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PubMed1993

Transient lupus anticoagulant associated with hypoprothrombinemia and factor XII deficiency following adenovirus infection.

A potent lupus anticoagulant (LA) was detected in four children, 1 week after the clinical onset of an adenovirus infection. The adenovirus infection was documented by direct virus detection in the stool of one patient and serologically in the others. None of the children had elevated titers of IgM- and only one of IgG-anticardiolipin antibodies (ACA). All patients had a marked reduction of prothrombin activity as well as antigen. Prothrombin-antibody complexes were demonstrated in the patients' plasma or mixtures of patient and normal plasma. Factor XII activity was moderately reduced in three of the patients. All coagulation abnormalities returned to normal within 4-12 weeks. Localized bleeding was observed in two cases, but there was no generalized bleeding tendency or evidence of thrombosis.

Adenoviridae Infections↗

PubMed2003

DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells.

Expression of adenovirus E1A deregulates cell proliferation to facilitate viral DNA replication, prompting the initiation of apoptosis signaled primarily through proapoptotic BAK in productively infected cells. We demonstrate here that in uninfected cells, BAK is complexed with the anti-apoptotic BCL-2 family member Myeloid Cell Leukemia 1 (MCL-1). E1A expression during infection resulted in the specific down-regulation of MCL-1 through destabilization of the protein and loss of the mRNA. Upon loss of the MCL-1-BAK complex, BAK complexed with either BAX in proapoptotic E1B mutant adenovirus-infected cells, or with the adenovirus BCL-2 homolog E1B 19K in cells infected with the wild-type virus in which apoptosis is inhibited. Loss of MCL-1 was required to initiate the apoptotic pathway in infected cells as restoration of MCL-1 expression rescued infected cells from E1A-induced apoptosis. Analogous to E1A expression, DNA damage down-regulates MCL-1, and adenovirus infection resulted in the accumulation of phosphorylated H2AX and ataxia-telangiectasia mutant protein (ATM), hallmarks of DNA double-strand breaks. Thus, MCL-1 may function by maintaining BAK in an inactive state, and the loss of MCL-1 upon activation of the DNA damage response, perhaps through replication stress induced in virus infected cells, may be required to initiate the apoptotic response.

Adenoviridae↗

PubMed2000

Adenovirus infections following haematopoietic cell transplantation: is there a role for adoptive immunotherapy?

Adenovirus has been recognised as an important pathogen in BMT recipients, especially in patients with GVHD and those receiving T cell-depleted allografts. We report adenovirus infections from an ongoing surveillance study in four patients after a non-myeloablative transplant and their improved outcome following withdrawal of immunosuppression in two patients and donor lymphocyte infusion for relapsed disease in the others. We discuss the control of adenovirus infections following immune manipulations and the feasibility of adoptive immunotherapy for post-transplant adenovirus infections.

Adenoviridae Infections↗

PubMed2004

Adenovirus infection in hospitalized immunocompetent children.

This study investigated the clinical features of immunocompetent children with adenovirus infection requiring hospitalization. The files of 78 children (mean age 17 +/- 10 months) with community-acquired adenovirus infection admitted over a 2-year period were reviewed. The children were referred after 5.7 +/- 3.4 days of illness, all with fever (mean peak 39.8 +/- 0.8 degrees C). Temperature normalized after 3.5 +/- 2 days. Duration of hospitalization (mean, 7.0 +/- 3.9 days) correlated with lethargy, lung crackles, cracked lips, hypoxia, impaired liver tests, and high serum lactic dehydrogenase (LDH) concentration at admission. Serum LDH concentrations and hypoxemia predicted 70% of the variance in hospital stay. All patients recovered. Adenovirus infection may cause considerable morbidity, even in immunocompetent children. Disease severity, defined by duration of hospitalization, correlates with serum LDH concentrations and oxygen saturation at admission.

Adenovirus Infections, Human↗

PubMed2004

Polymerase chain reaction in the management of disseminated adenovirus infection after stem cell transplantation.

We report a 20-month-old child with disseminated adenovirus infection after a haploidentical T cell-depleted stem cell transplantation. This case demonstrates the value of polymerase chain reaction surveillance for early detection of adenovirus infection and the role of quantitative polymerase chain reaction for monitoring antiviral therapy. It also emphasizes the importance of T cell immunity in controlling disseminated adenovirus infection after stem cell transplantation.

Adenovirus Infections, Human↗

PubMed1988

Nosocomial adenovirus infections: molecular epidemiology of an outbreak due to adenovirus 3a.

