[Contribution to the study of adenovirus infections. Adenoviruses and the Fiessinger-Leroy-Reiter syndrome].
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Adenoviridae↗
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[Inflammatory sequelae after adenovirus infection].
Adenovirus infections are common. The period of virus replication is short, hardly ever exceeding two weeks. In 216 patients we studied the post-inflammatory period after infection with adenovirus types 8, 4, 3, 7, 19 and 37, in some patients up to three years. In 49.5%, the initial infection also involved the cornea, in 79.5% bilaterally. In 50.5% there was only follicular conjunctivitis. The post-inflammatory period is most annoying as rather frequently a considerable period of chronic eye irritation can be expected. In our study the number of cases with post-infectious ocular irritation tended to decrease slowly. Treatment with 0.5% methylcellulose was of little help to alleviate the ocular irritation.
Adenoviridae Infections↗
Toxic shock-like syndrome caused by adenovirus infection.
Adenovirus infections commonly occur in childhood and produce a wide range of clinical disease. The most common sites of infection are the respiratory and gastrointestinal tracts but involvement of cardiovascular, neurological, cutaneous, ophthalmic, renal, and hepatic systems can also occur. A case of toxic shock-like syndrome with symptoms of multiorgan involvement resulting from adenovirus infection is reported.
Adenovirus Infections, Human↗
Neonatal adenovirus infection: a case report with in situ hybridization confirmation of ascending intrauterine infection.
Adenovirus infection is a rare, but serious infection, during the neonatal period. The actual model of infection at birth is currently unknown, however, several mechanisms have been proposed. We describe a case of fatal neonatal adenovirus pneumonia in a 25-wk gestational age infant. Adenovirus was confirmed by electron microscopy and by in situ hybridization. The maternal cervical/endocervical smear taken prior to the delivery contained epithelial cells with changes suggestive of adenovirus, which was confirmed by in situ hybridization on the smear. These findings suggest that ascending viral infection is a factor in the pathogenesis of neonatal adenovirus infection. The identification and reporting of adenovirus may be important during pregnancy in order to avoid delay in delivery of the fetus once membranes have ruptured.
Adenoviridae↗
The adenovirus EIIA enhancer. Analysis of regulatory sequences and changes in binding activity of ATF and EIIF following adenovirus infection.
Adenovirus EIIA upstream sequences which contain the binding sites for proteins ATF and EIIF act as an enhancer and can be trans-activated by both E1A and SV40 T/t-antigens. Specific mutation of either the ATF or EIIF binding site demonstrates that both act as positive regulators, decreasing transcription greater than 10-fold. Mutation of both the ATF and EIIF binding sites inhibited the EIIA enhancer 200-fold. Analysis of insertion mutations suggests that the spatial alignment of the upstream ATF and EIIF binding sites with respect to the downstream EIIF binding site on the DNA helix is important. Consistent with previous findings, using gel shift analysis we demonstrate that the binding activity of EIIF is increased following wild-type adenovirus infection. In contrast, using identical gel shift conditions, the binding activity of ATF is decreased by viral infection.
Adenovirus Early Proteins↗
Polymerase chain reaction for rapid detection of ocular adenovirus infection.
Adenoviruses are associated with endemic and epidemic acute conjunctivitis, large nosocomial outbreaks reflecting virus transmission on unwashed hands or inadequately sterilised ophthalmic instruments. The polymerase chain reaction (PCR) proved more sensitive than antigen detection by immune dot-blot test for the rapid diagnosis of ocular adenovirus infection (sensitivities in a retrospective study 112/123 (91%) versus 72/123 (59%), P < 0.001). Indeed, in a prospective comparison, DNA amplification and virus isolation generated similar numbers of positive results (34 versus 32), though five PCR positive results were possibly false positives. The sensitivity of the PCR was largely independent of adenovirus subgenus or serotype, though reduced sensitivity with subgenus B strains could not be excluded. Specimen preparation for DNA amplification using a simple lysis buffer proved more effective than phenol-chloroform extraction. The immune dot-blot test gave unavoidable false positive results, but with the PCR this problem could be minimized by technical modifications. The PCR could replace antigen detection and virus isolation as the initial test for adenoviruses in conjunctival swabs, with cell culture only being retained for adenovirus serotyping in PCR positive specimens and for other viruses such as herpes simplex.
