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Inhibition of vaccinia virus replication by adenosine in BSC-40 cells:: involvement of A₂ receptor-mediated PKA activation

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ARCHIVES OF VIROLOGY 2002年第7期147卷 1407-1423页

作者： Leao-Ferreira, LR Paes-De-Carvalho, R de Mello, FG Moussatché, N Univ Fed Fluminense Programa Neuroimmunol Inst Biol Outeiro Sao Joao Baptista Niteroi RJ Brazil Fed Univ Rio De Janeiro Inst Biophys Carlos Chagas Filho Rio De Janeiro Brazil

In the present study, we show that adenosine (Ado) affects vaccinia virus (W) replication in BSC-40 cells. In order to identify its effects on VV replicative cycle we analyzed the synthesis of virus macromolecules in cells incubated with 0.5 mM Ado. A 50% reduction in the steady-state level of virus DNA synthesis was observed. Consequently, virus post-replicative gene expression was also affected. A prolonged synthesis of the F11L early virus protein was also observed and it is likely related to a slow decline in the steady-state level of early mRNAs, as suggested by northern blot analysis of the VGF early transcript. The involvement of cAMP-signaling pathway as mediator of Ado response was also evaluated. Ado stimulated a three-fold increase in cAMP levels in BSC-40 cells and cAMP-mimetic agents reduced virus yield in a dose-dependent manner. Co-incubation of infected cells with H-89 reduced the inhibitory effects of 8-Br-cAMP and Ado on VV yields suggesting PKA involvement. A(2) receptor-mediated activation of PKA was indicated by antagonism of Ado response by theophylline and DMPX. Together, these results indicate that virus DNA replication is the main target of Ado. The mechanism involved is not related to reduction of the pyrimidine nucleotide synthesis. Furthermore, Ado-induced PKA activation modulates negatively an unidentified step of the virus replicative cycle.

关键词：腺苷/拮抗剂和抑制剂腺苷/药理学抗病毒药/药理学载体蛋白质类/药理学细胞系共同培养技术环AMP/分析环AMP/代谢环AMP依赖性蛋白激酶类/代谢剂量效应关系药物酶激活/药物作用上皮细胞/代谢上皮细胞/病毒学细胞内信号肽和蛋白质类磷酸二酯酶抑制剂/药理学蛋白质合成抑制药/药理学受体嘌呤能P1/拮抗剂和抑制剂受体嘌呤能P1/代谢信号传导可可碱/类似物和衍生物可可碱/药理学茶碱/药理学痘苗病毒/药物作用痘苗病毒/生理学病毒复制/药物作用动物

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Respiratory syncytial virus infection induces matrix metalloproteinase-9 expression in epithelial cells

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ARCHIVES OF VIROLOGY 2002年第2期147卷 229-242页

作者： Yeo, SJ Yun, YJ Lyu, MA Woo, SY Woo, ER Kim, SJ Lee, HJ Park, HK Kook, YH Seoul Natl Univ Coll Med Inst Endem Dis Dept Microbiol Seoul 151 South Korea Seoul Natl Univ Coll Med Inst Endem Dis Canc Res Inst Seoul 151 South Korea Seoul Natl Univ Hosp Clin Res Inst Seoul South Korea Canc Metastsais Res Ctr Seoul South Korea Chosun Univ Coll Pharm Kwangju South Korea Pochun CHA Med Sch Pundang CHA Gen Hosp Dept Pediat Sungnam South Korea Seoul Natl Univ Coll Med Dept Pediat Seoul South Korea Korea Inst Sci & Technol Div Appl Sci Seoul South Korea

