Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenovirus type 7 vaccine strain was engineered to express foreign antigens from both the E3 early promoter in the E3 region and the major late promoter inserted between the E4 region and the right inverted terminal repeat. This multiple expression vector was used to express hepatitis B core antigen (HBcAg), hepatitis B e antigen (HBeAg), and hepatitis B surface antigen (HBsAg). The gene inserted in the E3 region was derived from the core gene of the hepatitis B virus genome. When the precore region was present, an immunoreactive group of proteins with molecular weights ranging from 15,000 to 19,000 was secreted into the media. Velocity sedimentation centrifugation of media and lysates from cells infected with recombinants containing the core gene with the precore region resulted in peaks of HBeAg at the top of the gradient where authentic HBeAg should be found. In addition to the core gene in the E3 region, the surface antigen gene of hepatitis B virus was inserted behind the major late promoter in the E4 region resulting in an adeno-hepatitis recombinant virus capable of expressing both the core gene and the HBsAg cells. Cells infected with the adeno-hepatitis recombinants could also be stained with peroxidase-conjugates after reacting to antibody against HBcAg. Inoculation of dogs with the recombinant viruses which contained the core gene, with and without the precore sequence, resulted in a significant antibody response to HBcAg/HBeAg. The dogs also produced a significant antibody response to HBsAg as well as neutralizing antibody to adenovirus.
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PMID:Co-expression of hepatitis B virus antigens by a non-defective adenovirus vaccine vector. 182 60

A variety of factors were found to modify the toxicity of L-dopa in HeLa cells (D37 16 microM) and in dopa-sensitive, nonpigmented human melanoma cells (MM96) (D37 5 microM) having a similar size and doubling time. Dopa toxicity was decreased by concurrent treatment with superoxide dismutase, peroxidase or catalase, by erythrocytes, or by hypoxia. Toxicity could be increased by the enzyme inhibitors L- and D-penicillamine, sodium diethyldithiocarbamate or 3-amino-1,2,4-triazole. The two cell lines had similar levels of superoxide dismutase and peroxidase; in 6 human melanoma lines, no correlation was found between dopa killing and tyrosinase activity as determined either by formation of dopa from tyrosine or by formation of melanin from dopa. Uptake of L-dopa was similar in HeLa and MM96 cells, and the toxicity of D-dopa was the same in both lines as that of the L-isomer. Dopa decomposed within 12 hr in culture medium, the rate and products being influenced by addition of the above enzymes and by the cell density. Dopa-melanin and medium containing decomposed dopa were also selectively toxic to MM96 cells. Adenovirus 5 was used in two different ways to assess the relative importance of DNA damage and inhibition of DNA synthesis by dopa. Viral replication was found to be unaffected in cells being treated with dopa but was strongly inhibited in cells treated with the DNA polymerase inhibitor cytosine arabinoside. Secondly, the virus was itself inactivated by treatment with dopa for 24 hr (D37 1.3 mM); similar dose response curves were obtained for replication of dopa-treated virus in untreated HeLa or MM96 cells. These results show that the initial events of dopa toxicity occur outside the cell and lead to the formation of a stable, toxic product (probably melanin) which does not strongly inhibit DNA polymerase activity. Melanoma hypersensitivity was not due to differences in oxygen-metabolizing enzymes, dopa uptake, or DNA repair.
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PMID:Modification of dopa toxicity in human tumour cells. 392 49

New monoclonal antibodies (MAbs) to adenovirus hexon, highly active in ELISA and immunofluorescent analysis, were prepared. According to competitive ELISA, new MAbs differed in their blocking activity and were directed to 2 different hexon epitopes. MAb 3H8 did not modify antigen binding of the rest MAbs labeled with peroxidase (PAb x Pox), and none of unlabeled MAbs suppressed the reaction of MAb x Pox 3H8. MAbs 1E8 7F1, 1E11, and 3B1 reacted with each other but differed by the spectrum and level of competitive inhibition, which indicated that they were directed to different epitopes of adenovirus hexon. Comparison of the specific activity of MAbs 7F1 and 1E8 in direct immunofluorescent detection of adenovirus antigens in infected cell cultures and clinical materials from patients showed a good coincidence (90-97%) of the results with the IMAGEN Adenovirus test (Dako) and with polyclonal FITC conjugates to adenovirus hexon.
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PMID:[Isolation and characteristics of anti-adenovirus monoclonal antibodies in immunoenzyme and immunofluorescent reactions]. 1110 51

