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Results for “ADENOVIRUS INFECTIONS”

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PubMed2002

Mechanism of restriction of normal and cystic fibrosis transmembrane conductance regulator-deficient human tracheal gland cells to adenovirus infection and ad-mediated gene transfer.

CF-KM4 (cystic fibrosis transmebrane conductance regulator-deficient) and MM-39 (healthy) cells, two serous cell lines from submucosal tracheal glands, were found to be poorly susceptible to adenovirus (Ad)5 infection and Ad5-mediated gene transduction. The major limiting steps apparently resided in the primary events of Ad5 interaction, i.e., cell attachment and entry. Both CF-KM4 and MM-39 cells failed to express the Coxsackie-Ad receptor (CAR), and experimental data suggested that alpha[2-->6]-linked sialic acid residues of sialoglycoproteins (SAGP) in CF-KM4 cells, and heparan sulfate glycosaminoglycans (HS-GAG) in MM-39, were used as receptors by Ad5 virions. Ad5 attached to SAGP and HS-GAG receptors via its fiber knob domain, but entered the cells via a penton base- and Arg-Gly-Asp (RGD)-integrin-independent pathway. The block to Ad5-mediated gene transfer in MM-39 and KM4 cells could be overcome by conferring to the vector a novel cell-binding specificity. Thus, Ad5 vectors carrying a stretch of 7-lysine residues genetically inserted at the C-terminus of the fiber knob were found to transduce MM-39 cells with a 10- to 20-fold higher efficiency than the original vectors, but the transduction of CF-KM4 was not significantly improved. Retargeting Ad5 to integrin receptors via RGD peptide ligands, inserted at the extremity of the fiber shaft, resulted in a transducing efficiency of 20- and 50-fold higher in MM-39 and KM4 cells, respectively, compared with Ad5 vectors carrying fibers terminated by their natural knob domain.

Adenoviridae↗
PubMed2001

Detection of adenovirus infection in children in Jordan.

Between November 1997 and May 1998, 350 nasopharyngeal aspirates (NPA) were obtained from children admitted to the Respiratory Disease Unit at Princess Rahma Hospital, northern Jordan who were clinically diagnosed as suffering from respiratory tract infections. NPA were investigated for the presence of adenovirus using shell vial (SV) culture assay, conventional culture (CC) assay, and direct immunofluorescence assay (DFA). Of the 350 NPA, adenoviruses were detected in 54 (15.4%) by the combined techniques used. SV identified 34 (63%), CC 48 (89%) and DFA 30 (56%). Most virus isolations were in children aged 1-< 5 years old and were associated with pneumonia in 39% and bronchopneumonia in 32%. SV assay showed a sensitivity and specificity of 68.8% and 99.7%, respectively, for detecting adenovirus from NPA. These results emphasize that CC assay is still important for the diagnosis of adenovirus, although SV and DFA are superior diagnostic assays.

Adenoviridae↗
PubMed1991

Necrotizing tubulointerstitial nephritis associated with adenovirus infection.

We report 10 autopsy cases of necrotizing tubulointerstitial nephritis induced by adenovirus (ADV). Hemorrhagic, necrotizing tubulitis with intranuclear inclusion bodies was observed in the kidneys of five bone marrow transplant recipients and five patients treated with intensive chemotherapy for malignancies (four cases of leukemia and one case of lung cancer). It was histopathologically demonstrated that necrobiotic tubular cells had inclusion-bearing cells of three types: "smudge cells," Cowdry A intranuclear inclusion cells, and full-type intranuclear-containing cells. Immunofluorescent examination with anti-ADV antibody demonstrated specific fluorescence on the affected tubular cells of all 10 kidneys. Specific antigens for ADV type 11 were also revealed in all but one case by an immunofluorescent test using type-specific antiserum and convalescent serum containing high titer antibody to this serotype. Electron microscopy revealed intranuclear crystalline arrays of viral particles, 75 to 80 nm in diameter, in each of the seven cases examined. Extrarenal involvement, indicated by ADV-induced cytopathologic change, was confined to bladder or prostate. Hemorrhagic cystitis was recorded in all the bone marrow transplant cases as well as in one leukemia case. Adenovirus type 11 was isolated from urine in all five cases tested during these episodes. Renal failure was ascribed to ADV infection in two of five patients who died from renal dysfunction. The presence of hemorrhagic cystitis and localization of invasive infection in urogenital organs suggested that renal infection might occur by ascending route from the bladder. We propose that ADV should be added as a viral agent to the pathogenetic list of tubulointerstitial nephritis.

