 40 (Ad40) and anti-adenovirus type 41 (Ad41) monoclonal antibodies but were not detected by Adenoclone Type 40/41 enzyme immunoassay (EIA). The correlation between the Biotrin EIA and RIVM-ELISA results was low (26%). Immunospecific tests suggest that a significant proportion of enteric adenoviruses, possibly comprising previously unidentified or emerging types, are not detected by commercial diagnostic tests in South Africa.

Adenovirus Infections, Human↗

PubMed1972

Synthesis of viral ribonucleic acid during restricted adenovirus infection.

The mechanism by which simian virus 40 converts the abortive adenovirus type 7 infection of monkey cells into an efficient lytic infection has been investigated. Analysis of ribonucleic acid (RNA) synthesis during unenhanced and enhanced infection of monkey cells has shown that adenovirus RNA synthesized in the abortive infection contains both "early" and "late" sequences. In hybridization competition experiments, early adenovirus RNA from human cells prevented the hybridization of only 20% of the adenovirus RNA transcribed in unenhanced infection. Further, the RNA from unenhanced cells was able to completely block the hybridization of RNA synthesized during enhanced infection. Finally, virus-associated RNA, which is a late RNA transcribed in lytic adenovirus infection, is also produced in the unenhanced infection. An accompanying paper describes a marked deficiency in adenoviral capsid protein synthesis in the unenhanced infection. We conclude that RNA sequences, which are sufficient to code for the synthesis and assembly of structural proteins of adenovirus, are transcribed but are not efficiently translated in the unenhanced adenovirus infection of monkey cells.

Adenoviridae↗

PubMed2000

Enteric adenovirus infection in children in Taipei.

Enteric adenoviruses (EAds), including type 40 (Ad40) and 41 (Ad41), can cause acute and severe diarrhea in young children. To delineate the epidemiological features of pediatric EAds infection in Taiwan, we conducted a retrospective study of all cases of EAds gastroenteritis in children treated at National Taiwan University Hospital for the period from July 1993 to December 1997. Stool samples were tested for the presence of Ad40 or Ad41 by enzyme immunoassay (EIA). A total of 64 cases of EAds infection in 63 children aged from 8 days to 81 months old with a median age of 9.5 months treated during the study period were identified. The male-to-female ratio was 1.63 (39/24). No obvious seasonal clustering of EAds cases was noted. Most patients (76.6%) were infected before the age of 2 years. Clinical features included diarrhea (96.9%), fever (54.7%), vomiting (45.3%), mild dehydration (43.8%), symptoms of upper respiratory tract infection (21.9%), and abdominal pain (12.5%). Analysis of fecal samples in patients with diarrhea showed watery diarrhea in 72.2%, diarrhea with mucus in 20%, diarrhea with blood in 3.1% and diarrhea with mucus and blood in 1.6 % of all patients. Nearly one-half (43.5%) of the patients had diarrhea for more than 7 days. Thirty-seven patients (57.8%) were hospitalized due to gastroenteritis or other unrelated diseases, and 11 patients (17.2%) acquired enteric adenovirus infection during hospitalization for other underlying disease. Twelve patients (18.8%) had mixed infections, which included rotavirus, respiratory syncytial virus (RSV) and Salmonella species. There were no deaths in this series. The findings of this study suggest that EAds are important etiologic microbes of pediatric gastroenteritis.

Adenoviridae Infections↗

PubMed1997

Adenovirus infection enhances killing of melanoma cells by a mitotoxin.

Toxins are effective in cell killing if internalized efficiently. Conjugation of the plant toxin saporin with basic fibroblast growth factor has increased tumor killing due to better internalization, but toxin uptake by cells has remained relatively inefficient. We show here that infection of melanoma cells with a replication-defective adenovirus enhances cell killing by the mitotoxin basic fibroblast growth factor-saporin more than 10-fold, thus allowing tumor cell killing in vivo at nontoxic concentrations. Adenovirus infection leads to increased apoptosis by the mitotoxin due to enhanced internalization of the ligand-receptor complex and release of the active toxin from the endosomes.

Adenoviridae↗

PubMed1972

Studies of the mechanism of enhancement of human adenovirus infection in monkey cells by simian virus 40.

The defect which prevents human adenovirus replication in monkey cells and the mechanism whereby this restriction is overcome by coinfection with simian virus 40 (SV40) have been studied. Adenovirus capsid proteins are not synthesized efficiently in monkey cells in the absence of SV40. Adenovirus "enhancement" by SV40 was found to be the product of increased efficiency of replication by a small percentage of cells. This enhancement effect apparently occurred only when SV40 and adenovirus infected the same cells. These findings suggest that the replicative block occurs prior to virion assembly, and an accompanying report seeks to locate the site of restriction more precisely at the post-transcriptional level.

