Research
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Host antiviral defense mechanisms provide a powerful framework to uncover intrinsic viral vulnerabilities. Upon infection, cells produce interferons (IFNs), powerful antiviral cytokines that induce the expression of hundreds of interferon-stimulated genes (ISGs) and establish a broad antiviral state that limits viral replication and spread. Under this strong selective pressure, RNA viruses have evolved diverse strategies to evade or counteract these defenses.
Our research aims to dissect this dynamic interplay by identifying which ISGs restrict specific viruses, defining their mechanisms of action and cellular context, and determining how viruses overcome these barriers. Ultimately, we seek to reveal exploitable viral weaknesses exposed by the interferon-mediated antiviral response.
Identification of novel antiviral defense mechanisms
We identify and characterize cellular factors that restrict viral replication, focusing primarily on interferon-stimulated genes (ISGs) that target RNA viruses of major public health importance, including HIV-1, influenza viruses, SARS-CoV-2, and mosquito-borne flaviviruses such as dengue, Zika, and West Nile viruses. We investigate the molecular mechanisms underlying their antiviral activity and how these factors interfere with different stages of the viral life cycle.
Viral evasion of innate antiviral immunity
We investigate the strategies viruses use to evade innate antiviral defenses, including mechanisms that counteract interferon responses, circumvent ISG-mediated restriction, or interfere with the recognition of viral infection by host cells. Our research aims to uncover the molecular mechanisms that enable viruses to escape immune control and enhance their replication and transmission.
Innate immunity at the skin-vector interface
We investigate how mosquito-borne viruses interact with the skin, the first site of infection following transmission by an infected mosquito. We study how cutaneous immune defenses, resident cell populations, and mosquito saliva shape early viral replication, modulate innate immune responses, and influence viral dissemination within the host.
Host determinants of viral susceptibility
We investigate how differences in innate antiviral immunity across species shape susceptibility to viral infection. By comparing the antiviral activity of interferon-stimulated genes (ISGs) from different species against the same virus, we aim to identify host factors that determine the outcome of viral infection and understand how these differences influence host range and viral adaptation.
The Nisole Lab
Centre Armand-Frappier Santé Biotechnologie
531, boul. des Prairies
Laval H7V 1B7, Québec, Canada
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