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PubMed1965

ELECTRON MICROSCOPIC RADIOAUTOGRAPHY OF HELA CELLS INFECTED WITH ADENOVIRUS.

Harford, Carl G. (Washington University, St. Louis, Mo.), and Alice Hamlin. Electron microscopic radioautography of HeLa cells infected with adenovirus. J. Bacteriol. 89:1540-1547. 1965.-Because intracellular particles of adenovirus are not seen by light microscopy, radioautography with tritiated thymidine was carried out with an electron microscope. Reacted grains were present over many nuclei containing viral aggregates, but only 16% of these grains were over the aggregates. Control observations with tritium-labeled bacteria indicated that this low incidence of labeling of viral aggregates could not be attributed to errors of the method. We think that deoxyribonucleic acid (DNA) labeled with tritiated thymidine in these experiments was mainly the excess viral DNA that is known to accumulate in adenovirus-infected cells. We did not exclude the possibility that some cellular DNA was labeled.

Adenoviridae↗
PubMed1989

Nosocomial and endemic infections with a genome type of adenovirus type 5.

A unique genome type of adenovirus 5 was isolated from 37 specimens of 25 patients. DNA restriction analysis was performed with seven endonucleases. Part of the patients were treated at a bone marrow transplantation unit in Munich. Nosocomial spread, rather than activation of endogenous adenovirus infection, was likely for many of them. In addition, sporadic cases suggested an endemicity of this genome type in Bavaria.

Adenoviridae Infections↗
PubMed1989

Keratoconjunctivitis due to adenovirus type 8: a local outbreak.

An outbreak of acute keratoconjunctivitis occurred in 24 patients who had visited a private ophthalmology office between July and October 1986. The median incubation period was 12.6 days (range seven to 21 days). Adenovirus type 8 was isolated from three of the five patients in whom cultures were done. This outbreak illustrates the highly contagious nature of adenovirus infection and the potential for transmission during routine office visits.

Adenoviridae Infections↗
PubMed1979

[Virological diagnosis of epidemic keratoconjunctivitis (author's transl)].

Among 180 patients with proved adenovirus infection of the eye, 144 infections with adenovirus 8 (Ad 8) were found. 11 or 7 patients were infected with Ad 19 or Ad 4 respectively; further 18 cases were associated with 6 other serotypes. The main symptoms of epidemic keratoconjunctivitis (EKC) (pronounced inflammatory swelling of the plica and caruncula, nummular corneal infiltations) are not confined to Ad 8 infections. For the virological diagnosis, a combination of virus isolation and serology is recommended. Virus isolation is mostly successful from conjunctival swabs obtained during the first week of the disease. For serological investigation, the first blood specimen should be taken as early as possible, the second not earlier than 15 days after onset of disease. The mere application of the group-specific adenovirus complement-fixation is insufficient; it should be supplied by neutralization and hemagglutination-inhibition with Ad 8 (or Ad 19) virus, although these reactions are not invariably type-specific. A swifter diagnosis of the adenovirus infection by immunofluorescence performed in cell cultures inoculated with conjunctival material, 3 or 7 days after inoculation, was often successful; however, this procedure proved to be less sensitive than virus isolation.

Adenoviridae Infections↗
PubMed1999

Infectivity and expression of the early adenovirus proteins are important regulators of wild-type and DeltaE1B adenovirus replication in human cells.

An adenovirus mutant lacking the expression of the large E1B protein (DeltaE1B) has been reported to replicate selectively in cells lacking the expression of functionally wild-type (wt) p53. Based on these results the DeltaE1B or ONYX-015 virus has been proposed to be an oncolytic virus which might be useful to treat p53-deficient tumors. Recently however, contradictory results have been published indicating that p53-dependent cell death is required for productive adenovirus infection. Since there is an urgent need for new methods to treat aggressive, mutant p53-expressing primary tumors and their metastases we carefully examined adenovirus replication in human cells to determine whether or not the DeltaE1B virus can be used for tumor therapy. The results we present here show that not all human tumor cell lines take up adenovirus efficiently. In addition, we observed inhibition of the expression of adenovirus early proteins in tumor cells. We present evidence that these two factors rather than the p53 status of the cell determine whether adenovirus infection results in lytic cell death. Furthermore, the results we obtained by infecting a panel of different tumor cell lines show that viral spread of the DeltaE1B is strongly inhibited in almost all p53-proficient and -deficient cell lines compared to the wt virus. We conclude that the efficiency of the DeltaE1B virus to replicate efficiently in tumor cells is determined by the ability to infect cells and to express the early adenovirus proteins rather than the status of p53.

