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  • 1
    Abstract: Amphotropic murine leukemia virus (MLV) replicates in cells from various mammalian species including humans and is a potential contaminant in MLV vector preparations for human gene transfer studies. In general, MLV replication depends on the expression of viral genes under the control of 75 bp enhancer elements in the long terminal repeat. However, in specific human fibrosarcoma and lymphoma lines replication of amphotropic MLV is possible without these enhancers. Fibrosarcomas are malignant tumors of fibroblast origin. To test the replication potential of intact and enhancerless amphotropic MLV in untransformed cells, infection studies with these viruses were carried out in three types of primary human fibroblasts. Replication of amphotropic MLV is observed in two of three tested fibroblast strains. None of these primary human fibroblasts is permissive for enhancer-deficient MLV, suggesting that replication of this virus may be limited to transformed cells.
    Type of Publication: Journal article published
    PubMed ID: 12210420
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  • 2
    Keywords: RISK ; INFECTION ; ASSOCIATION ; antibodies ; PREDICTION ; AUTOANTIBODIES ; Myocarditis ; BETA-CELL AUTOIMMUNITY ; SUSPENSION ARRAY ; PICORNAVIRIDAE
    Abstract: Exposure to Ljungan virus (LV) is implicated in the risk of autoimmune (type 1) diabetes but possible contribution by other parechoviruses is not ruled out. The aim was to compare children diagnosed with type 1 diabetes in 2005-2011 (n = 69) with healthy controls (n = 294), all from the Jamtland County in Sweden, using an exploratory suspension multiplex immunoassay for IgM and IgG against 26 peptides of LV, human parechoviruses (HPeV), Aichi virus and poliovirus in relation to a radiobinding assay (RBA) for antibodies against LV and InfluenzaA/H1N1pdm09. Islet autoantibodies and HLA-DQ genotypes were also determined. 1) All five LV-peptide antibodies correlated to each other (P 〈 0.001) in the suspension multiplex IgM- and IgG-antibody assay; 2) The LV-VP1_31-60-IgG correlated with insulin autoantibodies alone (P = 0.007) and in combination with HLA-DQ8 overall (P = 0.022) as well as with HLA-DQ 8/8 and 8/X subjects (P = 0.013); 3) RBA detected LV antibodies correlated with young age at diagnosis (P 〈 0.001) and with insulin autoantibodies (P 〈 0.001) especially in young HLA-DQ8 subjects (P = 0.004); 4) LV-peptide-VP1_31-60-IgG correlated to RBA LV antibodies (P = 0.009); 5) HPeV3-peptide-IgM and -IgG showed inter-peptide correlations (P 〈 0.001) but only HPeV3-VP1_1-30-IgG (P 〈 0.001) and VP1_95-124-IgG (P = 0.009) were related to RBA LV antibodies without relation to insulin autoantibody positivity (P = 0.072 and P = 0.486, respectively). Both exploratory suspension multiplex IgG to LV-peptide VP1_31-60 and RBA detected LV antibodies correlated with insulin autoantibodies and HLA-DQ8 suggesting possible role in type 1 diabetes. It remains to be determined if cross-reactivity or concomitant exposure to LV and HPeV3 contributes to the seroprevalence. J. Med. Virol. 87:1130-1140, 2015. (c) 2015 Wiley Periodicals, Inc.
    Type of Publication: Journal article published
    PubMed ID: 25873230
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  • 3
    Keywords: PROTEINS ; INFECTION ; MOLECULAR-BIOLOGY ; antibodies ; virus ; PATHOGENESIS ; glutathione-S-transferase ; KIDNEY-TRANSPLANT ; RENAL-TRANSPLANTATION ; PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY
    Abstract: The human polyomaviruses BKV and JCV cause mostly subclinical infections in childhood. Systemical immunosuppression after organ transplantation can lead to reactivation of persistent polyomavirus infections which may cause rejection of the transplanted organ. BKV and JCV seroprevalence and serostability was measured in 441 European solid organ transplanted recipients. Baseline samples were collected on average 24 days post-transplantation and sera were then collected over an 18 months follow-up period on up to six different time points. The overall seroprevalence at baseline for BKV was 97% with very little change over time. Prevalence for JCV was 76% at baseline and increased to 80% at the end of follow-up. BKV seroprevalence was highest in the youngest age group (100%) and decreased with increasing age (92% in the oldest age group; P?〈?0.0001), while JCV increased with age (69% vs. 81%; P?=?0.020). Antibody reactivities for both BKV and JCV increased significantly with time (P?=?0.0002 and P?〈?0.0001, respectively). Among the 406 patients with several samples, 94% were stably seropositive for BKV and 1% remained seronegative during the follow-up. JCV antibody stability was somewhat lower: 67% remained stably seropositive and 13% seronegative. While seroprevalence of BKV and JCV decrease and increase with age, respectively, both polyomaviruses showed significant increasing antibody reactivity over time in organ transplanted recipients at the onset of immunosuppression.