An immunocompromised woman died of disseminated infection due to adenovirus type 3. During her hospitalization and after her death, 38 hospital personnel developed an acute respiratory illness. Adenovirus type 3 infection was documented by culture in 18 of the 38 individuals and by seroconversion in one additional employee. Four of 34 asymptomatic hospital personnel exposed to the index case also seroconverted. Thus, 23 personnel were considered to have confirmed infections, and 22 of these 23 reported direct contact with the index case. Acquisition of infection was associated with the number and type of contacts. Protection against infection was associated with detectable serum-neutralizing antibody in the early serological sample. Restriction enzyme analysis using six different endonucleases indicated that all isolates of virus were type 3a and had identical genetic composition. This study underscores the importance of adenovirus as a cause of nosocomial infection and indicates that genetic analysis of viral DNA is a powerful tool for studying common-source outbreaks.

Adenoviridae Infections↗

PubMed1984

Human adenovirus infection in phytohaemagglutinin treated mice.

The course of infection by human adenovirus type 12 has been studied in mice treated with phytohaemagglutinin (PHA) 1 day after infection or those infected with the virus 3 days after PHA treatment. Virus antigens were demonstrated by immunofluorescence in the cells of the thymus, spleen and lymph nodes and in some cases the supernatant of the cell homogenate was found to contain infective viruses. Virus antigens occurred sporadically in cells of the lymphoid organs of control animals infected only with adenovirus. Neither virus antigens nor infective virus could be detected in mice that were not infected by virus and not treated with PHA as controls. The results indicate that PHA treatment increased the sensitivity of mice to human adenovirus infection.

Adenoviridae Infections↗

PubMed2005

First reported outbreak of diarrhea due to adenovirus infection in a hematology unit for adults.

Numerous outbreaks of adenovirus infection from different types of health care settings, except a hematology unit, have been reported. This is the first report describing an outbreak of adenovirus infection causing diarrhea among adult hematopoietic stem cell transplant recipients. Six of 21 patients from the outbreak cohort were affected with diarrhea. Electron microscopy, cell culture, and direct DNA sequencing of amplicons generated from stool and blood samples were used to investigate this outbreak. Electron microscopy and cell culture detected adenovirus in stools from symptomatic patients. DNA sequencing of amplicons generated from stool samples confirmed nosocomial transmission of infection from a single index case. The outbreak strain was also detected in plasma of four of these patients, suggesting systemic infection. The outbreak strain was identified as type 12. Standard infection control measures were effective to control this outbreak.

Adenovirus Infections, Human↗

PubMed2003

Severe adenovirus infection in children.

During the period from July 1, 1999 to September 30, 2000, 9 children with severe adenovirus infection were treated at Chang Gung Children's Hospital. The mean age was 22 months (range, 5-50 months). All of them had lower respiratory tract infections, which manifested as lobar or segmental pneumonia and pleural effusion. Eight (88.9%) of the 9 patients required intensive care and 4 of them required mechanical ventilation. Abnormal laboratory findings included leukocytosis, elevated C-reactive protein, anemia, and prolonged prothrombin time and partial thromboplastin time. Extrapulmonary complications included hepatitis (6 cases), encephalitis (3), conjunctivitis (3), periorbital ecchymosis (1), and coagulopathy (2). One patient died, resulting in a mortality rate of 12.5%. Follow-up at 3 months postdischarge, 5 patients (62.5% of survivors) had bronchiolitis obliterans and/or organizing pneumonia. Seven patients were infected by serotype 3 adenovirus, 1 patient by serotype 2, and another by serotype 11. In conclusion, the clinical, laboratory, and radiographic features of severe adenovirus infection may mimic bacterial infection. Rapid progression of the clinical course despite antibiotic therapy and the presence of unusual extrapulmonary symptoms are important clinical clues in the diagnosis of severe adenoviral infection.

Adenovirus Infections, Human↗

PubMed2000

Adult adenovirus infections: loss of orphaned vaccines precipitates military respiratory disease epidemics. For the Adenovirus Surveillance Group.

Adenovirus vaccines have greatly reduced military respiratory disease morbidity since the 1970s. However, in 1995, for economic reasons, the sole manufacturer of these vaccines ceased production. A population-based adenovirus surveillance was established among trainees with acute respiratory illness at 4 US military training centers as the last stores of vaccines were depleted. From October 1996 to June 1998, 1814 (53.1%) of 3413 throat cultures for symptomatic trainees (78% men) yielded adenovirus. Adenovirus types 4, 7, 3, and 21 accounted for 57%, 25%, 9%, and 7% of the isolates, respectively. Unvaccinated trainees were much more likely than vaccinated trainees to be positive for types 4 or 7 (odds ratio [OR] = 28.1; 95% CI, 20.2-39.2). Two training centers experienced epidemics of respiratory disease affecting thousands of trainees when vaccines were not available. Until a new manufacturer is identified, the loss of orphaned adenovirus vaccines will result in thousands of additional preventable adenovirus infections.