Increased gelatinolytic activity was observed in respiratory syncytial virus (RSV)-infected HEp-2 cells by using zymography. The anti-matrix metalloproteinase-9 (MMP-9) antibody specifically reduced the gelatinolytic activity suggesting that the increased gelatinolytic activity was due to the MMP-9. It was also supported by the results from immunofluorescent staining, treatment of MMP inhibitors, and RSV infection of the cell clones that were transfected with plasmids to express more MMP-9 and tissue type inhibitor of metalloproteinase-1 (TIMP-1). The gelatinolytic activity of extracellular MMP-9 in RSV-infected HEp-2 cells increased 1.5 +/- 0.2 fold compared with the control (p < 0.01). Cell surface MMP-9 expression was also clearly detected by immunofluorescent staining. Treatment with 1,10-phenanthroline (0.05 mM), ethylenediamine-tetraacetate (EDTA) (1.5 mM), and penta-O-galloyl-beta-D-glucose (PGG) (3.3 muM) inhibited RSV multiplication as well as syncytia formation. Furthermore, the average syncytia size increased when the cells expressing more MMP-9 were infected by RSV. In contrast, syncytia formation was inhibited in the cells manipulated to express TIMP-1. Thus, this study concludes that although RSV infection induces MMP-9, which can enhance the syncytia formation leading to RSV multiplication and spread it can be inhibited by MMP inhibitors.

关键词：上皮细胞/代谢上皮细胞/病毒学巨细胞/生理学基质金属蛋白酶9/遗传学基质金属蛋白酶9/代谢呼吸道合胞体病毒感染/病毒学呼吸道合胞病毒/致病力呼吸道合胞病毒/生理学金属蛋白酶1组织抑制剂/遗传学金属蛋白酶1组织抑制剂/代谢转染肿瘤细胞培养的病毒复制人类

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Human mesothelial cells are unusually susceptible to simian virus 40-mediated transformation and asbestos cocarcinogenicity

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第18期97卷 10214-10219页

作者： Bocchetta, M Di Resta, I Powers, A Fresco, R Tosolini, A Testa, JR Pass, HI Rizzo, P Carbone, M Loyola Univ Cardinal Bernardin Canc Ctr Med Ctr Dept PatholCanc Immunol Program Maywood IL 60153 USA Fox Chase Canc Ctr Human Genet Program Philadelphia PA 19111 USA Wayne State Univ Karmanos Canc Inst Aerodigest Program Detroit MI 48201 USA

Mesothelioma, a malignancy associated with asbestos, has been recently linked to simian virus 40 (SV40). We found that infection of human mesothelial cells by SV40 is very different from the semipermissive infection thought to be characteristic of human cells. Mesothelial cells are uniformly infected but not lysed by SV40, a mechanism related to p53, and undergo cell transformation at an extremely high rate. Exposure of mesothelial cells to asbestos complemented SV40 mutants in transformation. Our data provide a mechanistic explanation for the ability of SV40 to transform mesothelial cells preferentially and indicate that asbestos and SV40 may be cocarcinogens.

关键词：石棉/毒性致癌物/毒性细胞转化肿瘤细胞培养的上皮细胞/药物作用上皮细胞/病理学上皮细胞/病毒学成纤维细胞/细胞学成纤维细胞/药物作用成纤维细胞/病毒学间皮瘤/病因学间皮瘤/病理学间皮瘤/病毒学猴病毒40 肿瘤抑制蛋白质p53/遗传学肿瘤抑制蛋白质p53/代谢人类

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Infection of breast epithelial cells with Epstein-Barr virus via cell-to-cell contact

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JOURNAL OF THE NATIONAL CANCER INSTITUTE 2000年第22期92卷 1849-1851页

作者： Speck, P Longnecker, R Northwestern Univ Sch Med Dept Microbiol Immunol Chicago IL 60611 USA

Epstein-Barr virus (EBV), a human herpesvirus present in more than 90% of adults, is a major viral cofactor in certain tumors of lymphoid and epithelial tissues (1). Persistent infection is associated with malignancies and proliferative syndromes typically of lymphoid and epithelial tissues (1), including Burkitt's lymphoma, Hodgkin's disease, certain adult T-cell lymphomas, and, in epithelium, nasopharyngeal carcinoma and oral hairy leukoplakia. In vitro, EBV efficiently infects, transforms, and immortalizes B cells, yielding lymphoblastoid cell lines (LCLs). Several studies have associated EBV with breast cancer. Bonnet et al. (2) detected EBV genomes and gene expression in breast cancer lesions by using polymerase chain reaction (PCR) analysis, Southern hybridization, and immunohistochemistry specific for EBV protein EBNA (i.e., EBV nuclear antigen)-1. Labrecque et al. (3) detected EBV in breast cancers by PCR and in situ hybridization. There are descriptions of EBV-associated lymphomas (4,5) localizing to breast and of bilateral breast cancer developing during the rare chronic active EBV infection syndrome (6). Recent reports (7,8) have described EBV infection of human carcinoma cells on cocultivation with LCLs by a mechanism requiring cell-to-cell contact. These findings and the reported association with breast cancer prompted us to address the question of whether EBV enters breast epithelium by cell-to-cell contact. We have developed an appropriate reagent: EBV bearing the gene encoding and expressing the protein known as enhanced green fluorescent protein (EGFP) (9,10). Cells infected by this virus, designated EBfaV-GFP, are readily detected by their green fluorescence (9–11). Here, we report that cells of human breast cancer epithelial lines T47D and MCF7, which are not infected on direct exposure to cell-free EBfaV-GFP virus, become infected when cocultivated with LCLs derived with and bearing EBfaV-GFP, as shown by expression of EGFP. This finding is consi

