Combination therapy of rabies-infected mice with inhibitors of pro-inflammatory host response, antiviral compounds and human rabies immunoglobulin

Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different comb...

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Vydané v:	Vaccine Ročník 37; číslo 33; s. 4724 - 4735
Hlavní autori:	Marosi, András, Dufkova, Lucie, Forró, Barbara, Felde, Orsolya, Erdélyi, Károly, Širmarová, Jana, Palus, Martin, Hönig, Václav, Salát, Jiří, Tikos, Réka, Gyuranecz, Miklós, Růžek, Daniel, Martina, Byron, Koraka, Penelope, Osterhaus, Albert D.M.E., Bakonyi, Tamás
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Netherlands Elsevier Ltd 02.08.2019 Elsevier Limited
Predmet:	Allergy and Immunology animal models Animals Antibodies antiviral agents Antiviral drugs Bats Blood-brain barrier Brain research Cascades Caspase Caspase-1 Central nervous system Combination Combination therapy Cytokines Disease Encephalitis enzyme inhibitors Experiments Exposure Fatalities Food chains HRIG humans Immune system Immunoglobulins Immunology Immunomodulation Immunotherapy Infections Inflammation Infliximab Inhibitor drugs Inhibitors Interferon interferons Kinases Lasionycteris noctivagans lethal dose 50 Lyssavirus Mannitol mice Monoclonal antibodies necrosis neoplasms Pathogenesis Rabies Rabies lyssavirus Rabies virus Ribavirin Sorafenib Survival survival rate Targeted cancer therapy therapeutics TNF inhibitors Toxicity tumor necrosis factor-alpha Tumor necrosis factor-TNF Tumor necrosis factor-α Tumors vaccines viral load virus replication Viruses St Louis Missouri United States > US Czech Republic HRIG Infliximab Rabies virus Survival Combination Sorafenib
ISSN:	0264-410X, 1873-2518, 1873-2518
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Abstract	Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different combinations of therapeutics were tested to evaluate their effect on survival in rabies-infected mice, as well as on viral load in the CNS. C57Bl/6 mice were infected with Silver-haired bat rabies virus (SHBRV)-18 at virus dose approaching LD50 and LD100. In one experimental group daily treatments were initiated 4 h before-, in other groups 48 or 96 h after challenge. In the first experiment therapeutic combination contained inhibitors of tumour necrosis factor-α (infliximab), caspase-1 (Ac-YVAD-cmk), and a multikinase inhibitor (sorafenib). In the treated groups there was a notable but not significant increase of survival compared to the virus infected, non-treated mice. The addition of human rabies immunoglobulins (HRIG) to the combination in the second experiment almost completely prevented mortality in the pre-exposure treatment group along with a significant reduction of viral titres in the CNS. Post-exposure treatments also greatly improved survival rates. As part of the combination with immunomodulatory compounds, HRIG had a higher impact on survival than alone. In the third experiment the combination was further supplemented with type-I interferons, ribavirin and favipiravir (T-705). As a blood-brain barrier opener, mannitol was also administered. This treatment was unable to prevent lethal consequences of SHBRV-18 infection; furthermore, it caused toxicity in treated mice, presumably due to interaction among the components. In all experiments, viral loads in the CNS were similar in mice that succumbed to rabies regardless of treatment. According to the findings, inhibitors of detrimental host response to rabies combined with antibodies can be considered among the possible therapeutic and post-exposure options in human rabies cases.