Adenoviridae↗
PubMed1989

Comparison of direct rapid tests for the detection of adenovirus antigen in routine conjunctival specimens.

Two direct rapid tests to detect adenovirus antigen, enzyme immunoassay (EIA) and immunofiltration (IF) were compared with regard to sensitivity, specificity, ease of interpretation, and technical complexity against 75 adenovirus culture-positive and 35 adenovirus culture-negative conjunctival swab specimens. Enzyme immunoassay and IF were equally sensitive (P = 0.5), with sensitivities of 80.6 and 79.0%, respectively, when swab specimens were collected from patients within 7 days of the onset of clinical symptoms of adenovirus infection. After 7 days of clinical onset, IF (46.2%) was more sensitive (P less than 0.01) than EIA (0.0%), and was able to detect residual antigen in three culture-negative specimens. Enzyme immunoassay and IF were equally specific (100%). Both tests were easy to interpret, but IF was more technically complex and is not yet commercially packaged. Enzyme immunoassay could benefit either an office practice or a central laboratory, whereas IF is better suited for the latter.

Adenoviridae Infections↗
PubMed1987

Genomic variation of adenovirus type 5 isolates recovered from bone marrow transplant recipients.

We characterized the genomic variation of adenovirus type 5 isolates recovered from bone marrow transplant recipients in Seattle between 1976 and 1982. By restriction endonuclease analysis, we identified three new adenovirus genomic variants, each associated with a single invasive adenovirus infection. In addition, we were able to obtain suggestive evidence for a nosocomial spread of a particular group of isolates within this population. This study demonstrates that the technique of restriction endonuclease analysis is an important epidemiological tool for investigating viral infections.

Adenoviridae Infections↗
PubMed1978

Mapping of adenovirus type 5 temperature-sensitive mutations by marker rescue in enhanced double DNA infections.

Adenovirus type 5 DNA has low infectivity (Graham & van der Eb, 1973) which can be increased by various techniques, one of which is the dimethyl sulphoxide (DMSO) boost (Stow & Wilkie, 1976). In this report, it is shown that DMSO treatment of adenovirus 5 DNA-infected HeLa cells results in a 10-fold increase in plaque formation, and that this can be used to facilitate marker rescue experiments. Double DNA infections were performed by the calcium phosphate method, co-precipitating intact temperature-sensitive mutant DNA with purified wild-type DNA restriction endonuclease fragments. Analysis of the plaquing ability of these mixtures and any progeny virus has resulted in the assignment of six temperature-sensitive mutations to discrete physical locations on the adenovirus type 5 genome. These locations are discussed with respect to the mutant phenotypes and the transcription-translation products of the appropriate regions.

Adenoviruses, Human↗
PubMed2001

Influenza A infection is an important cause of febrile seizures.

