Viral Antigens

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Helen G Porter - One of the best experts on this subject based on the ideXlab platform.

  • respiratory Viral Antigens in autopsy lung tissue specimens from patients with cancer or myocardial infarction
    Clinical Infectious Diseases, 1999
    Co-Authors: David D Porter, Helen G Porter

    Using immunoenzyme histochemical analysis, we retrospectively examined lung tissue specimens obtained at autopsy from 118 patients with cancer who had received chemotherapy and 20 patients who had died after myocardial infarction. Respiratory Viral Antigens were demonstrated in lung tissue specimens from eight of 118 cancer patients and two of 20 myocardial infarction patients. Most of the patients with demonstrable Viral Antigens were febrile and had signs of pulmonary infection, but in no case was pulmonary Viral infection considered clinically. The following Viral Antigens were demonstrated: influenza A virus (6 patients), respiratory syncytial virus (2), influenza B virus (1), and parainfluenza virus type 1 (1).

James M. Wilson - One of the best experts on this subject based on the ideXlab platform.

  • role of Viral Antigens in destructive cellular immune responses to adenovirus vector transduced cells in mouse lungs
    Journal of Virology, 1996
    Co-Authors: Yiping Yang, James M. Wilson

    Adenoviruses missing E1 have been used as gene delivery vectors to the lungs for the treatment of cystic fibrosis. Transient expression of the recombinant gene and the development of inflammation have been two major limitations to the application of first-generation recombinant adenoviruses for gene therapy. Studies with mouse models of liver- and lung-directed gene therapy suggested that CD8+ cytotoxic T lymphocytes (CTLs) are effectors that contribute to extinction of transgene expression. The precise Antigens responsible for activation of CTLs have not been identified. In this study, we examine the relative contributions of Viral proteins versus the transgene product to the activation of CTLs which eliminate transgene-containing cells in mouse lungs. Instillation of a lacZ-expressing virus into the lungs of C57BL/6 mice elicited CTL responses to both Viral proteins and the transgene product, beta-galactosidase, which collectively contribute to loss of trans-gene expression in mouse airways. Similar results were obtained in two experimental models in which the animals should be tolerant to the transgene, i.e., lacZ virus delivered to an animal transgenic for lacZ and a virus expressing the liver-specific enzyme ornithine transcarbamylase administered to the lungs of various strains of immune-competent mice. These data confirm the hypothesis that CTLs specific for Viral Antigens contribute to the problem of transgene instability in mouse lungs and indicate that CTLs specific for transgene product alone cannot account for the observed problem.

  • Immune responses to Viral Antigens versus transgene product in the elimination of recombinant adenovirus-infected hepatocytes in vivo.
    Gene therapy, 1996
    Co-Authors: Yiping Yang, Karin Jooss, Hildegund C.j. Ertl, James M. Wilson

    Human adenoviruses have been developed as an attractive vehicle for in vivo liver-directed gene therapy. Problems with the application of first generation recombinant adenoviruses to liver-directed gene therapy have been transient expression of the recombinant gene and development of hepatitis. Previous studies in mouse models of gene transfer to liver and lung suggested that MHC class I-restricted cytotoxic T lymphocytes (CTLs) to Viral Antigens may be effectors in the elimination of transgene expression. The goal of this study was to evaluate the importance of Viral Antigens versus transgene product in inducing CTL mediated hepatocyte destruction in vivo. Immunization of C57BL/6 mice with a lacZ-expressing adenovirus elicited CTL responses to both Viral Antigens and the transgene product, beta-galactosidase (beta-gal). Adoptive transfer experiments, as well as studies involving lacZ-transgenic mice (ROSA-26) revealed that CTLs to Viral Antigens are sufficient to destroy virus-infected hepatocytes, indicating that CTLs to beta-gal can not solely account for the observed hepatocyte destruction that has characterized the use of first generation viruses. In addition, we confirmed that B cell-mediated events do not participate in destruction of hepatocytes in vivo, despite the production of virus- and beta-gal-specific antibodies. These data confirm the hypothesis that Viral gene expression elicits host responses that contribute to the problem of transgene instability. Recombinant adenoviruses must be redesigned to diminish Viral gene expression if they are to be used in the treatment of chronic diseases.

  • cellular and humoral immune responses to Viral Antigens create barriers to lung directed gene therapy with recombinant adenoviruses
    Journal of Virology, 1995
    Co-Authors: Yiping Yang, Hildegund C.j. Ertl, James M. Wilson

    Recombinant adenoviruses are an attractive vehicle for gene therapy to the lung in the treatment of cystic fibrosis (CF). First-generation viruses deleted of E1a and E1b transduce genes into airway epithelial cells in vivo; however, expression of the transgene is transient and associated with substantial inflammatory responses, and gene transfer is significantly reduced following a second administration of the virus. In this study, we have used mice deficient in immunological effector functions in combination with adoptive and passive transfer techniques to define antigen-specific cellular and humoral immune responses that underlie these important limitations. Our studies indicate that major histocompatibility complex class I-restricted CD8+ cytotoxic T lymphocytes are activated in response to newly synthesized Antigens, leading to destruction of virus infected cells and loss of transgene expression. Major histocompatibility complex class II-associated presentation of exogenous Viral Antigens activates CD4+ T-helper (TH) cells of the TH1 subset and, to a lesser extent, of the TH2 subset. CD4+ cell-mediated responses are insufficient in the absence of cytotoxic T cells to completely eliminate transgene containing cells; however, they contribute to the formation of neutralizing antibodies in the airway which block subsequent adenovirus-mediated gene transfer. Definition of immunological barriers to gene therapy of cystic fibrosis should facilitate the design of rational strategies to overcome them.

