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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of postmortem examinations performed in 237 fatal cases of influenza and other acute respiratory diseases are presented. In smears of organs and tissue culture cells infected with these materials and heart blood the immunofluorescent procedure detected influenza virus antigens in 67% of the cases, antigens of other respiratory viruses in 53% including 18-19% of mixed infections. Parallel immunofluorescent studies in living patients and isolation of influenza virus and adenoviruses increased per cent of influenza case confirmation to 82%, other respiratory infections to 63%. Mixed infection was recorded in 22-28%. Antigens of influenza and parainfluenza viruses were more frequently found in smears of bronchi and trachea, antigens of respiratory syncytial virus and adenovirus in lung smears. Adenovirus antigen was also found in lymphoid cells of smears of the spleen, bronchial lymph node, tonsils. In immunofluorescent examinations of tissue cultures infected with the heart blood, virus antigen was detected most frequently in influenza and adenovirus infection (24% and 26% of cases, respectively), less frequently in respiratory syncytial virus infection (11%) and parainfluenza (5%). Virus antigens were also demonstrated in tissue culture cells infected with specimens of the liver, spleen, bronchial lymph node, tonsils, brain. The immunofluorescent studies demonstrated long-term persistence of virus antigens in the body. In a portion of cases of laboratory confirmed mixed infection there were no clinical-morphological signs of two virus diseases. In these, one of the infections was latent or was due to a previously experienced disease.
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PMID:[Recognition of influenza and other acute respiratory virus infections and their combinations by means of immunofluorescence]. 17 23

Adenovirus type 2-transformed hamster cell-induced newborn tumor lines were usually rejected when transplanted s.c. into 21-day-old syngeneic, weanling hamsters. The tumor-inducing capacity of two of these lines (Ad2HTL3 and Ad2HTL6) was tested in intact and neonatally thymectomized hosts. After s.c. injection of suspensions prepared from these lines, none of the weaning hamsters developed tumors while 100% of the newborns and 35.2% of neonatally thymectomized, weanling hamsters developed progressively enlarging neoplasms. The susceptibility of neonatally thymectomized hamsters to tumor challenge was directly related to the degree of immunosuppression observed following thymectomy as indicated by the amplitude of the in vitro response of blood leukocytes to concanavalin A. Pretreatment of thymectomized weanlings with syngeneic adult lymphoid cells (i.p.) resulted in a significant reduction in tumor susceptibility (p = 0.03). These findings suggest that acquisition of resistance to adenovirus type 2-transformed cells during the first 21 days of life may be a thymus-dependent cellular immune process.
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PMID:Age-related and thymus-dependent rejection of adenovirus 2-transformed cell tumors in the Syrian hamster. 31 31

HeLa cell OTF-1 has been purified on the basis of its DNA binding activity and used to raise a polyclonal rabbit antiserum. This antiserum is shown to recognize both native and denatured OTF-1 from both human and a similar protein from Xenopus culture cells, but to react either more weakly or not at all with the lymphoid cell-specific OTF-2. Separately, NFIII has been purified on the basis of its ability to stimulate Adenovirus DNA replication in vitro. On denaturing polyacrylamide gels OTF-1 and NFIII exhibit identical mobility. Anti-OTF-1 antiserum recognizes NFIII and neutralizes its stimulatory effect on DNA replication. Moreover, OTF-1 can functionally replace NFIII. Taken together with previously published DNA binding data, this indicates that OTF-1 and NFIII are either very closely related or identical.
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PMID:Anti-OTF-1 antibodies inhibit NFIII stimulation of in vitro adenovirus DNA replication. 292 10

Human peripheral blood lymphocytes were induced to proliferate indefinitely in vitro by fusion with cytoplasts from mouse L 929 cells or, alternatively, by transfection with DNA isolated from L929 cytoplasts. Since adenoviruses epidemically infect human lymphocytes, the newly established cell lines were assayed for the presence of adenoviral DNA sequences. In 8 of 10 lymphoid cell lines of both B and T cell origin, adenovirus type 5 (serogroup C) DNA sequences were detected. The cells harbor approximately 40 to 70 genome copies per cell. Adenovirus type 5 transcripts of the E1A and E1B early regions that are responsible for the transforming capacity of adenoviruses could not be detected in the lymphoid cell lines. Therefore we conclude that the adenovirus genome persisting in immortalized lymphoid cells is not involved in the maintenance of indefinite proliferation induced by fusion with L929 cytoplasts or by DNA transfection.
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PMID:Adenovirus type 5 persisting in human lymphocytes is unlikely to be involved in immortalization of lymphoid cells by fusion with cytoplasts or by transfection with DNA of mouse L cells. 295 95

