Viral infection in the context of regulation of interferon (IFN) signaling

The first line of antiviral defence is governed by innate immune responses. After recognition of a virus by pathogen recognition receptors (PRRs), a signalling cascade is triggered, resulting in the expression of inflammatory cytokines, such as type I interferon (IFN). IFN induces the expression of hundreds of IFN-stimulated genes (ISGs) that execute direct antiviral actions. Interferon induced transmembrane proteins (IFITMs) are important antiviral factors induced by IFN signalling. The immune-related IFITM1, IFITM2, and IFITM3 are capable of attenuating the entry of a wide range of viruses.

We investigate antiviral properties of interferons and IFITM proteins in several virus models, including hepatitis C virus (HCV), tick-borne encephalitis virus (TBEV) and coronavirus SARS-CoV-2. We described the role of IFITM proteins in the inhibition of TBEV infection and virus-mediated cell death. Interestingly, our data suggests that TBEV cell-to-cell spread may be less prone to both IFN- and IFITM-mediated suppression, potentially facilitating escape from IFITM-mediated immunity (Chmielewska, 2022).

For research of SARS-CoV-2 entry we use pseudoparticles – a convenient and safe model based on pseudotyped lentiviruseses (Chmielewska, 2021).

Chmielewska, AM, et al. „Immune response against SARS-CoV-2 variants: the role of neutralization assays.” npj Vaccines 6.1 (2021): 1-8.

Chmielewska, AM., et al. „The role of IFITM proteins in tick-borne encephalitis virus infection.” Journal of Virology (2022): 96: e01130-21