Immunotherapy With Interferon α11, But Not Interferon Beta, Controls Persistent Retroviral Infection.
Animals
Antiviral Agents
/ pharmacology
Biomarkers
Cell Line
Cytotoxicity, Immunologic
/ drug effects
Disease Management
Disease Models, Animal
Female
Friend murine leukemia virus
/ physiology
Host-Pathogen Interactions
/ immunology
Immunologic Factors
/ pharmacology
Interferon Type I
/ pharmacology
Interferon-alpha
/ pharmacology
Interferon-beta
/ pharmacology
Leukemia Virus, Murine
/ physiology
Lymphocytes
/ immunology
Mice
Retroviridae Infections
/ drug therapy
Treatment Outcome
Viral Load
/ drug effects
Virus Replication
/ drug effects
Friend retrovirus
Type I IFNs
cytotoxic CD8+ T cells
immunotherapy
persistent infection
retroviral infection
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
05
11
2021
accepted:
29
12
2021
entrez:
7
2
2022
pubmed:
8
2
2022
medline:
26
2
2022
Statut:
epublish
Résumé
Type I Interferons (IFNs), including numerous IFNα subtypes and IFNβ, are key molecules during innate and adaptive immune responses against viral infections. These cytokines exert various non-redundant biological activities, although binding to the same receptor. Persistent viral infections are often characterized by increased IFN signatures implicating a potential role of type I IFNs in disease pathogenesis. Using the well-established Friend retrovirus (FV) mouse model, we compared the therapeutic efficacy of IFNα11 and IFNβ in acute and chronic retroviral infection. We observed a strong antiviral activity of both IFNs during acute FV infection, whereas only IFNα11 and not IFNβ could also control persistent FV infection. The therapeutic treatment with IFNα11 induced the expression of antiviral IFN-stimulated genes (ISG) and improved cytotoxic T cell responses. Finally, dysfunctional CD8
Identifiants
pubmed: 35126368
doi: 10.3389/fimmu.2021.809774
pmc: PMC8810532
doi:
Substances chimiques
Antiviral Agents
0
Biomarkers
0
Immunologic Factors
0
Interferon Type I
0
Interferon-alpha
0
Interferon-beta
77238-31-4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
809774Informations de copyright
Copyright © 2022 Schwerdtfeger, Dickow, Schmitz, Francois, Karakoese, Malyshkina, Knuschke, Dittmer and Sutter.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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