    Type of Publication: Journal article published
    PubMed ID: 23172042
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  • 4
    Keywords: RISK ; ASSOCIATION ; IN-SITU HYBRIDIZATION ; HUMAN-PAPILLOMAVIRUS ; EPSTEIN-BARR-VIRUS ; WILD-TYPE P53 ; cytomegalovirus ; SOCIOECONOMIC-STATUS ; GERM-CELL TUMORS ; PARVOVIRUS B19
    Abstract: In 1984, Newell and coworkers were the first to suggest that testicular cancer might have a viral etiology since it showed similar characteristics to Hodgkin's lymphoma. A systematic literature review and meta-analysis was conducted to investigate a possible association between viral infections (EBV, CMV, Parvovirus B19, HPV, and HIV) and testicular cancer. Articles published from 1985 through June 2010 were located from MEDLINE and EMBASE databases, 21 articles were finally included in the review. For infection with EBV, CMV, Parvovirus B19, and HIV the pooled OR were 4.80 (95% CI 0.98-23.54), 1.85 (95% CI 0.92-3.70), 2.86 (95% CI 0.35-23.17), and 1.79 (95% CI 1.45-2.21) respectively. No pooling was possible for HPV infection studies due to small numbers. The results support a possible association, but more epidemiological studies with better viral identification and localization methods are needed to verify these findings.
    Type of Publication: Journal article published
    PubMed ID: 23959966
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  • 5
    Keywords: CELLS ; CELL ; Germany ; human ; GENERATION ; NEW-YORK ; GENE ; GENOME ; transcription ; TRANSDUCTION ; gene transfer ; GENE-TRANSFER ; murine ; recombination ; SEQUENCE ; SEQUENCES ; virus ; HOST RANGE ; VECTORS ; VECTOR ; PROMOTER ; REQUIRES ; leukemia ; inactivation ; MAMMALIAN-CELLS ; REPLICATION ; INCLUDING HUMANS ; INTEGRATION SITE ; RETROVIRAL VECTORS ; LONG TERMINAL REPEAT ; amphotropic ; COMPETENT RETROVIRUS ; murine leukemia virus
    Abstract: Amphotropic murine leukemia virus (MLV) replicates in cells from various mammalian species including humans and is a potential contaminant in MLV vector preparations for human gene transfer studies. Because MLV replication proceeds through an RNA genome that is generated under the control of viral enhancer and promoter elements, vectors were developed that delete such elements during transduction to reduce the generation of replication-competent virus. It was shown recently that replication of amphotropic MLV in certain human cells is possible without the 75 bp transcription enhancers. It is now demonstrated that enhancer-independent replication requires functional elements within U3 and is repressed by an extended deletion in the U3 region comprising enhancers, promoter and flanking sequences. It is concluded that the transcriptional inactivation of amphotropic MLV in human cells requires the combined deletion of enhancers and of additional elements in U3
    Type of Publication: Journal article published
    PubMed ID: 12683417
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  • 6
    Keywords: brain ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; tumor ; AGENTS ; evaluation ; human ; THERAPY ; VITRO ; GENE ; PROTEIN ; gene therapy ; PATIENT ; prognosis ; FLOW ; BINDING ; MUTANT ; VECTORS ; ASSAY ; VECTOR ; MUTATION ; PCR ; MUTATIONS ; REPLICATION ; specificity ; FLOW-CYTOMETRY ; GENE-THERAPY ; ADENOVIRUS ; MULTIFORME ; CYTOTOXICITY ; AGENT ; THERAPIES ; GLIOMA ; MALIGNANT GLIOMA ; oncolytic virus ; MS ; analysis ; ASSAYS ; VIROTHERAPY ; USA ; CANCERS ; GLIOBLASTOMA ; quantitative ; TYROSINASE ENHANCER/PROMOTER ; RETINOBLASTOMA GENE ; adenoviral vector ; Ad2/24 ; ADENOVIRUS-E1A PREVENTS ; CELLULAR TRANSCRIPTION FACTOR