Adenoviridae↗

PubMed1975

[Complement fixation reaction (CFR) in adenovirus infections of calves].

Studied was the complement-fixation reaction in the diagnosis of the adenovirus infections in calves. It was found that the test is specific and sensitive. A virus suspension of tissue cultures was used as an antigen, its titer varying from 1:8 up to 1:16. Specific complement-fixing antibodies were detected mainly in survivals at serum dilution of up to 1:64. Specific antibodies were established in undiluted sera too taken from animals of infected herds. In some of the tested sera there were both complement-fixing and precipitating antibodies. In calves treated with a live vaccine against adenoviruses the dynamics of the complement-fixing antibodies was followed up.

Adenoviridae Infections↗

PubMed2003

MAP kinases and NF-kappaB collaborate to induce ICAM-1 gene expression in the early phase of adenovirus infection.

Replication-defective adenoviruses (Ad) utilized as vectors for gene transfer are known to induce an inflammatory and immune response upon exposure to respiratory cells in vitro and in vivo. Among the different mediators of inflammation, we recently demonstrated that a replication-defective Ad serotype 5, deleted in the early genes E1 and E3 (Ad.CFTR), induces the proinflammatory intercellular adhesion molecule 1 (ICAM-1) in A549 respiratory cells in vitro and in lung portions of nonhuman primates in vivo, Gene Ther. 5, 131-136). More recently, we described the involvement of the nuclear factor kappaB (NF-kappaB) in the induction of ICAM-1 upon 24 h of exposure of the same Ad5-derived vector, Gene Ther. 8, 1436-1442). Here we investigated whether the early phase of virus-cell interaction is sufficient to stimulate ICAM-1 upregulation. A549 cells were exposed to wild-type Ad5 (Ad5), to Ad.CFTR, and to Ad5 inactivated by incubation at 56 degrees C (Ad5/56 degrees C). Ad5, Ad.CFTR, and Ad5/56 degrees C activated NF-kappaB and increased ICAM-1 mRNA levels within 4 h after exposure. The role of the mitogen-activated protein kinases (MAPKs) on the ICAM-1 mRNA induction was studied. ICAM-1 mRNA upregulation was inhibited upon incubation with several chemicals, namely, the ERK1/2 inhibitors PD98059 and AG1288 (by 98 and 67%, respectively), of the p38/MAPK pathway SB203580 (by 50%), of the JNK pathway dimethylaminopurine (by 83%), and of the NF-kappaB parthenolide (by 96%). Ad5 and Ad5/56 degrees C stimulated ERK1/2, p38/MAPK, and JNK1 starting 10 min and peaking 20-30 min after exposure. The present results indicate a link between the activation of the three major MAPK pathways, NF-kappaB, and the upregulation of ICAM-1 gene expression evoked by Ad5 in the very initial phase of infection.

Active Transport, Cell Nucleus↗

PubMed1983

Effect of butyrate on adenovirus infection in semipermissive cells.

Adenovirus 2 stimulated cellular DNA synthesis in quiescent cultures of semipermissive tsAF8 cells and 3T3 cells. Such stimulation was inhibited by Na-butyrate, which also inhibited viral DNA replication in tsAF8 cells. In addition, butyrate inhibited the expression of early regions E1A and E2 of adenovirus 2 in both tsAF8 and 3T3 cells, while it had little effect on permissive HeLa cells.

Adenoviruses, Human↗

PubMed2003

Budding and secretion of HIV Gag-Env virus-like particles from recombinant human adenovirus infected cells.

