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PubMed2004

Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly.

The cytoskeleton is critical to the viral life cycle. Agents like cytochalasin inhibit viral infections but cannot be used for antiviral therapy because of their toxicity. We report the efficacy, safety, and mechanisms by which gene delivery of human wild-type low-molecular-weight caldesmon (l-CaD) protects cell membrane integrity from adenovirus infection in a DF-1 cell line, an immortalized avian fibroblast that is null for l-CaD. Transfection with an adenovirus (Ad)-controlled construct mediated a dose-dependent decline in transcellular resistance. In accordance with a computational model of cytoskeletal membrane properties, Ad disturbed cell-cell and cell-matrix adhesion and membrane capacitance. Transfection with the Ad-l-CaD construct attenuated adenovirus-mediated loss in transcellular resistance. Quantitation of vinculin-stained plaques revealed an increase in total focal contact mass in monolayers transfected with the Ad-l-CaD construct. Expression of l-CaD protected transcellular resistance through primary effects on membrane capacitance and independently of actin solubility and effects on pre-stress, as measured by the decline in isometric tension in response to cytochalasin D. Expression of l-CaD exhibited less Trypan blue cell toxicity than cytochalasin, and, unlike cytochalasin, it did not interfere with wound closure or adversely effect transcellular resistance. These findings demonstrate the gene delivery of wild-type human l-CaD as a potentially efficacious and safe agent that inhibits some of the cytopathic effects of adenovirus.

Actins↗
PubMed1976

An immunopathologic study of interstitial nephritis associated with experimental canine adenovirus infection.

The localisation of canine adenovirus in the renal tubules induces a marked cellular response in the interstitium. A number of mechanisms appear to be involved in the genesis of the lesions. Direct lytic damage to tubular epithelial cells by the virus is probably augmented by immunological factors. The production of local anti-viral antibody by plasma cells in the vicinity of virus-containing cells may result in the formation of toxic antigen-antibody complexes while the accumulation of large populations of macrophages suggests that cell-mediated hypersensitivity is also operative.

Adenoviridae Infections↗
PubMed1986

Rapid diagnosis of respiratory adenovirus infections in young adult men.

Rapid viral diagnosis was attempted in 106 military conscripts with pneumonia and in 101 military conscripts with other types of respiratory infections. Nasopharyngeal suction specimens (NPS) were assayed for viral antigens by immunofluorescence and enzyme immunoassay (EIA). Sputum specimens from 97 pneumonia patients were assayed for viral antigens by EIA. Also, 71 NPS and 13 sputum specimens were examined for the presence of adenovirus DNA by a sandwich hybridization (HYB) method. The reference test was adenovirus isolation in cell culture from the NPS. Adenoviruses were isolated from 6 pneumonia patients and from 20 patients with other respiratory infections. Of these 26 NPS, rapid diagnosis was successful in 13, 16, and 14 cases by EIA, immunofluorescence, and HYB, respectively. Four antigen-positive specimens were found among the 181 specimens which were negative by virus isolation. Sputum was found to contain adenovirus antigen by EIA in 5 of 97 tested specimens. Of these 97 specimens, 13 were selectively tested in HYB, and a positive signal was observed in 4 cases. Serological testing of paired sera revealed 23 adenovirus infections in the pneumonia group and 42 in the group with other respiratory infections. Other viral infections were found only sporadically. All rapid virus detection methods showed excellent specificity but had a lower sensitivity (60%) than virus isolation. Our results show that rapid methods for diagnosing respiratory adenovirus infections can be successfully used in selected groups of adults.

Adenoviridae Infections↗
PubMed1998

The large E1B protein together with the E4orf6 protein target p53 for active degradation in adenovirus infected cells.