OBJECTIVES: To compare the incidence of febrile seizures in children hospitalized for influenza A infection with parainfluenza and adenovirus infection and to examine the hypothesis that children hospitalized for influenza A (variant Sydney/H3N2) during the 1998 season in Hong Kong had more frequent and refractory seizures when compared with other respiratory viruses, including the A/Wuhan H3N2 variant that was present in the previous year. METHODS: Medical records of children between 6 months and 5 years of age admitted for influenza A infection in 1998 were reviewed. For comparison, records of children of the same age group with influenza A infection in 1997, and with parainfluenza and adenovirus infections between 1996 and 1998 were reviewed. Children who were afebrile or who had an underlying neurologic disorder were excluded. RESULTS: Of children hospitalized for influenza A in 1998 and 1997, 54/272 (19.9%) and 27/144 (18.8%) had febrile seizures, respectively. The overall incidence of febrile seizures associated with influenza A (19.5%) was higher than that in children hospitalized for parainfluenza (18/148; 12.2%) and adenovirus (18/199; 9%) infection, respectively. In children who had febrile seizures, repeated seizures were more commonly associated with influenza A infection than with parainfluenza or adenovirus infection (23/81 [28%] vs 3/36 [8.3%], odds ratio [OR] 4.3, 95% confidence interval: 1.2 to 15.4). Alternatively, children with influenza A infection had a higher incidence (23/416, 5.5%) of multiple seizures during the same illness than those with adenovirus or parainfluenza infection (3/347, 0.86%; OR 6.7, 95% confidence interval: 2.0-22.5.) The increased incidence of febrile seizures associated with influenza A was not attributable to differences in age, gender, or family history of febrile seizure. Multivariate analysis, adjusted for peak temperature and duration of fever, showed that hospitalized children infected with infection A had a higher risk of febrile seizures than those who were infected with parainfluenza or adenovirus (OR 1.97). Influenza A infection was a significant cause of febrile seizure admissions. Of 250 and 249 children admitted to Queen Mary Hospital for febrile seizures in 1997 and 1998, respectively, influenza A infection accounted for 27 (10.8%) admissions in 1997 and 54 (21.7%) in 1998. During months of peak influenza activity, it accounted for up to 35% to 44% of febrile seizure admissions. In contrast, parainfluenza, adenovirus, respiratory syncytial virus, and influenza B had a smaller contribution to hospitalizations for febrile seizures, together accounting for only 25/250 (10%) admissions in 1997 and 16/249 (6.4%) in 1998. CONCLUSION: The influenza A Sydney variant (H3N2) was not associated with an increased risk of febrile seizures when compared with the previous influenza A Wuhan variant (H3N2) or H1N1 viruses. However, in hospitalized children, influenza A is associated with a higher incidence of febrile seizures and of repeated seizures in the same febrile episode than are adenovirus or parainfluenza infections. The pathogenesis of these observations warrants additional studies. Complex febrile seizures, particularly multiple febrile seizures at the time of presentation, have been thought to carry an adverse long-term prognosis because of its association with a higher incidence of epilepsy. Repeated febrile seizures alone, particularly if associated with influenza A infection, may not be as worrisome as children with complex febrile seizures because of other causes, which requires additional investigation. This may subsequently have an impact on reducing the burden of evaluation in a subset of children with complex febrile seizures.

Adenoviridae Infections↗
PubMed1979

Comparative sensitivity of a cultural test and the complement fixation test in the diagnosis of adenovirus ocular infection.

The sensitivity of human embryonic kidney (HEK) cell culture and the complement fixation test (cft) in the diagnosis of adenovirus ocular infection has been compared. The optimum time for collection of specimens to obtain the best results by each test has been examined. Sixty-one (53%) of 116 patients with moderate to severe follicular conjunctivitis, clinically indicative of adenovirus infection, had serological evidence of infection or had the virus isolated from ocular swabs. Virus was isolated from 53 patients (45%) and significant antibody rises were found in 33 (27%). When each test was carried out under optimum conditions, virus was isolated from 82% of cases and serological evidence of infection found in 72%. Serological responses as detected by the CFT appeared to be inferior in infections caused by adenovirus type 7 to those encountered in infections due to adenovirus types 3 and 8.

Adenoviridae Infections↗
PubMed1990

Expression of the type I DNA topoisomerase gene in adenovirus-5 infected human cells.

The amount of topoisomerase I specific mRNA increases three- to fivefold during the early phase of infection of HeLa cells with adenovirus-5. The observed increase in specific mRNA is mainly due to an increased rate of transcription of the gene. In human 293 cells, which constitutively express the viral E1A and E1B genes, we determined an elevated level of topoisomerase I mRNA, comparable to the amount of mRNA present in HeLa cells early after infection with adenovirus. In contrasts, in HeLa cells infected with adenovirus dI312, a mutant were the E1A region had been deleted, the amount of topoisomerase I mRNA remained constant, unless the cells were superinfected with wild type virus. Our experiments indicate that the topoisomerase I gene is transactivated by an early adenovirus protein product coded by the E1A region. In contrast to the increase in mRNA synthesis, the amount of topoisomerase I protein and the topoisomerase I activity remain constant up to 24 hours after infection.

