OBJECTIVES: To study the effects of the homeopathic preparation Engystol (Biologische Heilmittel HEEL GmbH, Baden-Baden, Germany) on a panel [corrected] of human pathogenic viruses in vitro. DESIGN: The effects of Engystol were studied using plaque-reduction assays and virus titration assays, and by quantification of newly synthesized viral proteins in virus-specific enzyme-linked immunoabsorbent assays (ELISAs). SUBJECTS: The DNA viruses Adeno 5 and herpes simplex type 1 (HSV-1), the RNA virus respiratory syncytial virus (RSV), and human rhinovirus (HRV). RESULTS: A 73% reduction of Adeno 5 specific proteins and an 80% reduction in HSV-1 specific proteins were observed in ELISAs of virus-infected cells treated with Engystol after infection. The effects appeared to be dose-dependent. With these viruses, similar results were observed in titration assays of viral offspring from cells treated with Engystol. Pretreatment of adenovirus with Engystol did not inhibit the infectivity of the virus suspension and no Engystol-induced stimulation of interferon-alpha could be observed. Plaque-reduction assays with the RNA viruses, RSV and HRV, showed reductions in infectivity by 37% (RSV) and 20% (HRV), respectively. CONCLUSIONS: The results indicate antiviral activity of Engystol independent of the activation of the cellular interferon system.
OBJECTIVES: To study the effects of the homeopathic preparation Engystol (Biologische Heilmittel HEEL GmbH, Baden-Baden, Germany) on a panel [corrected] of human pathogenic viruses in vitro. DESIGN: The effects of Engystol were studied using plaque-reduction assays and virus titration assays, and by quantification of newly synthesized viral proteins in virus-specific enzyme-linked immunoabsorbent assays (ELISAs). SUBJECTS: The DNA viruses Adeno 5 and herpes simplex type 1 (HSV-1), the RNA virus respiratory syncytial virus (RSV), and human rhinovirus (HRV). RESULTS: A 73% reduction of Adeno 5 specific proteins and an 80% reduction in HSV-1 specific proteins were observed in ELISAs of virus-infected cells treated with Engystol after infection. The effects appeared to be dose-dependent. With these viruses, similar results were observed in titration assays of viral offspring from cells treated with Engystol. Pretreatment of adenovirus with Engystol did not inhibit the infectivity of the virus suspension and no Engystol-induced stimulation of interferon-alpha could be observed. Plaque-reduction assays with the RNA viruses, RSV and HRV, showed reductions in infectivity by 37% (RSV) and 20% (HRV), respectively. CONCLUSIONS: The results indicate antiviral activity of Engystol independent of the activation of the cellular interferon system.