The feasibility of using adenovirus 5 as an in vitro probe for chemosensitivity in short-term cultures of human tumors was evaluated using human melanoma cell lines and primary cultures of melanoma biopsies. A convenient immunoperoxidase method was developed for quantitating viral replication 2 days after infection. Two different approaches were explored: the host cell reactivation assay (HCR) using drug-treated virus; and the viral capacity assay using drug-treated cells. The HCR assay detected sensitivity to 5-(3-methyl-1-triazeno)imidazole-4-carboxamide (MTIC) in Mer- (methyl excision repair deficient) cell lines as decreased ability of the cells to replicate MTIC-treated virus. This test should be applicable to DNA-damaging agents and repair-deficient tumors. Adenovirus replicated readily in nonproliferating primary cultures of melanoma biopsies; application of the HCR assays to this material identified one Mer- sample of 11 tested. Herpes viruses were not suitable for use in HCR because herpes simplex virus type 1 failed to distinguish Mer- from Mer+ melanoma cells; and nonproductive infection of MTIC-sensitive lymphoid cells with Epstein-Barr virus yielded an MTIC-resistant cell line. The second assay (viral capacity) involved determination of the inhibition of replication of untreated virus in treated cells. This approach correctly predicted sensitivity to hydroxyurea and deoxyadenosine in melanoma cell lines when compared with clonogenic survival assay. Viral capacity was also inhibited by cytosine arabinoside, fluorouracil, vincristine, adriamycin, 6-mercaptopurine and ionising radiation, and may therefore be useful for detecting sensitivity to a wide range of antitumor agents.
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PMID:Adenovirus replication as an in vitro probe for drug sensitivity in human tumors. 352 82

Chronic infection with adenovirus types 5 and 6 was established in primary mononuclear leukocytes from human umbilical cord blood and in Epstein-Barr virus (EBV)-transformed B lymphocytes from human umbilical cord blood and from woolly monkey blood. Adenovirus could be recovered from cultures of primary leukocytes and of EBV-transformed lymphocytes for two and three months, respectively, without visible alteration of cell growth. Infection in cultures of EBV-transformed lymphocytes from woolly monkey blood was obliterated by exposure to antibody, but EBV-transformed lymphocytes from human umbilical cord blood contained small amounts of virus for prolonged periods that restored infection in the culture when antibody was removed. Thus, chronic infection of lymphoid cells by some adenoviruses is maintained by at least two mechanisms: cell-to-cell spread of virus in the absence of antibody and intracellular persistence of infectious virus in the presence of antibody.
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PMID:Persistent infection with adenovirus types 5 and 6 in lymphoid cells from humans and woolly monkeys. 627 68

Rhesus monkey fetuses of either immune or nonimmune dams were inoculated in utero with Adenovirus SV-20 (AdSV-20), a virus capable of inducing fetal pneumonia, and studied immunologically at various intervals. AdSV-20 infection at 90-100 days gestational age resulted in absolute lymphopenia in a few fetuses, reduced numbers of peripheral blood lymphocytes (PBL) which formed rosettes with sheep erythrocytes (ERL) and reduced complement-receptor lymphocytes (CRL) in a majority, while Fc fragment-receptor lymphocytes (FcRL) were occasionally increased. There was a tendency for depression of ERL and CRL early in infection of 120-130-day fetuses, followed by stimulation of these populations and FcRL in later phases. Maternal immunity did not protect against these effects of AdSV-20 infection in fetuses. Immune and nonimmune dams were spared adverse clinical effects and had no changes in lymphoid cell populations following inoculation of their fetuses. Despite precocious production of circulating IgM, fetuses of nonimmune dams had little or no demonstrable anti-AdSV-20 serum neutralizing (SN) antibody, indicating that the ability to develop an effective immune response was suppressed or had not been acquired at the gestational ages studied. Nonimmune dams displayed little evidence of seroconversion following inoculation of their fetuses with AdSV-20, except in those dams whose fetuses died in utero, whereby there was a significant antibody response. SN antibody titers of immune dams were not boostered substantially subsequent to inoculation of their fetuses, and fetal SN titers were lower than maternal titers, suggesting absence of an active fetal antibody response in this group also. Direct inoculation of AdSV-20 into 90-130-day rhesus monkey fetuses provided a model system for immunologic study of fetal infection, probably involving complex fetal-maternal interactions, in a situation where the infected, viable fetus and its dam appeared to be microbiologically isolated from one another.
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PMID:Fetal and maternal immunologic manifestations of intrauterine Adenovirus SV-20 infection. 686 35