Adenoviridae Infections↗
PubMed1996

The activity of cytosolic phospholipase A2 is required for the lysis of adenovirus-infected cells by tumor necrosis factor.

Most cell types are resistant to apoptosis induced by tumor necrosis factor (TNF) unless the cells are treated with a sensitizing agent. Inhibitors of transcription or translation act as sensitizing agents, as do adenoviruses lacking one or more resistance genes. We have reported recently that the activity of cytosolic phospholipase A2 (cPLA2) is necessary for the TNF-induced lysis of cells that are sensitized by inhibitors of transcription or translation (C. Voelkel-Johnson, T. E. Thorne, and S. M. Laster, J. Immunol. 156:201-207, 1996). In this report we have asked whether the lysis of cells infected by the adenovirus dl758 (which lacks the E3 14.7-kDa resistance gene product) also involves the activity of cPLA2. We report that a phosphorothioate-modified antisense oligonucleotide specific for cPLA2, but not the control oligonucleotide, inhibited the TNF-induced release of both [3H]arachidonic acid and 51Cr from infected cells. Arachidonyltrifluoromethyl ketone (AA COCF3), an inhibitor of cPLA2, also inhibited the release of 51Cr, and we found that the release of [3H]arachidonic acid was highly selective and was preferred over the release of [3H]palmitic acid. Taken together, these results suggest strongly that cPLA2 is indeed the phospholipase responsible for the release of [3H]arachidonic acid during the lysis of infected cells and that its activity is necessary for cell death. Finally, since arachidonic acid serves as the substrate for the synthesis of inflammatory lipids, our results suggest a possible link between the TNF-induced lysis of infected cells and inflammation. The E3 14.7-kDa resistance protein may, therefore, play two roles: preventing TNF-induced cell death and, as our results show, preventing the TNF-induced release of arachidonic acid.

3T3 Cells↗
PubMed2000

Neutralisation of adenovirus infectivity by ascitic fluid from ovarian cancer patients.

Animal models and phase I clinical trials have shown that repeat virus delivery and subsequent transgene expression is limited by the generation of humoral and cellular immune responses directed towards the therapeutic vector. The presence of a pre-existing immune response may even prevent initial delivery. In order to determine the presence of pre-existing anti-adenovirus humoral immunity we analysed ascitic fluid, collected from the peritoneal cavity of patients with advanced ovarian cancer. Twelve ascitic fluid and four matched serum samples were examined. The titre and isotype of anti-adenovirus antibodies was determined by ELISA, and Western blotting identified the molecular basis of the immune response, which was primarily directed towards fibre and penton base. Neutralisation of virus infectivity was assessed in vitro by measurement of green fluorescent protein reporter gene expression. We found that the ascitic fluid samples contain antibodies that recognise both adenovirus types 2 and 5, were predominantly IgG and directed towards the viral antigens responsible for cell adhesion, and had virus neutralising activity.

Adenovirus Infections, Human↗
PubMed2003

Adenovirus infection in hematopoietic stem cell transplantation: effect of ganciclovir and impact on survival.

Adenoviruses (ADV) are emerging as important causes of morbidity and mortality in patients undergoing hematopoietic stem cell transplantation (HSCT). In mainly non-T-cell depleted HSCT recipients, we analyzed the incidence of ADV infection, risk factors for infection, the effect of ganciclovir administered for prevention of cytomegalovirus (CMV), and the impact of ADV infection on survival. The overall incidence of ADV, irrespective of the method of detection, was 8.5% (450/5233) and 12.3% (43/348) after the first or second allogeneic HSCT, and 6.3% (78/1219) and 6.5% (5/77) after the first or second autologous HSCT, respectively. The most frequent sites of infection and disease were stool and gastrointestinal tract, respectively. Statistically significant risk factors associated with ADV infections among allogeneic recipients included younger age, grade II to IV graft-versus-host disease, year of transplantation, and a second allogeneic HSCT. Furthermore, allogeneic patients seronegative for CMV at transplantation and seropositive allogeneic patients who did not receive ganciclovir, either at engraftment or as pre-emptive therapy on CMV reactivation, were at higher risk of developing ADV infections compared with seropositive patients who received ganciclovir (odds ratio=1.8, 95% confidence interval (CI) 1.2 to 2.8, P=.005 and odds ratio=3.4, 95% CI 2.1 to 5.55, P<.0001, respectively). The hazard of overall mortality was higher in patients who contracted ADV compared with those who did not (hazard ratio 1.5, 95% CI 1.3 to 1.7, P<.0001). This study shows that ADV infections are associated with poor transplantation outcome in T-cell repleted HSCT recipients. Ganciclovir, given for CMV prevention, may have a protective effect. Controlled treatment and prevention studies are warranted.