关键词：乳房/病理学乳房/病毒学细胞融合细胞培养的上皮细胞/病毒学疱疹病毒4型人/致病力女(雌)性人类

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Simian virus 40 and the human mesothelium

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第18期97卷 9830-9831页

作者： Klein, G Karolinska Inst Ctr Microbiol & Tumor Biol S-17177 Stockholm Sweden

DNA tumor viruses have evolved to replicate, not to cause tumors. Their carcinogenic effect depends on the blocking of the lytic cycle and the ability of latently infected, potentially proliferative cells to escape immune surveillance. These conditions can be satisfied by accidental "experiments of nature" or by the artifices of laboratory experimentation.

关键词：石棉/毒性细胞转化肿瘤上皮细胞/药物作用上皮细胞/病理学上皮细胞/病毒学间皮瘤/病因学间皮瘤/病毒学猴病毒40/致病力人类

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Q vectors, bicistronic retroviral vectors for gene transfer

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BIOTECHNIQUES 2000年第4期28卷 702-+页

作者： Julius, MA Yan, QY Zheng, ZL Kitajewski, J Columbia Univ Coll Phys & Surg Dept Pathol New York NY 10032 USA

We have developed a retroviral vector that incorporates unique features of some previously described vectors. This vector includes: 3' long terminal repents (LTRs) of the self-inactivating class;a 5' LTR that is a hybrid of the cytomegalovirus (CMV) enhancer and the mouse sarcoma virus promoter;nn internal CMV immediate early region promoter to drive expression of the transduced gene and the neomycin phosphotransferase selectable marker an expanded,multiple cloning site and an internal ribosome entry site. An SV40 ori was introduced into the vector backbone to promote high copy number replication in packaging cell lines that express the SV40 large T antigen. We demonstrate that these retrocil al constructs, designated Q vectors, can be used in applications where high viral titers and high level stable or transient gene expression are desirable.

关键词：抗原病毒肿瘤/代谢细胞系巨细胞病毒/遗传学上皮细胞/细胞学上皮细胞/病毒学成纤维细胞/细胞学成纤维细胞/病毒学基因转移技术基因/遗传学基因报告/遗传学遗传载体/化学遗传载体/遗传学乳腺动物/细胞学乳腺动物/病毒学质粒/化学质粒/遗传学启动区遗传/遗传学原癌基因蛋白质类/生物合成原癌基因蛋白质类/遗传学逆转录病毒科/遗传学逆转录病毒科/生长和发育肉瘤病毒鼠/遗传学转染 Wnt蛋白质类斑马鱼蛋白质类 β半乳糖苷酶类/生物合成 β半乳糖苷酶类/遗传学动物女(雌)性小鼠大鼠

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Rhinovirus infection induces expression of its own receptor intercellular adhesion molecule 1 (ICAM-1) via increased NF-κB-mediated transcription

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第14期274卷 9707-9720页

作者： Papi, A Johnston, SL Univ Southampton Southampton Gen Hosp Southampton SO16 6YD Hants England

