The Roles of Type I Interferons in Viral Coinfection: Immune Cell Recruitment and Virus Inhibition
Additional Funding Sources
The project described was supported by the Research Experience for Undergraduates Program Site: Molecular and organismal evolution at the University of Idaho under Award No. 1757826.
Presentation Date
7-2019
Abstract
Previous studies have discovered that respiratory viral coinfections by influenza A virus (PR8) and rhinovirus (RV1B) reduces disease severity compared to PR8 infection in mouse models. When mice are given RV1B two days before PR8, the severity of PR8 induced disease is reduced. This reduction in disease severity is dependent upon type I IFN signaling, which induces antiviral immune responses and limits viral replication. Our goal is to determine which of these roles is important for RV-mediated protection by studying IFN inhibition in mice coinfected with RV1B and PR8. To study the role of IFN in inducing an immune response, we quantified cell populations in the airways of coinfected mice. Bronchoalveolar lavage (BAL) cells obtained from infected mice samples were stained using Hema 3 staining protocol to differentiate between the recruitment of immune cells such as macrophages, lymphocytes and neutrophils. To study the role of IFN in reducing viral replication, we quantified viral titers in lungs of coinfected mice by performing 50% tissue culture infectious dose (TCID50) assays. Coinfected mice inoculated with the control antibody presented lower virus titers as opposed to mice that were IFN inhibited; IFN inhibition yields increased virus titer. Therefore, when IFN is working normally viral replication is limited. This confirms the necessity of type I IFN signaling to reduce disease severity in RV1B/PR8 coinfections.
The Roles of Type I Interferons in Viral Coinfection: Immune Cell Recruitment and Virus Inhibition
Previous studies have discovered that respiratory viral coinfections by influenza A virus (PR8) and rhinovirus (RV1B) reduces disease severity compared to PR8 infection in mouse models. When mice are given RV1B two days before PR8, the severity of PR8 induced disease is reduced. This reduction in disease severity is dependent upon type I IFN signaling, which induces antiviral immune responses and limits viral replication. Our goal is to determine which of these roles is important for RV-mediated protection by studying IFN inhibition in mice coinfected with RV1B and PR8. To study the role of IFN in inducing an immune response, we quantified cell populations in the airways of coinfected mice. Bronchoalveolar lavage (BAL) cells obtained from infected mice samples were stained using Hema 3 staining protocol to differentiate between the recruitment of immune cells such as macrophages, lymphocytes and neutrophils. To study the role of IFN in reducing viral replication, we quantified viral titers in lungs of coinfected mice by performing 50% tissue culture infectious dose (TCID50) assays. Coinfected mice inoculated with the control antibody presented lower virus titers as opposed to mice that were IFN inhibited; IFN inhibition yields increased virus titer. Therefore, when IFN is working normally viral replication is limited. This confirms the necessity of type I IFN signaling to reduce disease severity in RV1B/PR8 coinfections.
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