    Abstract: Malignant glioma, in particular glioblastoma multiforme (GBM), represents one of the most devastating cancers currently known and existing treatment regimens do little to change patient prognosis. Conditionally replicating adenoviral vectors (CRAds) represent attractive experimental anti-cancer agents with potential for clinical application. However, early protein products of the wild type adenovirus backbone-such as E1A-limit CRAds' replicative specificity. In this study, we evaluated the oncolytic potency and specificity of CRAds in which p300/CPB and/or pRb binding capacities of E1A were ablated to reduce nonspecific replicative cytolysis. In vitro cytopathic assays, quantitative PCR analysis, Western blot, and flow cytometry studies demonstrate the superior anti-glioma efficacy of a double-mutated CRAd, Ad2/24CMV, which harbors mutations that reduce E1A binding to p300/CPB and pRb. When compared to its single-mutated and wild type counterparts, Ad2/24CMV demonstrated attenuated replication and cytotoxicity in representative normal human brain while displaying enhanced replicative cytotoxicity in malignant glioma. These results have implications for the development of double-mutated CRAd vectors for enhanced GBM therapy
    Type of Publication: Journal article published
    PubMed ID: 18649343
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  • 7
    Keywords: Germany ; THERAPY ; HEPATOCELLULAR-CARCINOMA ; NEW-YORK ; GENOME ; RNA ; SAMPLE ; SAMPLES ; PATIENT ; DNA ; INFECTION ; SERA ; CONTRAST ; SEQUENCE ; treatment ; ACID ; ACIDS ; NUCLEIC-ACID ; NUCLEIC-ACIDS ; PARTICLES ; TARGET ; virus ; COPY NUMBER ; COPY-NUMBER ; PATTERNS ; DECREASE ; NUMBER ; PCR ; REPLICATION ; hepatitis B virus ; SEGMENTS ; DECLINE ; COMPETITIVE PCR ; REPRESENTATION ; drug-induced coexistence of viral ; immature particles ; quantitation of particle numbers ; STRAND VIRAL-DNA ; TRANSCRIPTS
    Abstract: We examined whether lamivudine treatment, in addition to the rapid decline of HBV serum DNA described in a large number of laboratories, causes changes in composition and amount of discernable circulating viral DNA and RNA. Nucleic acids were extracted from serial serum samples of a patient infected chronically and treated with lamivudine for 14 weeks. Three sequence segments of the HBV genome synthesized successively during replication, X, C, and X-preC, were analyzed by competitive PCR and RT/PCR. In addition, RNA was examined for differential polyadenylation. Before treatment, identical DNA copy numbers (10(9)/ml) were found in all three segments. C segment DNA displayed the expected rapid decline. X-preC, a target contiguous only on plus-strand DNA behaved similarly. In contrast, the X segment DNA copy numbers showed a less pronounced decrease remaining at higher values (10(7)/Ml) than the C and X-preC segment (both about 2 x 10(5)/ml) at the end of therapy. X segment RNA displayed a persisting copy number of about 10(7)/Ml, while C and X-preC RNA decreased to about 10(5) copies/ml. Polyadenylated HBV RNA, full-length and truncated, persisted initially at 10(5) but decreased to 10(4) to 10(3) copies/ml at the end of treatment. The major conclusions are the actual numbers of virus particles during lamivudine therapy can only be assessed via X segment DNA, since it is reverse transcribed first, and Lamivudine induced coexistence of DNA and RNA for the C and X segment at similar levels indicates drug-arrested intermediates of reverse transcribed HBV DNA minus-strand. Packaged RNA lacks a poly(A) tail whereas polyadenylated RNA is likely not packaged. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12858405
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