It has recently been shown that an adenovirus mutant lacking expression of the large E1B protein (deltaE1B) selectively replicates in p53 deficient cells. However, apart from the large E1B protein the adenovirus early region encodes the E1A and E4orf6 proteins which also have been reported to affect p53 expression as well as its functioning. After infection with wild-type adenovirus we observed a dramatic decrease in wild-type p53 expression while no down-regulation of p53 could be detected after infection with the deltaE1B virus. The different effects of the wild-type and deltaE1B adenovirus on p53 expression were not only found in cells expressing wild-type p53 but were also observed when tumor cells expressing highly stabilized mutant p53 were infected with these two viruses. Infection with different adenovirus mutants indicated the importance of a direct interaction between p53 and the large E1B protein for reduced p53 expression after infection. Moreover, coexpression of the E4orf6 protein was found to be required for this phenomenon, while expression of E1A is dispensable. In addition, we provide evidence that p53 is actively degraded in wild-type adenovirus-infected cells but not in deltaE1B-infected cells.

Adenoviridae↗
PubMedDate not supplied

Evaluation of immunofluorescent reagents, centrifugation, and conventional cultures for the diagnosis of adenovirus infection.

In this study we have evaluated four fluorescent antibody reagents, three monoclonal and one polyclonal, for identification of adenovirus isolates and compared four conventional cultures (human embryonic kidney, A549, HEp-2, and MRC-5 cells) with centrifugation culture for rapid diagnosis. For identification of adenovirus isolates by immunofluorescence, CDC reagent and Adenoclone, both monoclonal antibodies to the hexon group-reactive antigen, were more sensitive and easier to interpret than the other two reagents tested. HEK and A549 cells were the most sensitive for isolation of adenovirus. Although A549 cells were an inexpensive alternative to HEK, A549 cell monolayers deteriorated more rapidly and passages were more often required. Centrifugation cultures with A549 cells detected 77% of positives within 2 days and 100% within 5 days, whereas isolation in conventional culture required up to 10 days for HEK and up to 20 days for MRC-5 cells.

Adenoviridae Infections↗
PubMed1970

Origin of thymidine kinase in adenovirus-infected human cell lines.

Human adenovirus type 5 enhances the thymidine kinase activity of KB cells but does not induce the enzyme in kinase-deficient HeLa (BU25) cells. Vaccinia induces thymidine kinase activity in both KB and HeLa (BU25) cells. Human adenovirus types 2, 4, 7, and 12 also fail to induce the enzyme in HeLa (BU25) cells. Vaccinia replicates equally well in the presence or absence of HATG (hypoxanthine-aminopterin-thymidine-glycine) in KB and HeLa (BU25) cells. Adenovirus type 5 replicates in KB and in HeLa (BU25) cells in the absence of HATG, and adenovirus type 5 replicates in kinase-positive KB cells in the presence of HATG. However, replication of adenovirus type 5 is grossly inhibited in HeLa (BU25) cells in the presence of HATG. These results suggest that human adenoviruses do not code for a new virus-specific thymidine kinase.

Adenoviridae↗
PubMed1990

[Prevention of adenovirus infection and antiviral activity of a hand disinfectant, Welpas].

A commercial alcoholic disinfectant (Welpas) was tested for its activity against adenovirus type 3 (Ad 3) by using two procedures, the in vitro suspension test and the in vivo fingertip test. Other available techniques for the sterilization of fingers were also evaluated for removal of Ad by using the fingertip test. In the suspension tests, the infectivity of Ad 3 was reduced to undetectable levels within 30-60 seconds. This results suggest the effectiveness of this disinfectant in reducing Ad infectivity. In the fingertip tests, the viruses were recovered from fingertips in varying titers after using one of the following techniques: wiping with tissue papers, washing with running water, washing with soap and rinsing with water, rubbing with Welpas, wiping with cotton soaked in 70% alcohol, or washing with a brush under running water. However, the viruses were not recovered when the fingertip was washed with water, wiped with paper, and rubbed with Welpas successively. This technique was found to be the most effective method currently available.

Adenoviridae Infections↗
PubMedDate not supplied

Necrotizing pancreatitis and gizzard erosion associated with adenovirus infection in chickens.

Cases of focal necrotic pancreatitis and gizzard erosion in chickens are reported. Intranuclear inclusion bodies were seen in necrotic pancreatic acinar cells and necrotic epithelial cells of the gizzard, and electron microscopy demonstrated virus particles in affected gizzard epithelium. Adenovirus antigens were detected immunohistochemically in these intranuclear inclusion bodies. These findings suggest that the necrotizing pancreatitis and gizzard erosion were associated with adenovirus infection.