AbstractList	Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different combinations of therapeutics were tested to evaluate their effect on survival in rabies-infected mice, as well as on viral load in the CNS. C57Bl/6 mice were infected with Silver-haired bat rabies virus (SHBRV)-18 at virus dose approaching LD50 and LD100. In one experimental group daily treatments were initiated 4 h before-, in other groups 48 or 96 h after challenge. In the first experiment therapeutic combination contained inhibitors of tumour necrosis factor-α (infliximab), caspase-1 (Ac-YVAD-cmk), and a multikinase inhibitor (sorafenib). In the treated groups there was a notable but not significant increase of survival compared to the virus infected, non-treated mice. The addition of human rabies immunoglobulins (HRIG) to the combination in the second experiment almost completely prevented mortality in the pre-exposure treatment group along with a significant reduction of viral titres in the CNS. Post-exposure treatments also greatly improved survival rates. As part of the combination with immunomodulatory compounds, HRIG had a higher impact on survival than alone. In the third experiment the combination was further supplemented with type-I interferons, ribavirin and favipiravir (T-705). As a blood-brain barrier opener, mannitol was also administered. This treatment was unable to prevent lethal consequences of SHBRV-18 infection; furthermore, it caused toxicity in treated mice, presumably due to interaction among the components. In all experiments, viral loads in the CNS were similar in mice that succumbed to rabies regardless of treatment. According to the findings, inhibitors of detrimental host response to rabies combined with antibodies can be considered among the possible therapeutic and post-exposure options in human rabies cases. AbstractRecent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different combinations of therapeutics were tested to evaluate their effect on survival in rabies-infected mice, as well as on viral load in the CNS. C57Bl/6 mice were infected with Silver-haired bat rabies virus (SHBRV)-18 at virus dose approaching LD 50 and LD 100. In one experimental group daily treatments were initiated 4 h before-, in other groups 48 or 96 h after challenge. In the first experiment therapeutic combination contained inhibitors of tumour necrosis factor-α (infliximab), caspase-1 (Ac-YVAD-cmk), and a multikinase inhibitor (sorafenib). In the treated groups there was a notable but not significant increase of survival compared to the virus infected, non-treated mice. The addition of human rabies immunoglobulins (HRIG) to the combination in the second experiment almost completely prevented mortality in the pre-exposure treatment group along with a significant reduction of viral titres in the CNS. Post-exposure treatments also greatly improved survival rates. As part of the combination with immunomodulatory compounds, HRIG had a higher impact on survival than alone. In the third experiment the combination was further supplemented with type-I interferons, ribavirin and favipiravir (T-705). As a blood-brain barrier opener, mannitol was also administered. This treatment was unable to prevent lethal consequences of SHBRV-18 infection; furthermore, it caused toxicity in treated mice, presumably due to interaction among the components. In all experiments, viral loads in the CNS were similar in mice that succumbed to rabies regardless of treatment. According to the findings, inhibitors of detrimental host response to rabies combined with antibodies can be considered among the possible therapeutic and post-exposure options in human rabies cases. Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different combinations of therapeutics were tested to evaluate their effect on survival in rabies-infected mice, as well as on viral load in the CNS. C57Bl/6 mice were infected with Silver-haired bat rabies virus (SHBRV)-18 at virus dose approaching LD and LD . In one experimental group daily treatments were initiated 4 h before-, in other groups 48 or 96 h after challenge. In the first experiment therapeutic combination contained inhibitors of tumour necrosis factor-α (infliximab), caspase-1 (Ac-YVAD-cmk), and a multikinase inhibitor (sorafenib). In the treated groups there was a notable but not significant increase of survival compared to the virus infected, non-treated mice. The addition of human rabies immunoglobulins (HRIG) to the combination in the second experiment almost completely prevented mortality in the pre-exposure treatment group along with a significant reduction of viral titres in the CNS. Post-exposure treatments also greatly improved survival rates. As part of the combination with immunomodulatory compounds, HRIG had a higher impact on survival than alone. In the third experiment the combination was further supplemented with type-I interferons, ribavirin and favipiravir (T-705). As a blood-brain barrier opener, mannitol was also administered. This treatment was unable to prevent lethal consequences of SHBRV-18 infection; furthermore, it caused toxicity in treated mice, presumably due to interaction among the components. In all experiments, viral loads in the CNS were similar in mice that succumbed to rabies regardless of treatment. According to the findings, inhibitors of detrimental host response to rabies combined with antibodies can be considered among the possible therapeutic and post-exposure options in human rabies cases. Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different combinations of therapeutics were tested to evaluate their effect on survival in rabies-infected mice, as well as on viral load in the CNS. C57Bl/6 mice were infected with Silver-haired bat rabies virus (SHBRV)-18 at virus dose approaching LD50 and LD100. In one experimental group daily treatments were initiated 4 h before-, in other groups 48 or 96 h after challenge. In the first experiment therapeutic combination contained inhibitors of tumour necrosis factor-α (infliximab), caspase-1 (Ac-YVAD-cmk), and a multikinase inhibitor (sorafenib). In the treated groups there was a notable but not significant increase of survival compared to the virus infected, non-treated mice. The addition of human rabies immunoglobulins (HRIG) to the combination in the second experiment almost completely prevented mortality in the pre-exposure treatment group along with a significant reduction of viral titres in the CNS. Post-exposure treatments also greatly improved survival rates. As part of the combination with immunomodulatory compounds, HRIG had a higher impact on survival than alone. In the third experiment the combination was further supplemented with type-I interferons, ribavirin and favipiravir (T-705). As a blood-brain barrier opener, mannitol was also administered. This treatment was unable to prevent lethal consequences of SHBRV-18 infection; furthermore, it caused toxicity in treated mice, presumably due to interaction among the components. In all experiments, viral loads in the CNS were similar in mice that succumbed to rabies regardless of treatment. According to the findings, inhibitors of detrimental host response to rabies combined with antibodies can be considered among the possible therapeutic and post-exposure options in human rabies cases.Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can enhance survival in mouse model and that certain antiviral compounds interfere with rabies virus replication in vitro. In this study different combinations of therapeutics were tested to evaluate their effect on survival in rabies-infected mice, as well as on viral load in the CNS. C57Bl/6 mice were infected with Silver-haired bat rabies virus (SHBRV)-18 at virus dose approaching LD50 and LD100. In one experimental group daily treatments were initiated 4 h before-, in other groups 48 or 96 h after challenge. In the first experiment therapeutic combination contained inhibitors of tumour necrosis factor-α (infliximab), caspase-1 (Ac-YVAD-cmk), and a multikinase inhibitor (sorafenib). In the treated groups there was a notable but not significant increase of survival compared to the virus infected, non-treated mice. The addition of human rabies immunoglobulins (HRIG) to the combination in the second experiment almost completely prevented mortality in the pre-exposure treatment group along with a significant reduction of viral titres in the CNS. Post-exposure treatments also greatly improved survival rates. As part of the combination with immunomodulatory compounds, HRIG had a higher impact on survival than alone. In the third experiment the combination was further supplemented with type-I interferons, ribavirin and favipiravir (T-705). As a blood-brain barrier opener, mannitol was also administered. This treatment was unable to prevent lethal consequences of SHBRV-18 infection; furthermore, it caused toxicity in treated mice, presumably due to interaction among the components. In all experiments, viral loads in the CNS were similar in mice that succumbed to rabies regardless of treatment. According to the findings, inhibitors of detrimental host response to rabies combined with antibodies can be considered among the possible therapeutic and post-exposure options in human rabies cases.
Author	Erdélyi, Károly Koraka, Penelope Osterhaus, Albert D.M.E. Dufkova, Lucie Felde, Orsolya Širmarová, Jana Tikos, Réka Palus, Martin Růžek, Daniel Hönig, Václav Salát, Jiří Martina, Byron Bakonyi, Tamás Marosi, András Gyuranecz, Miklós Forró, Barbara