We have characterized the assembly, budding and extra-cellular release of human immunodeficiency virus (HIV) Gag-Env virus-like particles (VLPs) from human embryonic kidney cells (293 cells expressing the E1a protein of adenovirus) infected with recombinant replication-defective human adenovirus type 5. Recombinant human adenovirus vectors expressing the chimeric Gag-Env protein were constructed by inserting the gag-env fusion gene into the E1a region of the human adenovirus type 5. Biochemical and immunological analyses of VLPs recovered from the culture supernatant revealed that these particles contain the HIV-2 Gag protein and segments of Env protein from the HIV-1 gp120. This chimeric Gag-Env protein interacted with HIV-1 positive patient sera and with HIV-2 Gag monoclonal antibody. Immunoelectron microscopy of the 293 cells infected with the recombinant adenoviruses showed that the HIV Gag-Env antigen is present in the VLPs. Thin-section electron microscopy (EM) revealed that the Gag-Env VLPs bud through the cytoplasmic membrane, as well as through membranes of intracellular vacuoles. The thin-section EM showed that the Gag-Env VLPs have a spherical morphology with an electron-dense ring. The size of VLPs range from 110 to 140 nm in diameter, which is slightly larger than that of the Gag particles without Env protein fusion. Mice immunized with recombinant adenoviruses generated antibodies that specifically reacted with Gag-Env chimeric proteins. Our results support the idea that the replication-defective adenovirus could be used to induce immune responses that might be useful in a vaccine against HIV/AIDS.

Adenovirus E1A Proteins↗

PubMed1988

Nuclear matrix-intermediate filament system and its alteration in adenovirus infected HeLa cell.

The nuclear matrix-intermediate filament (NM-IF) of normal and adenovirus infected HeLa cells were investigated by means of both electron microscopy and two-dimensional gel electrophoresis. After infection there were some changes in NM-IF, and the viral factory was suspended in nuclear matrix. Two new polypeptides appeared in 2-D gel of NM-IF after infection. They are probably not viral proteins but cellular polypeptides. During viral replication, all of vimentin were degraded and phosphorylated keratin 18 increased. These facts suggest that NM-IF plays a certain role in adenovirus replication.

Adenoviruses, Human↗

PubMed1995

Gastrointestinal adenovirus infections in a tertiary referral centre in Saudi Arabia.

To determine the prevalence of adenovirus and its serotypes in diarrhoeal stools in Saudi Arabia, 3,000 stool specimens were collected prospectively from subjects of all ages over a 28-month period. A total of 220 positive isolates were obtained. Fifteen serotypes were found, serotypes 40 and 41 being the most prevalent. Underlying disorders were found in the majority of patients, leukaemia being the most common single underlying condition. This investigation represents the first detailed study of the epidemiology of gastrointestinal adenovirus infections in Saudi Arabia.

Adenoviridae↗

PubMed1996

Systemic adenovirus infection associated with high mortality in mule deer (Odocoileus hemionus) in California.

Seventeen counties in northern California experienced epizootics of high mortality in the mule deer (Odocoileus hemionus) population during the latter half of 1993. Thirteen deer submitted to the California Veterinary Diagnostic Laboratory System as part of this natural die-off had systemic adenovirus infection. Pulmonary edema was present in all 13 deer. Erosions, ulceration, and abscessation of the upper alimentary tract occurred in 7/13 deer. Four of 13 deer had hemorrhagic enteritis. All 13 deer had widespread systemic vasculitis with endothelial intranuclear inclusions. Fluorescein isothiocyanate-labeled antibody directed against bovine adenovirus type 5 bound to antigen in endothelial cells. Adenovirus was identified by transmission electron microscopy within the nuclei of endothelial cells in 6/6 deer examined. An adenovirus was isolated from lung homogenates of one deer that were cultured on black-tailed deer pulmonary artery endothelial cells. With the exception of the intranuclear inclusions evident on histologic evaluation, gross and histologic changes were similar to those described for bluetongue virus infection and epizootic hemorrhagic disease virus infection in white-tailed deer. Nine additional deer were emaciated and had pharyngeal abscesses with focal vasculitis, which may represent the chronic affects of previous nonfatal adenovirus infection.

Adenoviridae↗

PubMed1999

Basolateral localization of fiber receptors limits adenovirus infection from the apical surface of airway epithelia.

Recent identification of two receptors for the adenovirus fiber protein, coxsackie B and adenovirus type 2 and 5 receptor (CAR), and the major histocompatibility complex (MHC) Class I alpha-2 domain allows the molecular basis of adenoviral infection to be investigated. Earlier work has shown that human airway epithelia are resistant to infection by adenovirus. Therefore, we examined the expression and localization of CAR and MHC Class I in an in vitro model of well differentiated, ciliated human airway epithelia. We found that airway epithelia express CAR and MHC Class I. However, neither receptor was present in the apical membrane; instead, both were polarized to the basolateral membrane. These findings explain the relative resistance to adenovirus infection from the apical surface. In contrast, when the virus was applied to the basolateral surface, gene transfer was much more efficient because of an interaction of adenovirus fiber with its receptors. In addition, when the integrity of the tight junctions was transiently disrupted, apically applied adenovirus gained access to the basolateral surface and enhanced gene transfer. These data suggest that the receptors required for efficient infection are not available on the apical surface, and interventions that allow access to the basolateral space where fiber receptors are located increase gene transfer efficiency.