The Rev trans-activator of human immunodeficiency virus type 1 (HIV-1) is a protein that regulates the simultaneous appearance in the cytoplasm of both spliced and unspliced forms of viral mRNAs from the same viral transcripts by way of recognition of a target sequence termed the Rev-responsive element (RRE). Whether Rev acts directly on RNA export or by inhibition of splicing, or both, is still a matter of debate. We have addressed this issue in Xenopus laevis oocytes by microinjecting RNA molecules containing RRE along with purified recombinant Rev protein into the oocyte nuclei. Adenovirus pre-mRNA containing an RRE in the intron was spliced equally well in the absence and presence of Rev protein. Only in the presence of Rev was non-spliced pre-mRNA exported from the nucleus; more surprisingly, the excised intron lariat (containing RRE) was also exported. Furthermore, an RRE-containing mRNA molecule that lacked intron sequences was also efficiently exported from the nucleus in a Rev-dependent manner. Therefore our results demonstrate that Rev can act directly at the level of nuclear export, independent of any inhibitory effect that it may exert on the splicing of pre-mRNA. Finally, our finding that the Rev mutant M10, shown previously to be inactive in human lymphoid cells, was also unable to export RRE-containing RNA molecules from oocyte nuclei suggests that one or more cellular factors, evolutionarily conserved between humans and Xenopus, interact with Rev in both cell systems to promote nuclear RNA export.
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PMID:Evidence that HIV-1 Rev directly promotes the nuclear export of unspliced RNA. 807 6

Adenovirus vectors have been used to transfer genes into both hematopoietic progenitor cells and tumor cells, including carcinoma cells that have metastasized to bone marrow (BM). However, the relative susceptibility of different subsets of hematopoietic cells is unknown. In permissive cells adenoviral-mediated gene transfer is mediated by the coxsackievirus and adenovirus receptor (CAR) protein and alpha(v) integrins expressed on the cell surface of the target cells. This prompted us to investigate the expression of CAR on subpopulations of hematopoietic cells, determine whether this protein played a role in adenovirus-mediated gene transfer of hematopoietic cells and whether we could modulate CAR to enhance gene transfer efficiency. In this report we show that CAR is expressed on approximately 40% of all human BM cells, including erythroid and myeloid cells, but not lymphoid cells. Of the CD34(+) cells, 10%-15% expressed CAR, but this did not include most colony-forming progenitor cells, nor the most primitive CD38(-) subpopulation. The presence of CAR correlated well with gene transfer efficiency, but we were unable to induce CAR expression on immature, noncommitted progenitor cells. In conclusion, our results show that primitive hematopoietic progenitor cells lack CAR expression, but that expression is acquired during erythroid and myeloid differentiation.
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PMID:Maturation and lineage-specific expression of the coxsackie and adenovirus receptor in hematopoietic cells. 1084 70

Adenovirus-p53-mediated apoptosis has been extensively evaluated in animal xenografts derived from human epithelial tumors and recently began testing in phase I clinical trials, but has not been evaluated for lymphoid malignancies. Cell lines derived from anaplastic large cell lymphoma (ALCL) carrying the t(2;5) translocation are efficiently transduced by adenoviral vector expressing p53 and undergo apoptosis. To test the in vivo efficiency of adenovirus-mediated-p53 expression and apoptosis induction, SUDHL-1 cells (derived from human ALCL) were injected subcutaneously into athymic nude mice. Cells from the xenograft had typical morphology of human ALCL by standard hematoxylin-eosin staining, CD5+, CD45+ and CD30+ immunophenotype, the t(2;5) translocation by PCR. Six tumors from an initial set of mice were evaluated for apoptosis by TUNEL and for necrosis by hematoxylin-eosin staining 48-72 h after injection with 1 x 108 p.f.u. of AdWTp53 (adenoviral vector expressing p53), of AdNull (adenoviral vector backbone) and PBS (mock), respectively. TUNEL staining was positive only in tumors injected with AdWTp53 and was mainly localized around the needle track. Differences of the means of the counts of the necrotic cells were statistically significant at P = 0.02 between AdWTp53 and mock and only borderline between AdWTp53 and AdNull. Twenty-three tumors from a separate set of mice were subsequently injected with AdWTp53, AdNull and PBS and evaluated for in vivo tumor response. Three total injections of viral vectors (1 x 108 p.f.u.) and PBS were given every 48-72 h. Only tumors injected with AdWTp53 showed tumor growth inhibition with a mean final tumor volume that was statistically significantly smaller than AdNull (P = 0.007) and mock (P = 0.002). Based on these results we foresee a potential application of adenovirus-mediated p53 apoptosis as gene therapy of lymphomas.
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PMID:Adenovirus-p53-mediated gene therapy of anaplastic large cell lymphoma with t(2;5) in a nude mouse model. 1084 52


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