Adenoviridae↗
Chronic keratoconjunctivitis associated with ocular adenovirus infection.
Adenovirus (types 3, 4, 5) was implicated as the etiologic agent in three cases of persistent keratoconjunctivitis. In two, virus was isolated 25 and 29 months after the onset of symptoms; the third patient has suffered intermittent flares of kerato-conjunctivitis since the initial isolation of virus 13 weeks after the onset of the disease. Such patients may represent a previously unsuspected source of adenovirus in the population. All were given corticosteroids topically. This treatment may have prolonged the adenoviral disease.
Adenoviridae Infections↗
Effect of ribavirin on the plasma viral DNA load in patients with disseminating adenovirus infection.
Adenovirus (AdV) infections are an increasingly frequent and potentially fatal complication in allogeneic stem cell transplant recipients. To determine the antiviral potential of ribavirin in an unbiased way, 4 patients without immune recovery were prospectively analyzed by quantitative measurement of plasma AdV DNA load. Administration of ribavirin at the first signs of AdV dissemination was not accompanied by a decrease in the plasma AdV DNA load in any of these patients, and an increase in the AdV load was even documented in 3. These observations question the potential of ribavirin to improve the outcome for patients with disseminating AdV infection and support a critical evaluation of antiviral treatments for AdV infection that involves the kinetics of virus DNA load as an objective parameter of viral replication.
Adenovirus Infections, Human↗
Expression of human cholesterol 7alpha-hydroxylase in atherosclerosis-susceptible mice via adenovirus infection.
Adenovirus is a vector for the delivery of genes mainly to the liver. Short-term (approximately 3 days) studies using adenovirus transfection have provided valuable insights into how genes can complement normal and pathological phenotypes. When atherosclerosis-susceptible C57BL/6 mice were infected with an adenovirus vector containing the human 7alpha-hydroxylate cDNA (AV17h1) and fed on a chow diet, human 7alpha-hydroxylase mRNA and enzyme activity doubled compared with that in mice infected with an adenovirus vector (AV1Null) alone. In AV17h1-infected mice fed on a high fat cholic acid (HFCA) diet, mRNA expression and activity of both the endogenous and adenovirus (human) 7alpha-hydroxylase were repressed. AV17h1-infected mice fed on a HFCA diet and killed at mid-light had increased 7alpha-hydroxylase activity and mRNA compared with mice killed at mid-dark. Since expression of AV17h1 is driven by a constitutive Rous sarcoma virus promoter, the repression of human 7alpha-hydroxylase by the HFCA diet was unexpected. In spite of this post-transcriptional repression by the HFCA diet, AV17h1-infected mice expressed the human 7alpha-hydroxylase mRNA, causing its enzyme activity to be 3-fold greater than in AV1Null-infected mice. In AV17h1-infected mice, the 7alpha-hydroxylase enzyme activity varied as a linear function of human mRNA abundance. In conclusion, the accumulation of apolipoprotein B-containing lipoproteins in plasma of C57BL/6 mice fed on the HFCA diet was not reduced by longer-term (2 weeks) 7alpha-hydroxylase expression, probably because of its diminished expression caused by the diet and hepatic inflammation from the adenovirus infection. These results may suggest that adenovirus is effective in promoting longer-term (2 weeks) expression of 7alpha-hydroxylase.
Adenoviridae Infections↗
Remodelling of the host cell RNA splicing machinery during an adenovirus infection.
Adenovirus makes extensive use of RNA splicing to produce a complex set of spliced mRNAs during virus replication. All transcription units, except pIX and IVa2, encode multiple alternatively spliced mRNAs. The accumulation of viral mRNAs is subjected to a temporal regulation, a mechanism that ensures that proteins that are needed at certain stages of the viral life cycle are produced. The complex interaction between host cell RNA splicing factors and viral regulatory elements has been studied intensely during the last decade. Such studies have begun to produce a picture of how adenovirus remodels the host cell RNA splicing machinery to orchestrate the shift from the early to the late profile of viral mRNA accumulation. Recent progress has to a large extent focused on the mechanisms regulating E1A and L1 alternative splicing. Here we will review the current knowledge of cis-acting sequence element, trans-acting factors and mechanisms controlling E1A and L1 alternative splicing.
