Original research
Antiviral activity of Engystol® and Gripp-Heel®: an in-vitro assessment
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* Corresponding author: Kerstin Roeska Roeska.kerstin@heel.de
Biologische Heilmittel Heel GmbH, Baden-Baden, Germany
Journal of Immune Based Therapies and Vaccines 2010, 8:6 doi:10.1186/1476-8518-8-6
Published: 16 November 2010Abstract
Background
Infections with respiratory viruses can activate the innate immune response - an important host defence mechanism in the early stage of viral infection. Interferon (IFN) release, triggered by virus infection, is an important factor in establishing an antiviral state, where IFN activation occurs prior to the onset of the adaptive immune response.
The two ultra-low-dose combination medications, Engystol® and Gripp-Heel®, have documented efficacy for the treatment of the respiratory infections. However, the underlying antiviral mechanisms remain elusive.
Methods
It was the goal to investigate whether Engystol® and Gripp-Heel® display antiviral activity in a prophylactic treatment protocol (2, 24 and 48 h pre-incubation) using a plaque reduction assay and whether the medications affect the release of type 1 IFN in virus-susceptible cell lines and human peripheral blood mononuclear cells (PBMCs).
Results
Both medications demonstrate prophylactic effect against viral respiratory virus replication. However, when the incubation was continued for up to 5 days, both medications exhibited a pronounced antiviral effect which was dependent on the pre-incubation time. Moreover, in co-stimulated HeLa cells as well as in activated PBMCs Gripp-Heel® and Engystol® demonstrated an increased type 1 IFN production.
Conclusions
Engystol® and Gripp-Heel® inhibited the replication of a variety of respiratory viruses. Additionally, we showed that pre-incubation affects the magnitude of the inhibitory effect differently for the various tested viruses. Both medications stimulate type 1 IFN release in different cell systems which suggests that their antiviral activity may be mediated possibly via modulation of the antiviral type 1 IFN host response.