Gillis R Otten - One of the best experts on this subject based on the ideXlab platform.

  • the role of non Viral Antigens in the cotton rat model of respiratory syncytial virus vaccine enhanced disease
    Vaccine, 2013
    Co-Authors: Christine A Shaw, Jeanrene Galarneau, Kathryn E Bowenkamp, Kurt Swanson, Gene A Palmer, Giuseppe Palladino, Judit Markovits, Nicholas M Valiante, Philip R Dormitzer, Gillis R Otten

    In the 1960s, infant immunization with a formalin-inactivated respiratory syncytial virus (FI-RSV) vaccine candidate caused enhanced respiratory disease (ERD) following natural RSV infection. Because of this tragedy, intensive effort has been made to understand the root causes of how the FI-RSV vaccine induced a pathogenic response to subsequent RSV infection in vaccinees. A well-established cotton rat model of FI-RSV vaccine-enhanced disease has been used by numerous researchers to study the mechanisms of ERD. Here, we have dissected the model and found it to have significant limitations for understanding FI-RSV ERD. This view is shaped by our finding that a major driver of lung pathology is cell-culture contaminants, although FI-RSV immunization and RSV challenge serve as co-factors to exacerbate disease. Specifically, non-Viral products from the vaccine and challenge preparations that are devoid of RSV give rise to alveolitis, which is considered a hallmark of FI-RSV ERD in the cotton rat model. Although FI-RSV immunization and RSV challenge promote more severe alveolitis, they also drive stronger cellular immune responses to non-Viral Antigens. The severity of alveolitis is associated with T cells specific for non-Viral Antigens more than with T cells specific for RSV. These results highlight the limitations of the cotton rat ERD model and the need for an improved animal model to evaluate the safety of RSV vaccine candidates.

M B Pensaert - One of the best experts on this subject based on the ideXlab platform.

  • Virus production and Viral antigen expression in porcine blood monocytes inoculated with pseudorabies virus.
    Archives of virology, 1994
    Co-Authors: H J Nauwynck, M B Pensaert

    Interactions of pseudorabies virus (PRV) with peripheral blood mononuclear cells (PBMC) were studied. T-lymphocytes, B-lymphocytes and monocytes were selected or depleted from the PBMC fraction by means of several separation techniques. After inoculation with virulent PRV in vitro, the percentage of cells that expressed Viral Antigens was determined in the different subpopulations by immunofluorescence. The susceptibility of monocytes depended on the method of isolation. When plasma-coated polystyrene culture grade dishes were used, 17 to 26% of the monocytes showed expression of Viral Antigens. However, PRV Antigens were detected in only 2% of the monocytes when the cells had first been labelled with monoclonal antibodies against a monocyte marker and subsequently separated on polystyrene bacteriological Petri disches coated with anti-mouse monoclonal antibodies. In subpopulations of unstimulated T- and B-lymphocytes only 0.4 to 0.7% of the cells were found positive by immunofluorescence. Viral Antigens appeared in the cytoplasm and on the cell membrane of monocytes isolated on plasma-coated dishes starting 5 h after inoculation and the expression was found in a maximal number of monocytes, 7 to 8 h after inoculation. The intracellular and extracellular virus progeny titers obtained in monocyte cultures were low, ranging from 10(4.3) to 10(5.2) TClD50 per 10(6) inoculated monocytes. The percentage of inoculated monocytes which produced infectious PRV was 0.1% in two experiments and less than 0.01% in one experiment. The results indicate that although monocytes are the most susceptible subpopulation of unstimulated PBMC to a PRV infection in vitro, replication is clearly restricted. Only a subset of monocytes expresses Viral Antigens and an even smaller fraction produces infectious virus.

Mai Anh Tuan - One of the best experts on this subject based on the ideXlab platform.

  • a novel biosensor based on serum antibody immobilization for rapid detection of Viral Antigens
    Talanta, 2011
    Co-Authors: Nguyen Thi Hanh, Nguyen Thanh Thuy, Pham Van Chung, Mai Anh Tuan

    Abstract In this paper, we represent a label-free biosensor based on immobilization of serum antibodies for rapid detection of Viral Antigens. Human serum containing specific antibodies against Japanese encephalitis virus (JEV) was immobilized on a silanized surface of an interdigitated sensor via protein A/glutaraldehyde for electrical detection of JEV Antigens. The effective immobilization of serum antibodies on the sensor surface was verified by Fourier transform infrared spectrometry and fluorescence microscopy. The signal of the biosensor obtained by the differential voltage converted from the change into non-Faradic impedance resulting from the specific binding of JEV Antigens on the surface of the sensor. The detection analyzed indicates that the detection range of this biosensor is 1–10 μg/ml JEV Antigens, with a detection limit of 0.75 μg/ml and that stable signals are measured in about 20 min. This study presents a useful biosensor with a high selectivity for rapid and simple detection of JEV Antigens, and it also proposes the biosensor as a future diagnostic tool for rapid and direct detection of Viral Antigens in clinical samples for preliminary pathogenic screenings in the case of possible outbreaks.