Adenovirus Infections, Human↗

PubMed2004

Treatment of adenovirus infections in the immunocompromised host.

Adenovirus infections are increasing as causes of morbidity and mortality in severely immunocompromised patients. The currently available antiviral agents, ribavirin and cidofovir, have yielded mixed results in case reports and small case series. Similar to cytomegalovirus disease, established adenovirus disease is often difficult to treat. Therapy may yield poor results, even when effective antiviral drugs are used. New strategies, including pre-emptive therapy, should be tested in prospective, clinical trials. New agents and adoptive transfer of specific T-cells to adenovirus might improve the current situation.

Adenoviridae Infections↗

PubMed1984

Differences in sequence content of nuclear and cytoplasmic polyribosomal RNA from adenovirus-infected cells.

RNA molecules from nuclear and cytoplasmic polyribosomes of adenovirus-infected HeLa cells were compared by hybridization to analyse the sequence content. Nuclear polyribosomes were released by exposure of intact detergent-washed nuclei to poly(U) and purified. Cytoplasmic polyribosomes were also purified from the same cells. To show that nuclear polyribosomes contain ribosomes linked by mRNA, polyribosomes were labelled with methionine and uridine in the presence of actinomycin D in adenovirus-infected cells. Purified nuclear polyribosomes were treated with EDTA under conditions which dissociate polyribosomes into ribosomes and subunits with a simultaneous release of mRNA, and sedimented. The treatment dissociated these polyribosomes, releasing the mRNA from them. Radiolabelled total RNA from each polyribosome population was fractionated in sucrose gradients into several pools or hybridized to intact adenovirus DNA to select virus-specific RNA. Sucrose-gradient-fractionated pool-3 RNA (about 28S) and virus-specific RNA were then hybridized to fragments of adenovirus DNA cleaved by restriction endonucleases SmaI, HindIII and EcoRI by the Southern-blot technique and by filter hybridization. The results showed that nuclear RNA contained sequences, from about 0 to 18 map units, which were essentially absent from cytoplasmic RNA. Furthermore, the amount of virus-specific RNA for a particular sequence was also different in the two populations.

Adenoviridae Infections↗

PubMed2003

Real-time blood plasma polymerase chain reaction for management of disseminated adenovirus infection.

We evaluated the usefulness of quantifying blood plasma adenovirus DNA loads for the management of adenovirus infection. Quantification of adenovirus A, B, and C DNA loads was done with real-time polymerase chain reaction (PCR) assays. Blood plasma specimens obtained from 44 immunocompromised patients were screened prospectively with this method. PCR findings for 36 patients were negative, and none of the patients developed disseminated adenoviral disease. PCR findings for 8 patients were positive; all 8 had invasive adenoviral disease and were treated with cidofovir. Sequential measurements of adenovirus DNA loads were performed to monitor the effect of cidofovir therapy. Decrease in the blood plasma DNA load was significantly higher in patients with a good response to cidofovir than in patients with a poor response and was therefore correlated with survival. Detection of adenovirus DNA in blood plasma appears to be useful for identifying patients at risk for invasive disease. Moreover, quantification of adenovirus DNA loads in plasma is helpful for monitoring the efficacy of antiviral therapy.

Adenoviridae↗

PubMed1961

Nucleuc acid synthesis in types 4 and 5 adenovirus-infected HeLa cells.

Type 4 adenovirus infection of HeLa cells effected a marked increase in synthesis of the saline-soluble DNA fraction, but not the host-cell DNA (the water-soluble fraction). This was demonstrated by the marked increase in specific activity of saline-soluble DNA but not water-soluble DNA when P(32)-inorganic phosphate or sodium formate-C(14) was employed. When these isotopes were used to label cells before viral infection rather than during the process of viral propagation, the saline-soluble DNA from infected cells had a specific activity of 10 to 20 per cent less than that of uninfected cells, indicating that the saline-soluble DNA was synthesized both from prelabeled precursors of the cell pools and unlabeled materials from the medium. Saline-soluble DNA began to increase between 10 to 12 hours after viral infection and 3 to 4 hours before appearance of newly propagated infectious virus. The specific activity of the acid-soluble pool of infected cells also increased between 10 to 12 hours after viral inoculation when sodium formate-C(14) was used as a radioisotope. When P(32)-inorganic phosphate was utilized, the specific activity of infected-cell RNA was increased approximately the same relative amount as when total RNA was determined chemically; i.e., 30 to 40 per cent. With type 5 adenovirus, not only did a 3- to 5-fold increase in saline-soluble DNA occur, but also an increase was measured in specific activity of RNA when P(32)-inorganic phosphate was used.

Adenoviridae↗

PubMedDate not supplied

Monitoring adenovirus infections with on-line and off-line methods.