Adenoviruses, Human↗
PubMed2004

[Two cases of acute encephalitis/encephalopathy associated with adenovirus type 3 infection].

Although adenovirus type 3 is a common pathogen of pediatric infection, there have been few reports on encephalitis and encephalopathy caused by this virus. We report two cases, one of acute encephalitis and another of transient encephalopathy, associated with adenovirus type 3 infection. Case 1, an 11-year-old boy with unconsciousness and convulsions, was diagnosed as having acute encephalitis because adenovirus type 3 was isolated from the cerebrospinal fluid. Case 2, a 3-year-old boy with intermittent excitement and hallucinations, was diagnosed as having transient encephalopathy. MRI, EEG, and cerebrospinal fluid studies were normal. Our cases and previously reported cases exhibit a wide clinico-pathological spectrum of the central nervous system involvement by adenovirus type 3.

Acute Disease↗
PubMed1987

Reduced allorecognition of adenovirus-2 infected cells.

The early region 3 of adenovirus 2 encodes the membrane glycoprotein E19. This protein specifically binds class I transplantation antigens of a variety of species. Concomitant with this interaction the intracellular transport of newly synthesized class I heavy chains is abrogated. At late stages of the virus infection this leads to a notable decrease in the cell surface expression of class I antigens. We have studied how infection with adenovirus 2 influences target cell recognition by alloreactive cytolytic T lymphocytes. We found that the E19 protein-induced reduction of the HLA-B7 cell surface expression led to a greatly reduced lysis of the infected cells. These findings support our hypothesis that the E19 protein has evolved to facilitate the in vivo replication of the virus by reducing the expression of HLA class I antigens.

Adenoviridae Infections↗
PubMed1998

Adenovirus facilitated infection of human cells with ecotropic retrovirus.

Retroviral infection is restricted by the expression of a viral receptor on the surface of the target cell. Retrovirus-mediated gene transfer is therefore not possible in cells that fail to express sufficient levels of the appropriate receptor, representing one major obstacle to the use of recombinant retroviruses in experimental and clinical applications. In this study, we utilized an adenoviral vector to express transiently the receptor for the ecotropic murine leukemia virus in a panel of human cell lines. Following adenoviral infection, the susceptibility to ecotropic retroviral particles of A549, HeLa, RC39 and Meso 33 cells, derived from human lung epithelium, cervical epithelium, kidney and mesothelium, respectively, was measured on a single-cell basis by the detection of a cell surface marker encoded by the recombinant retrovirus. The marker, termed NTP, was found in 10-30%, 25-50% and 50-90% of cells infected at 5, 50 and 250 adenovirus multiplicity of infection, respectively. Southern blot analysis demonstrated the integration of intact retroviral DNA. The integrated vector copy number increased with the adenoviral multiplicity of infection, suggesting that retrovirus infection is proportional to receptor expression by the target cell, albeit not in a linear fashion. Susceptibility to ecotropic retroviral infection was maintained undiminished for at least 3 days, indicating the persistent expression of ecotropic receptor by the adenovirus-transduced cells in that time period and the lack of a major cellular defense triggered by adenovirus infection against the subsequent retroviral infection. Thus, the infection of human cells of various tissues with a recombinant adenovirus expressing the ecotropic murine leukemia virus receptor generates a window of susceptibility where a high retroviral infection rate can be achieved. Increased efficiency of retroviral infection obtained in this fashion is amenable to specific regulation via the controlled expression of the adenovirus-encoded retroviral receptor.

Adenoviridae↗
PubMed2001

The mechanisms of placental viral infection.

