作者: Jennifer L. Craigen , Jane E. Grundy
DOI: 10.1097/00007890-199610270-00014
关键词: Ganciclovir 、 Biology 、 Foscarnet 、 Virus 、 Foscarnet Sodium 、 CD58 、 Virology 、 Cell adhesion molecule 、 Proinflammatory cytokine 、 Immunology 、 Intercellular Adhesion Molecule-1
摘要: Cytomegalovirus (CMV) is a major pathogen in transplant recipients and AIDS patients, the virus may also play role allograft rejection. Previous work from this laboratory demonstrated increased cell surface expression of adhesion molecules ICAM-1 (CD54) LFA-3 (CD58) following CMV infection vitro. We investigated whether induction by was direct viral effect or secondary to cytokine induction. Cytokines known up-regulate ICAM-1, such as TNFalpha IL-1beta, were not detected supernatants infected fibroblasts, neutralizing antibodies against these cytokines did abrogate either CMV. Infected had levels IL-6, IL-8 IFNbeta however, addition recombinant forms affect molecule expression. Neither virus-free nor UV-inactivated up-regulated molecules, demonstrating that requiring infectious virus. Effective antiviral treatment with ganciclovir foscarnet accentuated rather than abrogated up-regulation suggesting immediate early/early gene expression, which blocked treatment, responsible for Thus, despite effective therapy recipient, cells continue provide focus proinflammatory activity, could contribute immunopathology and/or accentuate graft rejection graft-versus-host disease vivo.