Several known process monitoring methods were tested for their efficacy in the detection of adenovirus infections. The methods that we explored include several indirect indications of viral infections, including metabolic rate analysis, secondary gauges of respiration, cell size measurement, cell number and cell viability determination, and changes in capacitance. Direct indications of the adenovirus infection were also applied, including total viral particle and infectious particle measurements, as well as a flow cytometry method for detecting infected cells. All of the methods tested in the study provide some positive indication of an adenovirus infection. Many of the methods require repeated sampling, which may limit their utility in a manufacturing process. All of the indirect measures of viral infection may be limited by the fact that they do not uniquely identify an infection. The simplest monitoring methods appear to be detection of changes in respiration or the capacitance of the culture, both of which seem to provide a clear indication of an infection. Further work will be required to demonstrate that these indications are characteristic of only a successful and productive adenovirus infection.

Adenoviridae↗

PubMed2000

Outcome and clinical course of 100 patients with adenovirus infection following bone marrow transplantation.

We conducted a retrospective review of the clinical features and outcome of adenovirus infection in 572 consecutive patients transplanted in a single centre over a 10 year period. One hundred patients (17%) had a total of 105 episodes of adenovirus infection diagnosed at a median of 18 days post transplant (range 2-150 days). The incidence was higher in children than adults (21% vs 9%, P < 0.001) and in unrelated donor vs matched sibling donor transplants (26% vs 9%, P < 0.001). Diarrhoea and fever were the most common presenting features. Reflecting these symptoms, the most common site of isolation was the stool. Serotypes 1, 2 and 7 were the most frequently seen (total of 41/68 or 60% of evaluable cases). In six patients (6%) adenovirus infection was the direct cause of death occurring at a median of 72 days post transplant (range 18-365 days). Five of these six patients had pulmonary involvement and four had associated graft-versus-host disease (GVHD). Three further patients were considered to have severe adenoviral disease (total incidence 9%). Isolation of virus from multiple sites correlated with a poor outcome (P < 0.001). Comorbid viral infection was common in this group with 50% of all patients having other viruses isolated (predominantly polyoma virus and cytomegalovirus). We conclude that adenovirus is commonly isolated after bone marrow transplant and is a cause of significant morbidity but was a rare cause of mortality (6/572 = 1%) in our patient group as a whole. The relative infrequency of severe infection will make it difficult for the transplant physician to decide which patients should receive experimental antiviral drugs such as ribavirin and cidofovir or immunomodulatory therapy with donor white cell infusions.

Adenovirus Infections, Human↗

PubMed1976

Crippling lung disease after measles and adenovirus infection.

Four children who developed severe lung disease after measles are described. One child died and three have been left with severe impairment of lung function. It is suggested that secondary infection with an adenovirus was responsible for causing the lung disease in these patients. The immune response to measles was abnormal. Measles virus may have rendered the children more susceptible to serious complications from infection with the adenovirus. The many deaths from 'measles pneumonia' in developing countries and the occasional occurence of post-measles bronchiectasis in this country may be due to secondary adenovirus infections. Further viral and serological studies are required to confirm this hypothesis.

Adenoviridae Infections↗

PubMed1999

The role of the L4 33K gene in adenovirus infection.

The late phase of adenovirus infection is characterized not only by the synthesis of late proteins and the assembly of new virions, but also by the inhibition of early gene expression and host cell translation. Previous work has demonstrated that both of these inhibitory effects depend upon expression from the major late transcription unit (MLTU), controlled by the major late promoter (MLP). Furthermore, the repression of early gene expression has been shown to be mediated in trans, suggesting a role for one or more MLTU-encoded soluble factor(s). A possible candidate for such a factor is the L4-encoded 33K gene product, a protein conserved throughout the Mastadenoviridae, but of no known function. To test the role of this protein in viral infection, a stop codon was placed at the 20th position of the 33K ORF. Viable virus with genomes containing the mutation were recovered in an overlap recombination assay. Phenotypic analysis revealed that the mutant virus had a significant deficiency in both kinetics of replication and final yield, as compared to the wild-type virus. Detailed analysis of infected cells showed that there was no detectable change in the regulation of expression of several early genes and the pIX gene. This suggests either that 33K is not involved in this late phase phenomenon or that this function is replaceable by another late protein(s). Late protein synthesis and accumulation were similar to those in wild-type-infected cells. However, the reduced yield of infectious mutant virus could be accounted for by a marked deficiency in the accumulation of intermediate particles and completed capsids, suggesting a role for 33K in the process of assembly. In addition there was a small but reproducible deficiency in the shutoff of host cell translation. These results show that the 33K protein plays an important, although apparently not essential, function in the late phase of virus infection.

Capsid↗