Adenoviridae Infections↗
Nuclear perturbations following adenovirus infection.
Adenoviruses are processed and assembled in the nuclei of infected cells and thereby produce significant perturbations to their structure and function. As the complex interactions that occur in the nuclei of uninfected cells are not yet fully understood many of the changes seen on infection have been described mainly in morphological terms. This chapter attempts to place more recent findings into this context and demonstrates that adenoviruses are able to hijack many cellular processes and enzymes to their advantage. In particular, modifications to nuclear PODs and nucleoli have more recently been explored in greater detail.
Adenoviridae Infections↗
[Adenovirus infections. I. Adenoviruses in epidemics of respiratory infections].
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Adenoviridae↗
Cyclic nucleotide-independent protein kinases bound to cytoplasmic and nuclear polyribosomes in non-infected and adenovirus-infected HeLa cells.
Cyclic nucleotide-independent protein kinase activity bound to cytoplasmic and nuclear polyribsomes from non-infected and adenovirus-infected HeLa cells was compared. The enzymes catalysed the incorporation of phosphate from gamma-(32)P-labelled ATP or GTP into acid-precipitable material in the absence of exogenous substrates. Their activity was not affected by cyclic AMP or cyclic GMP and was not inhibited by a cyclic nucleotide-dependent protein kinase-inhibitor protein. The kinases are tightly bound to polyribosomes of either origin from infected and non-infected cells, since treatment with 0.5m-NaCl did not dissociate the activity. The enzymes and the enzyme-associated endogenous substrates of cytoplasmic polyribosomes are significantly different from those of the nucleus, and adenovirus infection of the cells did not alter the nature of the enzymes or the substrates at 18-20h after infection. Nuclear kinases catalysed 3-4-fold more phosphate incorporation than did the cytoplasmic kinases. They did not phosphorylate endogenous substrates in the cytoplasmic preparations, and vice versa, which suggests that such substrates for cytoplasmic and nuclear kinases are specific. Polyacrylamide-gel electrophoresis of the phosphorylated proteins revealed the presence of a higher number of endogenous substrates in the nuclear preparation. The nuclear kinases phosphorylated all histones from HeLa cells, but the cytoplasmic ones phosphorylated predominantly the histone of mol.wt. 12000. Bovine heart kinase phosphorylated several low-molecular-weight cytoplasmic proteins and no nuclear proteins. With a DEAE-cellulose column either enzyme activity could be resolved into a number of peaks. The substrate specificities of these peaks indicate that there are at least two different forms of the enzyme in each preparation of polyribosomes.
Adenoviridae Infections↗
Replication of minute virus of mice DNA in adenovirus-infected or adenovirus-transformed cells.
The effect of adenovirus infection or transformation on the DNA replication of Minute Virus of Mice (MVM) was studied in human fibroblast cell lines. In WI38, HeLa, and 293 cells MVM infection allowed production of viral NS-1 and capsid proteins with or without adenovirus 2 (Ad2) co-infection. However, MVM DNA replication varied markedly. In HeLa cells MVM DNA was replicated weakly in host nucleoli, and replication was increased markedly by Ad2 co-infection as well as recompartmentalized to Ad2 replication factories. In Ad-transformed 293 cells MVM DNA was replicated very efficiently when infected alone or with Ad2 co-infection although recompartmentalization from nucleoli to replication factories was also seen. In WI38 cells MVM DNA was not replicated under any conditions. The variation in DNA replication in WI38, HeLa, and 293 cells despite viral protein production in all cases suggests that MVM DNA replication is uncoupled from viral gene expression and that host factors required for MVM DNA replication are induced or recompartmentalized by adenovirus infection or transformation.
Adenoviruses, Human↗
Dynamic organization of splicing factors in adenovirus-infected cells.