Adenoviridae Infections↗
PubMed1999

Replication-defective adenovirus infection reduces Helicobacter felis colonization in the mouse in a gamma interferon- and interleukin-12-dependent manner.

Helicobacter infection leads to chronic inflammation of the stomach. Although the infection persists in spite of an immune response, animal studies have shown that adjuvant-based oral vaccines can protect against infection and even eliminate established infection. These vaccines are thought to induce a Th2 immune response, counterbalancing the Th1 response seen with natural infections. As a prelude to using adenovirus vectors carrying cytokine genes to modulate the immune response to established Helicobacter felis infection, we first examined the effect of the replication-defective adenovirus (RDA) vector itself. C57BL/6 mice chronically infected with H. felis (8 to 10 weeks) received intramuscular injections of RDA. The effect of RDA on the severity of H. felis colonization and the degree of gastric inflammation was assessed 2 weeks later. RDA caused a significant decrease in H. felis colonization without significantly altering the associated inflammation. RDA did not alter the H. felis-specific immunoglobulin G1 (IgG1), IgG2a, and IgA responses in the serum but was associated with an increase in gamma interferon (IFN-gamma)-producing CD8(+) spleen cells. To determine if IFN-gamma or Th1 cytokines were involved in the response to RDA, we examined RDA treatment of H. felis infection in mice lacking either IFN-gamma or interleukin-12 (IL-12). RDA failed to alter H. felis colonization in either of these two mouse strains. Thus, viral infection of mice chronically infected with H. felis led to a significant decrease in H. felis colonization in an IFN-gamma- and IL-12-dependent manner. These results demonstrate that Th1 responses associated with systemic viral infection can influence an established H. felis infection.

Adenoviridae Infections↗
PubMed2003

Inhibition of adenovirus infection and adenain by green tea catechins.

Green tea catechins have been reported to inhibit proteases involved in cancer metastasis and infection by influenza virus and HIV. To date there are no effective anti-adenoviral therapies. Consequently, we studied the effect of green tea catechins, and particularly the predominant component, epigallocatechin-3-gallate (EGCG), on adenovirus infection and the viral protease adenain, in cell culture. Adding EGCG (100 microM) to the medium of infected cells reduced virus yield by two orders of magnitude, giving and IC(50) of 25 microM and a therapeutic index of 22 in Hep2 cells. The agent was the most effective when added to the cells during the transition from the early to the late phase of viral infection suggesting that EGCG inhibits one or more late steps in virus infection. One of these steps appears to be virus assembly because the titer of infectious virus and the production of physical particles was much more affected than the synthesis of virus proteins. Another step might be the maturation cleavages carried out by adenain. Of the four catechins tested on adenain, EGCG was the most inhibitory with an IC(50) of 109 microM, compared with an IC(50) of 714 microM for PCMB, a standard cysteine protease inhibitor. EGCG and different green teas inactivated purified adenovirions with IC(50) of 250 and 245-3095, respectively. We conclude that the anti-adenoviral activity of EGCG manifests itself through several mechanisms, both outside and inside the cell, but at effective drug concentrations well above that reported in the serum of green tea drinkers.

Adenoviridae↗
PubMed1981

Diffuse meningocerebral angiodysplasia and adenovirus infection: an improbable relationship.

A case of diffuse meningocerebral angiodysplasia is described in which type 4 adenovirus was isolated from the brain biopsy. The pathological features were similar to those previously described by various authors (1,3,4,5) and were not indicative of an infective process. Status epilepticus in the presence of extensive arteriovenous shunting in this dysgenetic cerebromeningeal vasculature is probably responsible for the extensive necrosis observed in the cortex and white matter.

Adenoviridae Infections↗
PubMed2005

Mitochondrial localization of p53 during adenovirus infection and regulation of its activity by E1B-19K.