Adenoviridae↗

PubMed1965

Characterization of a Tumorlike Antigen in Type 12 and Type 18 Adenovirus-Infected Cells.

Gilead, Zvee (University of Pennsylvania, Philadelphia), and Harold S. Ginsberg. Characterization of a tumor-like antigen in type 12 and type 18 adenovirus-infected cells. J. Bacteriol. 90:120-125. 1965.-An antigen that reacts with antibody from type 12 adenovirus tumor-bearing hamsters was identified in extracts of KB cells infected with type 12 or 18 adenovirus. In contrast, viral structural proteins separated by chromatography on diethylaminoethyl-cellulose did not react with the sera from tumorous hamsters. The tumorlike (T) antigen in infected cells was found to be smaller than the viral structural antigens and, therefore, could be separated from them by centrifugation in a linear sucrose gradient. Investigation of the production of the T antigen in virus-infected cells further distinguished it from viral structural proteins by the following properties: (i) the T antigen was first detected 3 to 4 hr after infection, whereas viral antigens were synthesized 17 to 20 hr after infection; and (ii) the T antigen was produced when deoxyribonucleic acid (DNA) biosynthesis was inhibited by 5-fluorodeoxyuridine (10(-6)m), but viral proteins were not synthesized in the absence of viral DNA replication.

Journal Article↗

PubMed1996

Polymerase chain reaction for rapid diagnosis of respiratory adenovirus infection.

Endemic (type 1, 2, 5 and 6) and epidemic (type 3, 4 and 7) respiratory adenovirus infections are associated with upper respiratory tract symptoms, pharyngoconjunctival fever, and pneumonia. Improved methods of diagnosis are needed, particularly in immunocompromized patients. We examined 93 throat swabs or nasopharyngeal aspirates from patients with acute respiratory disease using virus isolation and an adenovirus-specific polymerase chain reaction (PCR) based on consensus primers H1 and H2 derived from the hexon region DNA sequences of serotypes 2 and 5. Specimens which yielded viruses other than adenovirus in cell culture (n = 23) or which were negative for infectious viruses (n = 25) were negative in the PCR. The sensitivity of DNA amplification was 76% (34/45) in comparison with virus culture, being markedly lower with subgenus B (types 3 and 7) strains than with subgenus C (type 1, 2, 5 and 6) isolates (8/16 (50%)) vs. 26/28 (93%). P = 0.004) despite the use of a low annealing temperature to maximize detection of adenoviruses belonging to subgenera other than C. Of the 11 samples falsely negative in a single-round PCR but yielding adenovirus type 1 (n = 1), type 2 (n = 1). type 3 (n = 7), type 7 (n = 1), or untyped isolates (n = 1) in cell culture, nine (82%) gave positive results after nested DNA amplification. Possible approaches to further improving the performance of adenovirus PCR with respiratory specimens are discussed.

Adenoviridae Infections↗

PubMed1985

Fatal disseminated adenovirus infection featuring liver necrosis and prolonged viremia in an immunosuppressed child with malignant histiocytosis.

Truly disseminated adenovirus disease is rare and appears to be limited to patients with severe combined T and B cell deficiency. This report describes an 18-month-old child with malignant histiocytosis treated with chemotherapy who developed a fatal disseminated type 2 adenovirus infection. Histologic changes in the tissues of multiple organs as well as the presence of typical crystalline structures in sections of the liver seen with electron microscopy provided evidence of viral replication. Adenovirus was recovered from the involved organs and from daily serum samples obtained over a 2-week period prior to death. The possibility that the child may have had virus associated histiocytic disease prior to chemotherapy is discussed.

Adenoviridae Infections↗

PubMedDate not supplied

Concomitant intestinal adenovirus infection and pulmonary cytomegalovirus infection in children causing fatal enteritis and pneumonia.

Three children in Bangladesh who presented with diarrhoea, cough, dyspnoea, fever, and signs of malnutrition and died in the hospital were shown at post-mortem examination to have both adenovirus infection of the intestine (by immunofluorescence) and cytomegalovirus infection of the lung (by immunoperoxidase staining). This finding of dual viral infections of the intestine and lung in patients with concomitant enteritis and pneumonia provides a basis for symptoms emanating simultaneously from these two organ systems.

Adenovirus Infections, Human↗