Virus infections, the majority of which are rhinovirus infections, are the major cause of asthma exacerbations. Treatment is unsatisfactory, and the pathogenesis unclear. Lower airway lymphocyte and eosinophil recruitment and activation are strongly implicated, but the mechanisms regulating these processes are unknown. Intercellular adhesion molecule-1 (ICAM-1) has a central role in inflammatory cell recruitment to the airways in asthma and is the cellular receptor for 90% of rhinoviruses. We hypothesized that rhinovirus infection of lower airway epithelium might induce ICARI-1 expression, promoting both inflammatory cell infiltration and rhinovirus infection. We therefore investigated the effect of rhinovirus infection on respiratory epithelial cell ICAM-1 expression and regulation to identify new targets for treatment of virus-induced asthma exacerbations. We observed that rhinovirus infection of primary bronchial epithelial cells and the A549 respiratory epithelial cell line increased ICAM-1 cell surface expression over 12- and 3-fold, respectively. We then investigated the mechanisms of this induction in A549 cells and observed rhinovirus-induction of ICAM-1 promoter activity and ICAM-1 mRNA transcription. Rhinovirus induction of ICAM-1 promoter activity was critically dependent upon up-regulation of NP-kappa B proteins binding to the -187/-178 NF-kappa B binding site on the ICAM-1 promoter. The principal components of the rhinovirus-induced binding proteins were NF-kappa B p65 homo- or heterodimers. These studies identify ICAM-1 and NF-kappa B as new targets for the development of therapeutic interventions for virus-induced asthma exacerbations.

关键词：哮喘/并发症哮喘/病毒学结合部位支气管/代谢支气管/病毒学细胞系上皮细胞/代谢上皮细胞/病毒学胞间黏附分子1/生物合成 NF-κB/代谢细小RNA病毒科感染/并发症细小RNA病毒科感染/代谢细小RNA病毒科感染/病毒学 RNA 信使/代谢鼻病毒属/代谢鼻病毒属/致病力鼻病毒属/生理学转录因子AP-1/代谢转录遗传病毒复制人类

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Effect of nitrogen dioxide on respiratory viral infection in airway epithelial cells

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ENVIRONMENTAL RESEARCH 1999年第2期81卷 159-166页

作者： Becker, S Soukup, JM US EPA Natl Hlth & Environm Effects Res Lab Res Triangle Pk NC 27711 USA

Nitrogen dioxide (NO2) is a common air pollutant outdoors and indoors in homes with unvented combustion sources. It is also a constituent of tobacco smoke. Epidemiological studies suggest that children exposed to NO2, or living with smoking parents, have an increased incidence of respiratory viral infections. The most common virus causing severe respiratory symptoms in infants and young children is respiratory syncytial virus (RSV), In the present study we investigated whether NO2 exposure affects RSV infection in airway epithelial cells, the host cells for viral replication and virus-induced cytokine production. Cultures of the bronchial epithelial cell line BEAS-2B exposed to 0.5, 1.0, and 1.5 ppm NO2 for 60 min were infected with RSV Viral replication, as well as RSV-induced interleukin (IL)-6 and IL-8, was assessed at various times postinfection, The NO2 doses used were not toxic to the BEAS-2B cells as measured by release of lactic dehydrogenase (LDH). The internalization of RSV was increased by exposure to 0.5 ppm NO2 and decreased by exposure to 1.5 ppm NO2, On the other hand, the release of infectious virus 48 h postexposure was not affected by the two lower doses of NO2, but was significantly reduced in cells exposed to 1.5 ppm NO2, Virus-induced cytokine production was also significantly reduced in cells exposed to 1.5 ppm NO2, and not affected by 0.5 and 1.0 ppm. It is likely that the decrease in cytokine production is related to the decrease in viral burden. These data suggest that possible increases in viral clinical symptoms associated with NO2 may not be caused by increased susceptibility of the epithelial cells to infection but may result from effects of NO2 on host defenses that prevent the spread of virus. (C) 1999 Academic Press.