Adenovirus infection affects the nuclear distribution of host splicing factors. Late phase-infected cells contain discrete clusters of small nuclear ribonucleoproteins (snRNPs) that are separate from centers containing the viral 72-kilodalton DNA-binding protein (72K protein). In the present study, we demonstrate that these snRNP clusters also contain splicing factors from the SR protein family. We show that a previously described monoclonal antibody, 3C5, detects SR proteins. Furthermore, we demonstrate that late region 3 transcription occurs at a maximal rate in infected cultures in which greater than 90% of the cells contain the snRNP clusters, indicating that such cells are actively transcribing their late genes. During the onset of the late phase, the intranuclear distribution of splicing factors is very different from that seen after the late phase is established. When late viral transcription commences, cells with snRNP clusters are less prevalent than in cultures that are maintaining maximum levels of late transcription. Instead, a cell type which shows snRNPs, concentrated in foci that also contain the viral 72K DNA-binding protein is detected. This cell type disappears from cultures by 18 to 20 h after a high-multiplicity infection. These results suggest a dynamic organization of splicing factors in infected cells that can be correlated to the status of viral gene expression. Our work also provides an explanation for the differing results that have been published concerning the organization of splicing factors in the adenovirus-infected cell nucleus (L. F. Jiménez-García and D. L. Spector, Cell 73:47-59, 1993). During the present study we observed that a monoclonal antibody against the SC-35 protein, which was used by Jiménez-García and Spector to study the localization of the SC-35 splicing factor in adenovirus-infected cells, cross-reacts with the adenovirus 72K DNA-binding protein and is thus unsuitable for this type of study.
Adenoviridae↗
[Experimental study of combined staphylococcal, streptococcal and adenovirus infections in tissue culture].
Associated adenoviral, staphylococcus, and streptococcus infection was studied in the cultures of cells HEp-2 and PAO. Under conditions of monoinfection the cell culture largely inhibited the reproduction of staphylococci, and failed to influence the streptococci. In double and triple associated infections staphylococci overcame the inhibitory action of the cell culture. The pathogenic properties of cocci (plasma coagulation, hemotoxic properties) grown in the cell culture both under conditions of monoinfection, and in associations, failed to change. In double and triple associated infections adenoviruses did reproduce, but in lower titre than in monoinfection. Under conditions of mixed infection cocci penetrated and reproduced in the cell cytoplasm more intensively than in monoinfection. The cytopathic action was determined by viral associate, and was identical by its character to adenoviral monoinfection. A statistically significant increase in the activity of aldolase and transaminase enzymes was noted in mixed infection. The changes in the enzyme activity proved to depend on the character of the associations studied.
Adenoviridae Infections↗
Still's disease associated with adenovirus infection and defect in adenovirus directed natural killing.
Low natural killer (NK) activity towards adenovirus infected fibroblasts was detected in the peripheral blood of a child with Still's disease and was not normalised by the addition of interferon alfa or interleukin 2. NK cytotoxicity directed at K 562 target cells or polio infected fibroblasts was normal. This specific NK deficiency might have contributed to the development of the child's Still's disease.
Adenoviridae Infections↗
Fatal adenovirus infections in infants probably infected with HIV.
Adenovirus infections occur commonly in infants and children but are rarely fatal. Although immunosuppression has been associated recently with fatal outcome of adenovirus infections, reports of major morbidity or mortality caused by adenovirus infection in HIV positive patients are infrequent. This is the first report on fatal adenovirus infections in presumably HIV-positive infants in Thailand. Three infants, aged 4, 8 and 5 months, were hospitalized with diagnoses of pneumonia and ARDS, pneumonia with hepatomegaly and ARDS, and pediatric AIDS with pneumonia, respectively. All the infants died within a few weeks after hospitalization. Serologic tests revealed positive anti-HIV in all three infants. Unfortunately, no additional investigation for definite diagnosis of HIV infection was employed. Pathological findings from autopsy and post mortem needle biopsies revealed adenovirus pneumonia in the first two infants, and massive adenovirus infection of the liver in the third infant. Diagnoses were based on characteristic light microscopic pathological findings, and demonstration of viral particles arranged in crystalline arrays in the nucleus of the infected cells by electron microscopy.
AIDS-Related Opportunistic Infections↗