Recent studies indicate that inflammatory reaction occurs around hematoma after intracerebral hemorrhage (ICH). In this study the authors examine the hypothesis that overexpression of IL-1ra in the brain attenuate brain edema formation after ICH. Adenoviruses expressing IL-1ra (Ad.RSVIL-1ra) or LacZ (Ad.RSVLacZ) or saline were injected into the lateral ventricle. On the fifth day after virus injection, 100 microl of autologous blood or 5 U thrombin was infused into the right basal ganglia. Rats with ICH were killed 24 or 72 hours later for measurement of brain water content. Thrombin-treated rats were killed 24 hours later for edema measurements and an assessment of polymorphonuclear leukocyte (PMNL) infiltration by myeloperoxidase (MPO) assay. Compared with control groups, Ad.RSVIL-1ra treated rats had less brain edema formation in the ipsilateral basal ganglia 3 days after ICH (81.5 +/- 0.3% compared with 83.4 +/- 0.4% and 83.3 +/- 0.5% in control animals). Ad.RSVIL-1ra treated rats had also less brain edema following thrombin injection. The reduction of brain edema induced by thrombin was involved in the reduction of PMNL infiltration in basal ganglia, as assessed by MPO assay. Adenovirus-mediated overexpression of IL-1ra attenuated brain edema formation following ICH, perhaps by reduction of thrombin-induced brain inflammation.
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PMID:Overexpression of interleukin-1 receptor antagonist reduces brain edema induced by intracerebral hemorrhage and thrombin. 1475 87

The cornea contains a heterogeneous population of antigen-presenting cells with the capacity to contribute to immune responses. Adenovirus keratitis is a severe corneal infection with acute and chronic phases. The role of resident corneal antigen-presenting cells in adenovirus keratitis has not been studied. We utilized transgenic MaFIA mice in which c-fms expressing macrophages and dendritic cells can be induced to undergo apoptosis, in a mouse model of adenovirus keratitis. Clinical keratitis and recruitment of myeloperoxidase and CD45(+) cells were diminished in c-fms depleted, adenovirus infected mice, as compared to controls, consistent with a role for myeloid-lineage cells in adenovirus keratitis.
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PMID:Resident corneal c-fms(+) macrophages and dendritic cells mediate early cellular infiltration in adenovirus keratitis. 2718 63

Inflammatory reaction plays a crucial role in the pathophysiology of acquired hearing loss such as ototoxicity and labyrinthitis. In our earlier work, we showed the pivotal role of otic fibrocytes in cochlear inflammation and the critical involvement of proinflammatory cytokines in cisplatin ototoxicity. We also demonstrated that otic fibrocytes inhibit monocyte chemoattractant protein 1 (CCL2) upregulation in response to interleukin-10 (IL-10) via heme oxygenase 1 (HMOX1) signaling, resulting in suppression of cochlear inflammation. However, it is still unclear how IL-10 affects inflammation-mediated cochlear injury. Here we aim to determine how hypochlorous acid, a model inflammation mediator affects cochlear cell viability and how IL-10 affects hypochlorous acid-mediated cochlear cell injury. NaOCl, a sodium salt of hypochlorous acid (HOCl) was found to induce cytotoxicity of HEI-OC1 cells in a dose-dependent manner. Combination of hydrogen peroxide and myeloperoxidase augmented cisplatin cytotoxicity, and this synergism was inhibited by N-Acetyl-L-cysteine and ML-171. The rat spiral ligament cell line (RSL) appeared to upregulate the antioxidant response element (ARE) activities upon exposure to IL-10. RSL cells upregulated the expression of NRF2 (an ARE ligand) and NR0B2 in response to CoPP (a HMOX1 inducer), but not to ZnPP (a HMOX1 inhibitor). Adenovirus-mediated overexpression of NR0B2 was found to suppress CCL2 upregulation. IL-10-positive cells appeared in the mouse stria vascularis 1 day after intraperitoneal injection of lipopolysaccharide (LPS). Five days after injection, IL-10-positive cells were observed in the spiral ligament, spiral limbus, spiral ganglia, and suprastrial area, but not in the stria vascularis. IL-10R1 appeared to be expressed in the mouse organ of Corti as well as HEI-OC1 cells. HEI-OC1 cells upregulated Bcl-xL expression in response to IL-10, and IL-10 was shown to attenuate NaOCl-induced cytotoxicity. In addition, HEI-OC1 cells upregulated IL-22RA upon exposure to cisplatin, and NaOCl cytotoxicity was inhibited by IL-22. Taken together, our findings suggest that hypochlorous acid is involved in cochlear injury and that IL-10 potentially reduces cochlear injury through not only inhibition of inflammation but also enhancement of cochlear cell viability. Further studies are needed to determine immunological characteristics of intracochlear IL-10-positive cells and elucidate molecular mechanisms involved in the otoprotective activity of IL-10.
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PMID:Interleukin-10 Attenuates Hypochlorous Acid-Mediated Cytotoxicity to HEI-OC1 Cochlear Cells. 2905 1