Recent results have revealed that the p53 tumor suppressor protein possesses a direct transcription-independent apoptotic activity. During apoptosis induced by genotoxic stress, a small fraction of p53 is targeted to mitochondria where it initiates apoptosis by causing mitochondrial dysfunction. In adenovirus-infected cells, the expression of E1A protein enhances the accumulation of p53 during early phases of infection and during late times after infection, it is targeted for degradation by the combined action of E1B-55K and E4-orf6 proteins. The functional significance of E1A-mediated accumulation of p53 during early phases of viral replication is not known. Our studies with isogenic epithelial cell lines that differ only on the status of p53 indicate that Ad infection induces apoptosis by p53-dependent and -independent pathways and both pathways are suppressed by E1B-19K. We show that during early phase of Ad infection, a fraction of p53 is targeted to the mitochondria. In virus infected cells, a large fraction of the viral antiapoptosis protein E1B-19K is also localized in mitochondria during early and late phases of infection. Coimmunoprecipitation analysis has revealed that p53 and E1B-19K form a complex in mitochondria. The interaction of 19K involves two noncontiguous regions located around amino-acid residues 14-15 and 123-124. On p53, the mutations within the DNA-binding domain reduce interaction with E1B-19K. Our studies also suggest that 19K may additionally complex with the multidomain mitochondrial proapoptotic protein BAK, thereby reducing the level of p53 interaction with BAK. We suggest that p53-induced apoptosis may be important for efficient cell lysis and viral spread and that E1B-19K may neutralize the apoptotic activity of p53 at multiple levels.

Adenoviridae↗
PubMed1998

Enhancement of phospholipase D activity following baculovirus and adenovirus infection in Sf9 and COS-7 cells.

In order to purify the human phospholipase D1 (hPLD1) for analysis of its functional properties, we applied a baculovirus-based high-expression system. As expected, Sf9 cells infected with a baculovirus encoding for the hPLD1 displayed a 7.5-fold increase in PLD activity compared to uninfected cells. Sf9 cells infected with the wild-type (WT) and other recombinant baculoviruses were used as an expression control. Surprisingly, all baculoviruses tested led to a 3-5 fold increase in basal PLD activity when compared to uninfected cells. To further characterize the nature of the increased PLD activity, the influence of ADP-ribosylation factor (ARF) and phorbol 12-myristate 13-acetate (PMA) was studied. In contrast to membranes containing the hPLD1, the PLD activity in membranes from uninfected and WT-infected Sf9 cells was not stimulated by ARF. PMA did not affect the increase in PLD activity in any case. To further study whether the virus-mediated increase in PLD activity is a more general phenomenon, we infected COS-7 cells with recombinant and WT adenoviruses. Only the infection with the WT adenovirus resulted in an approx. 2-fold increase in PLD activity. Our results demonstrate for the first time that a viral infection elevates the PLD activity in insect and mammalian cells.

ADP-Ribosylation Factors↗
PubMed1995

Adenovirus infection induces reentry into the cell cycle of terminally differentiated skeletal muscle cells.

Different cell types in the body of higher animals undergo terminal differentiation. In such a process, cells acquire specialized functions and irreversibly lose their ability to divide, therefore entering the postmitotic state. Terminally differentiated cells do not proliferate in response to growth factors or following the expression of activated, retroviral oncogenes. In this paper we demonstrate that adenovirus infection is an efficient and convenient means to induce terminally differentiated cells to reenter the cell cycle. These findings constitute a first step toward defining the molecular determinants of the irreversible withdrawal from the cell cycle of terminally differentiated cells. They may also open the way to therapeutic applications.

Adenoviruses, Human↗
PubMed2002

Fatal adenovirus infection during alemtuzumab (anti-CD52 monoclonal antibody) treatment of a patient with fludarabine-refractory B-cell chronic lymphocytic leukemia.

Alemtuzumab (Campath-1H) is a humanized CD52 monoclonal antibody that targets normal as well as malignant B- and T-lymphocytes. Alemtuzumab has significant antitumor activity in chronic lymphocytic leukemia (B-CLL) but also induces immunosuppression. We describe a case of fatal adenovirus infection in a heavily pretreated patient with fludarabine-refractory B-CLL receiving alemtuzumab therapy, drawing attention to the fact that also viruses other than cytomegalovirus (CMV) and herpes simplex (HSV) need to be considered in B-CLL patients with fever of unknown origin while on alemtuzumab treatment.

Adenoviridae Infections↗