Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment
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...
Ausführliche Beschreibung
Autor*in: |
Roeska, Kerstin [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2010 |
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Schlagwörter: |
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Anmerkung: |
© Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 |
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Übergeordnetes Werk: |
Enthalten in: Journal of immune based therapies and vaccines - London : Biomed Central, 2003, 8(2010), 1 vom: 16. Nov. |
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Übergeordnetes Werk: |
volume:8 ; year:2010 ; number:1 ; day:16 ; month:11 |
Links: |
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DOI / URN: |
10.1186/1476-8518-8-6 |
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Katalog-ID: |
SPR029446600 |
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520 | |a 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. | ||
650 | 4 | |a Respiratory Syncytial Virus |7 (dpeaa)DE-He213 | |
650 | 4 | |a Antiviral Activity |7 (dpeaa)DE-He213 | |
650 | 4 | |a Respiratory Virus |7 (dpeaa)DE-He213 | |
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10.1186/1476-8518-8-6 doi (DE-627)SPR029446600 (SPR)1476-8518-8-6-e DE-627 ger DE-627 rakwb eng Roeska, Kerstin verfasserin aut Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 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. Respiratory Syncytial Virus (dpeaa)DE-He213 Antiviral Activity (dpeaa)DE-He213 Respiratory Virus (dpeaa)DE-He213 Antiviral Effect (dpeaa)DE-He213 Test Preparation (dpeaa)DE-He213 Seilheimer, Bernd aut Enthalten in Journal of immune based therapies and vaccines London : Biomed Central, 2003 8(2010), 1 vom: 16. Nov. (DE-627)362770271 (DE-600)2100016-5 1476-8518 nnns volume:8 year:2010 number:1 day:16 month:11 https://dx.doi.org/10.1186/1476-8518-8-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1 16 11 |
spelling |
10.1186/1476-8518-8-6 doi (DE-627)SPR029446600 (SPR)1476-8518-8-6-e DE-627 ger DE-627 rakwb eng Roeska, Kerstin verfasserin aut Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 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. Respiratory Syncytial Virus (dpeaa)DE-He213 Antiviral Activity (dpeaa)DE-He213 Respiratory Virus (dpeaa)DE-He213 Antiviral Effect (dpeaa)DE-He213 Test Preparation (dpeaa)DE-He213 Seilheimer, Bernd aut Enthalten in Journal of immune based therapies and vaccines London : Biomed Central, 2003 8(2010), 1 vom: 16. Nov. (DE-627)362770271 (DE-600)2100016-5 1476-8518 nnns volume:8 year:2010 number:1 day:16 month:11 https://dx.doi.org/10.1186/1476-8518-8-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1 16 11 |
allfields_unstemmed |
10.1186/1476-8518-8-6 doi (DE-627)SPR029446600 (SPR)1476-8518-8-6-e DE-627 ger DE-627 rakwb eng Roeska, Kerstin verfasserin aut Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 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. Respiratory Syncytial Virus (dpeaa)DE-He213 Antiviral Activity (dpeaa)DE-He213 Respiratory Virus (dpeaa)DE-He213 Antiviral Effect (dpeaa)DE-He213 Test Preparation (dpeaa)DE-He213 Seilheimer, Bernd aut Enthalten in Journal of immune based therapies and vaccines London : Biomed Central, 2003 8(2010), 1 vom: 16. Nov. (DE-627)362770271 (DE-600)2100016-5 1476-8518 nnns volume:8 year:2010 number:1 day:16 month:11 https://dx.doi.org/10.1186/1476-8518-8-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1 16 11 |
allfieldsGer |
10.1186/1476-8518-8-6 doi (DE-627)SPR029446600 (SPR)1476-8518-8-6-e DE-627 ger DE-627 rakwb eng Roeska, Kerstin verfasserin aut Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 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. Respiratory Syncytial Virus (dpeaa)DE-He213 Antiviral Activity (dpeaa)DE-He213 Respiratory Virus (dpeaa)DE-He213 Antiviral Effect (dpeaa)DE-He213 Test Preparation (dpeaa)DE-He213 Seilheimer, Bernd aut Enthalten in Journal of immune based therapies and vaccines London : Biomed Central, 2003 8(2010), 1 vom: 16. Nov. (DE-627)362770271 (DE-600)2100016-5 1476-8518 nnns volume:8 year:2010 number:1 day:16 month:11 https://dx.doi.org/10.1186/1476-8518-8-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1 16 11 |
allfieldsSound |
10.1186/1476-8518-8-6 doi (DE-627)SPR029446600 (SPR)1476-8518-8-6-e DE-627 ger DE-627 rakwb eng Roeska, Kerstin verfasserin aut Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 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. Respiratory Syncytial Virus (dpeaa)DE-He213 Antiviral Activity (dpeaa)DE-He213 Respiratory Virus (dpeaa)DE-He213 Antiviral Effect (dpeaa)DE-He213 Test Preparation (dpeaa)DE-He213 Seilheimer, Bernd aut Enthalten in Journal of immune based therapies and vaccines London : Biomed Central, 2003 8(2010), 1 vom: 16. Nov. (DE-627)362770271 (DE-600)2100016-5 1476-8518 nnns volume:8 year:2010 number:1 day:16 month:11 https://dx.doi.org/10.1186/1476-8518-8-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1 16 11 |
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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. 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Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment Respiratory Syncytial Virus (dpeaa)DE-He213 Antiviral Activity (dpeaa)DE-He213 Respiratory Virus (dpeaa)DE-He213 Antiviral Effect (dpeaa)DE-He213 Test Preparation (dpeaa)DE-He213 |
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antiviral activity of $ engystol^{®} $ and gripp-$ heel^{®} $: an in-vitro assessment |
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Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment |
abstract |
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. © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 |
abstractGer |
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. © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 |
abstract_unstemmed |
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. © Roeska and Seilheimer; licensee BioMed Central Ltd. 2010 |
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Antiviral activity of $ Engystol^{®} $ and Gripp-$ Heel^{®} $: an in-vitro assessment |
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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.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Respiratory Syncytial Virus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Antiviral Activity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Respiratory Virus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Antiviral Effect</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Test Preparation</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Seilheimer, Bernd</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of immune based therapies and vaccines</subfield><subfield code="d">London : Biomed Central, 2003</subfield><subfield code="g">8(2010), 1 vom: 16. 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