Author_xml	– sequence: 1 givenname: András surname: Marosi fullname: Marosi, András email: Marosi.Andras@univet.hu organization: Department of Microbiology and Infectious Diseases, University of Veterinary Medicine, Hungária krt. 23 – 25, 1143 Budapest, Hungary – sequence: 2 givenname: Lucie surname: Dufkova fullname: Dufkova, Lucie organization: Department of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100 Brno, Czech Republic – sequence: 3 givenname: Barbara surname: Forró fullname: Forró, Barbara organization: Institute for Veterinary Medical Research, Centre for Agricultural Research, Hungarian Academy of Sciences, Hungária krt. 21, 1143 Budapest, Hungary – sequence: 4 givenname: Orsolya surname: Felde fullname: Felde, Orsolya organization: Institute for Veterinary Medical Research, Centre for Agricultural Research, Hungarian Academy of Sciences, Hungária krt. 21, 1143 Budapest, Hungary – sequence: 5 givenname: Károly surname: Erdélyi fullname: Erdélyi, Károly organization: National Food Chain Safety Office, Veterinary Diagnostic Directorate, Tábornok u. 2, 1149 Budapest, Hungary – sequence: 6 givenname: Jana surname: Širmarová fullname: Širmarová, Jana organization: Department of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100 Brno, Czech Republic – sequence: 7 givenname: Martin surname: Palus fullname: Palus, Martin organization: Department of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100 Brno, Czech Republic – sequence: 8 givenname: Václav surname: Hönig fullname: Hönig, Václav organization: Department of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100 Brno, Czech Republic – sequence: 9 givenname: Jiří surname: Salát fullname: Salát, Jiří organization: Department of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100 Brno, Czech Republic – sequence: 10 givenname: Réka surname: Tikos fullname: Tikos, Réka organization: Department of Microbiology and Infectious Diseases, University of Veterinary Medicine, Hungária krt. 23 – 25, 1143 Budapest, Hungary – sequence: 11 givenname: Miklós surname: Gyuranecz fullname: Gyuranecz, Miklós organization: Institute for Veterinary Medical Research, Centre for Agricultural Research, Hungarian Academy of Sciences, Hungária krt. 21, 1143 Budapest, Hungary – sequence: 12 givenname: Daniel surname: Růžek fullname: Růžek, Daniel organization: Department of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100 Brno, Czech Republic – sequence: 13 givenname: Byron surname: Martina fullname: Martina, Byron organization: Artemis One Health Research Foundation, Delft, The Netherlands – sequence: 14 givenname: Penelope surname: Koraka fullname: Koraka, Penelope organization: Viroscience Lab, Erasmus Medical Centre, Wytemaweg 80 3015CN, Rotterdam, The Netherlands – sequence: 15 givenname: Albert D.M.E. surname: Osterhaus fullname: Osterhaus, Albert D.M.E. organization: Artemis One Health Research Foundation, Delft, The Netherlands – sequence: 16 givenname: Tamás surname: Bakonyi fullname: Bakonyi, Tamás organization: Department of Microbiology and Infectious Diseases, University of Veterinary Medicine, Hungária krt. 23 – 25, 1143 Budapest, Hungary
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43 start-page: 2786 year: 2005 ident: 10.1016/j.vaccine.2018.05.066_b0165 article-title: Development of a real-time, TaqMan reverse transcription-PCR assay for detection and differentiation of lyssavirus genotypes 1, 5, and 6 publication-title: J Clin Microbiol doi: 10.1128/JCM.43.6.2786-2792.2005 – volume: 14 start-page: 119 year: 2008 ident: 10.1016/j.vaccine.2018.05.066_b0215 article-title: Furious and paralytic rabies of canine origin: neuroimaging with virological and cytokine studies publication-title: J Neurovirol doi: 10.1080/13550280701883857 – volume: 26 start-page: 163 year: 2015 ident: 10.1016/j.vaccine.2018.05.066_b0065 article-title: Exogenous interferon prolongs survival of rabies infected mice publication-title: Virus Dis – volume: 81 start-page: 7993 year: 2007 ident: 10.1016/j.vaccine.2018.05.066_b0105 article-title: Lethal silver-haired bat rabies virus infection can be prevented by opening the blood-brain barrier publication-title: J Virol doi: 10.1128/JVI.00710-07 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Snippet	Recent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS) can... AbstractRecent studies demonstrated that inhibitors of pro-inflammatory molecular cascades triggered by rabies infection in the central nervous system (CNS)...
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SubjectTerms	Allergy and Immunology animal models Animals Antibodies antiviral agents Antiviral drugs Bats Blood-brain barrier Brain research Cascades Caspase Caspase-1 Central nervous system Combination Combination therapy Cytokines Disease Encephalitis enzyme inhibitors Experiments Exposure Fatalities Food chains HRIG humans Immune system Immunoglobulins Immunology Immunomodulation Immunotherapy Infections Inflammation Infliximab Inhibitor drugs Inhibitors Interferon interferons Kinases Lasionycteris noctivagans lethal dose 50 Lyssavirus Mannitol mice Monoclonal antibodies necrosis neoplasms Pathogenesis Rabies Rabies lyssavirus Rabies virus Ribavirin Sorafenib Survival survival rate Targeted cancer therapy therapeutics TNF inhibitors Toxicity tumor necrosis factor-alpha Tumor necrosis factor-TNF Tumor necrosis factor-α Tumors vaccines viral load virus replication Viruses
Title	Combination therapy of rabies-infected mice with inhibitors of pro-inflammatory host response, antiviral compounds and human rabies immunoglobulin
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