Adenoviridae Infections↗
PubMed1999

Group D adenoviruses infect primary central nervous system cells more efficiently than those from group C.

Group C adenovirus-mediated gene transfer to central nervous system cells is inefficient. We found that wild-type group D viruses, or recombinant adenovirus type 2 (Ad2) (group C) modified to contain Ad17 (group D) fiber, were more efficient in infecting primary cultures of neurons. Together with studies on primary vascular endothelial cells and tissue culture cell lines, our results indicate that there is not a universally applicable adenovirus serotype for use as a gene transfer vector.

Adenoviruses, Human↗
PubMed1974

Experimental adenovirus infection of the mouse adrenal gland. II. Electron microscopic observations.

A strain of mouse adenovirus, found to have a striking tropism for the weanling mouse adrenal gland, enabled electron microscopic examination of adrenals in various stages of infection. Nucleolar hypertrophy and the successive formation of three types of inclusion bodies in association with nucleoli preceded virion production. Angular crystals of virions formed in the affected nuclei. Virus was released by lysis of nuclear membranes; rapid degeneration of cytoplasmic organelles followed. Rupture of external cell membranes released virus into the extracellular spaces where virions crossed vascular basement membranes to enter endothelial cells. Virions were also phagocytized by inflammatory cells which reentered vascular sinusoids, and by adrenal parenchymal cells. Disruption of virus-laden phagocytic vacuoles in parenchymal cells released virions into the cytoplasm. Typical viral inclusion bodies also formed in vascular endothelial cells and in inflammatory cells, but virion replication was not detected. The possibility that virus directly entered parenchymal cells through the external cell membrane without phagocytosis is discussed.

Adenoviridae Infections↗
PubMed2005

[Neurologic disease due to adenovirus infection].

The aim of this study was to assess the prevalence of adenovirusm (ADV) infections in neurological disorders. A total of 108 cerebrospinal fluid (CSF) samples from 79 encephalitis cases, 7 meningitis and 22 other neurological diseases analysed in our laboratory between 2000 and 2002 were studied. Forty nine (47.4%) belonged to immunocompromised patients. Viral genome was detected using nested polymerase chain reaction (Nested-PCR) and ADV genotypes were identified using partial gene sequence analysis of hexon gene. Adenovirus were detected in 6 of 108 (5.5%) CSF samples tested. All of these were from encephalitis cases, 6/79, representing 7.6% of them. No statistically significant differences were observed (p > 0.05) between the immunocompromised and non immunocompromised patients with ADV infection of the central nervous system. Two ADV genotypes (B1 and C) were identified. In conclusion, our results describe the role of ADV in neurologic infections in Argentina. The results contribute to the knowledge of ADV epidemiology, specially in encephalitis.

Adenovirus Infections, Human↗
PubMed1995

Clearance of adenovirus-infected hepatocytes by MHC class I-restricted CD4+ CTLs in vivo.

E1-deleted recombinant adenoviruses have been developed for liver-directed gene therapy because efficient gene transfer to hepatocytes can be achieved in vivo. However, these viruses also express viral proteins in hepatocytes, leading to the development of destructive immune responses. Our previous studies indicated that MHC class I-restricted C D8+CTLs are major effectors in eliminating virus-infected cells, and CD4+ cells are also necessary in developing a fully competent CTL response by secretion of IFN-gamma, which sensitizes the virus-infected hepatocytes to CTLs through up-regulation of MHC class I expression. In this study, we have used adoptive transfer techniques in combination with mice deficient in immune functions to further define the role of CD4+ cells in the primary response to adenovirus-mediated gene transfer to the liver. Our studies indicate that CD4+ cells alone are capable of destroying virus-infected hepatocytes. Adoptive transfer experiments with beta 2m- mice along with in vitro CTL assays suggest that these CD4+ can act as CTL effectors, which are MHC class I-restricted. Depletion of these CD4+ effectors in vivo leads to prolongation of adenovirus-mediated transgene expression in hepatocytes. These results suggest that class I-restricted CD4+ CTLs contribute to elimination of adenovirus-transduced hepatocytes and extend our understanding of functional importance of CD4+ cells in viral pathogenesis.

Adenoviridae↗