关键词：空气污染物/毒性支气管/药物作用支气管/免疫学支气管/病毒学细胞系细胞因子类/生物合成剂量效应关系药物上皮细胞/药物作用上皮细胞/免疫学上皮细胞/病毒学二氧化氮/毒性呼吸道合胞病毒/药物作用病毒复制/药物作用人类

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Goat milk epithelial cells are highly permissive to CAEV infection in vitro

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VIROLOGY 1999年第1期259卷 67-73页

作者： Mselli-Lakhal, L Guiguen, F Fornazero, C Du, J Favier, C Durand, J Grezel, D Balleydier, S Mornex, JF Chebloune, Y Ecole Vet Lyon INRA Lab Associe Rech Lentivirus Petits Ruminants F-69280 Marcy Etoile France

The main route of small ruminant lentivirus dissemination is the ingestion of infected cells present in colostrum and milk from infected animals. However, whether only macrophages or other cell subtypes are involved in this transmission is unknown. We derived epithelial cell cultures, 100% cytokeratin positive, from milk of naturally infected and noninfected goats. One such culture, derived from a naturally infected goal, constitutively produced a high titer of virus in the absence of any cytopathic effect. The other cultures, negative for natural lentivirus infection, were tested for their susceptibility to infection with the CAEV-CO strain and a French field isolate CAEV-3112. We showed that milk epithelial cells are easily infected by either virus and produce viruses at titers as high as those obtained in permissive goat synovial membrane cells. The CAEV-CO strain replicated in milk epithelial cells in absence of any cytopathic effect, whereas the CAEV-3112 field isolate induced both cell fusion and cell lysis. Our results suggest that CAEV-infected milk epithelial cells of small ruminants may play an important role in virus transmission and pathogenesis. (C) 1999 Academic Press.

关键词：关节炎脑炎病毒山羊/生理学细胞培养的上皮细胞/病毒学山羊慢病毒感染/病理学慢病毒感染/病毒学乳/细胞学乳/病毒学动物女(雌)性

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Sexual transmission and propagation of SIV and HIV in resting and activated CD4⁺ T cells

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SCIENCE 1999年第5443期286卷 1353-1357页

作者： Zhang, ZQ Schuler, T Zupancic, M Wietgrefe, S Staskus, KA Reimann, KA Reinhart, TA Rogan, M Cavert, W Miller, CJ Veazey, RS Notermans, D Little, S Danner, SA Richman, DD Havlir, D Wong, J Jordan, HL Schacker, TW Racz, P Tenner-Racz, K Letvin, NL Wolinsky, S Haase, AT Univ Minnesota Sch Med Dept Microbiol Minneapolis MN 55455 USA Harvard Univ Beth Israel Hosp Div Viral Pathogenesis Boston MA 02215 USA Univ Pittsburgh Dept Infect Dis & Microbiol Pittsburgh PA 15261 USA Calif Reg Primate Res Ctr Davis CA 95616 USA Univ Amsterdam Acad Med Ctr Acad Hosp Div Infect Dis Trop Med & AIDS NL-1105 AZ Amsterdam Netherlands Univ Calif San Diego Dept Pathol La Jolla CA 92093 USA Univ Calif San Diego Dept Med La Jolla CA 92093 USA Univ Minnesota Sch Med Dept Med Minneapolis MN 55455 USA Bernhard Nocht Inst Trop Med D-20359 Hamburg Germany Northwestern Univ Sch Med Div Infect Dis Chicago IL 60611 USA San Diego VA Hlth Care Syst La Jolla CA 92093 USA

In sexual transmission of simian immunodeficiency virus, and early and later stages of human immunodeficiency virus-type 1 (HIV-1) infection, both viruses were found to replicate predominantly in CD4(+) T cells at the portal of entry and in Lymphoid tissues, infection was propagated not only in activated and proliferating T cells but also, surprisingly, in resting T cells. The infected proliferating cells correspond to the short-lived population that produces the bulk of HIV-1. Most of the HIV-1-infected resting T cells persisted after antiretroviral therapy. Latently and chronically infected cells that may be derived from this population pose challenges to eradicating infection and developing an effective vaccine.

关键词：抗HIV药/治疗应用 CD4阳性T淋巴细胞/细胞学 CD4阳性T淋巴细胞/免疫学 CD4阳性T淋巴细胞/病毒学细胞周期子宫颈/病毒学上皮细胞/病毒学 HIV感染/药物疗法 HIV感染/传播 HIV感染/病毒学 HIV-1/生理学淋巴结/病毒学淋巴细胞活化猕猴 RNA 病毒/分析猴获得性免疫缺陷综合征/传播猴获得性免疫缺陷综合征/病毒学猴免疫缺陷病毒/生理学时间因素病毒复制动物女(雌)性

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