The placenta is a dynamic organ whose structure and function change throughout pregnancy. There is compelling evidence that the placenta plays an integral role in the vertical transmission of viruses, such as cytomegalovirus and human immunodeficiency virus, from the mother to the fetus. Although the sequelae of congenital viral infection (i.e., fetal anomalies, intrauterine fetal death, and persistent postnatal infection) may be devastating, very little is known about the passage of viruses across the placenta and the pathologic consequences of placental viral infection. We postulate that the syncytiotrophoblast, which forms a continuous barrier between the maternal and fetal circulation, is relatively resistant to viral infection. In support of this hypothesis, we observed that the susceptibility of trophoblast cells to infection by adenovirus and herpes simplex virus and the expression of viral receptors were reduced as trophoblast cells terminally differentiated into syncytiotrophoblast. Conversely, we observed that undifferentiated, extravillous trophoblast cells, which are susceptible to adenovirus infection, underwent pathologic changes (i.e., apoptosis) when infected by adenovirus in the presence of decidual lymphocytes (which were used to simulate the maternal immune response to viral infection). Based on these findings, we speculate that viral infection of extravillous trophoblast cells may negatively impact the process of placental invasion and predispose the mother and fetus to adverse reproductive outcomes that result from placental dysfunction.

Female↗
PubMed1975

DNA binding proteins in the cytoplasm and in a nuclear membrane complex isolated from uninfected and adenovirus 2 infected cells.

The DNA binding proteins in a nuclear membrane fraction that can synthesize DNA in vitro (referred to as "nuclear membrane complex") and in the cytoplasm of adenovirus infected and uninfected cells were isolated and characterized. Suspension cultures of human KB cells infected with human adenovirus 2 were treated with 25 mu-g/ml of arabinosylcytosine starting at 2 hr to block the synthesis of viral structural proteins, and then labeled with (3H)leucine from 6 to 24 hr after infection. Uninfected cells were treated similarly and labeled with (14C)leucine. The 3H-labeled proteins (infected cells) and 14C-labeled proteins (uninfected cells) isolated from the cytoplasm were mixed, as were the corresponding proteins isolated from the membrane complex, and each mixture was fractionated by stepwise elution from single-stranded DNA-cellulose columns. From 50 to 60% of the labeled protein in the membrane complex from infected cells and 40 to 50% of that from uninfected cells bound to DNA-cellulose in 0.05 M NaCl. Much less protein from the cytoplasm was bound to DNA cellulose, 20% from infected cells and 11% from uninfected cells. Gel electrophoresis of the mixture of 3H- and 14C-labeled proteins eluted from DNA-cellulose by different concentrations of NaCl revealed the following. (1) The 0.15 and 0.40 M NaCl eluates from the membrane complex of infected and uninfected cells contained a heterogenous mixture of similar polypeptides. (2) The 0.6 M NaCl eluate from the membrane complex derived from infected cells contained two major DNA binding proteins with molecular weights of 75,000 and 45,000 that were absent from uninfected cells. Large quantities of these two proteins were present in highly purified form in the 0.6 M NaCl eluate from the cytoplasm of infected cells. The DNA binding proteins of molecular weight 75,000 and 45,000 that are present in the cytoplasm are identical with those present in the membrane complex, as established by coelectrophoresis. (3) Two major cell-specific proteins of molecular weight 40,000 and 15,000-17,000 were present in the 2 M NaCl eluate of the membrane complex from uninfected and infected cells. A major cell-specific protein of molecular weight 33,000 was present in the 0.15 and 0.4 M NaCl eluates of the uninfected and infected cell cytoplasmic fractions. Aanalysis of cells labeled at 2-6 hr after infection in the absence of arabinosyl cytosine indicated that the synthesis of the DNA binding proteins of molecular weight 75,000 and 45,000 begins early after infection prior to the onset of viral DNA replication.

Adenoviridae↗
PubMed2005

Nuclear actin is partially associated with Cajal bodies in human cells in culture and relocates to the nuclear periphery after infection of cells by adenovirus 5.

Cajal bodies are intra-nuclear structures enriched in proteins involved in transcription and mRNA processing. In this study, immunofluorescence microscopy experiments using a highly specific antibody to actin revealed nuclear actin spots that colocalized in part with p80 coilin-positive Cajal bodies. Actin remained associated with Cajal bodies in cells extracted to reveal the nuclear matrix. Adenovirus infection, which is known to disassemble Cajal bodies, resulted in loss of actin from these structures late in infection. In infected cells, nuclear actin was observed to relocate to structures at the periphery of the nucleus, inside the nuclear envelope. Based on these findings, it is suggested that actin may play an important role in the organization or function of the Cajal body.

Actins↗