Inflammatory Response to Viral Infections
Viral infections trigger a range of acute and chronic diseases and can predispose individuals to long-term inflammatory conditions. While the immune system is essential for controlling viral pathogens, an overactive or dysregulated response can lead to excessive inflammation, tissue damage, and disease. The IRVIn research group investigates the molecular mechanisms that govern this balance between protective immunity and pathological inflammation.
Keywords
Viral infections; Virus-induced senescence; Interferon-inducible genes; Transplantation; Kidney; Intrinsic immunity; Antivirals.
A key focus of our research is virus-induced senescence (VIS)—a cellular response to viral infection characterized by stable cell cycle arrest and a pro-inflammatory secretory profile known as the senescence-associated secretory phenotype (SASP). They study how VIS contributes to tissue inflammation and dysfunction, using cytomegalovirus (CMV) and BK polyomavirus (BKPyV) as infection models, with particular emphasis on the kidney transplant setting. Their goal is to identify therapeutic strategies to target VIS and restore homeostasis.
In collaboration with the Laboratory of Viral Pathogenesis at the University of Turin, where the IRVIn’s PI is currently based, we also explore how viruses, including herpesviruses and coronaviruses, manipulate post-translational modifications (PTMs) such as citrullination—a process mediated by peptidyl-arginine deiminases (PADs). PAD dysregulation is linked to autoimmunity and cancer, and this line of investigation aims to clarify how viral infections contribute to autoimmune disease and identify novel host-targeting antivirals (HTAs).
A third research area focuses on IFI16, an interferon-inducible protein that functions as a damage-associated molecular pattern (DAMP) when released extracellularly during infection. IFI16 activates TLR4 signaling, amplifying inflammation in synergy with microbial components such as LPS. They seek to elucidate how IFI16 contributes to inflammation in viral, bacterial, and autoimmune contexts.
Together, their work aims to uncover the molecular links between viral infections, inflammation, and immune-mediated disease.
GROUP MEMBERS
Marco De Andrea
Group Leader
Associate Professor
Stefano Garagnani
PhD Student
Federica Castiglioni
PhD Student
Mirco Romanelli
PhD Student
Vincenzo Cantaluppi
Co-leader
(Kidney-transplant unit)
Full Professor
Marisa Gariglio
Co-leader (Virology unit)
Full Professor
Anna Gerbi
PhD Student
For any information, please contact
corefacilities.ipazia@uniupo.it
or segreteria.caad@uniupo.
CAAD
Center for Translational Research on
Autoimmune and Allergic Disease
Centro di Ricerca Traslazionale
sulle Malattie Autoimmuni e Allergiche
Corso Trieste 15/A
Novara – 28100 (ITALY)
Inflammatory Response
to Viral Infections
Viral infections trigger a range of acute and chronic diseases and can predispose individuals to long-term inflammatory conditions. While the immune system is essential for controlling viral pathogens, an overactive or dysregulated response can lead to excessive inflammation, tissue damage, and disease. The IRVIn research group investigates the molecular mechanisms that govern this balance between protective immunity and pathological inflammation.
Keywords
Viral infections; Virus-induced senescence; Interferon-inducible genes; Transplantation; Kidney; Intrinsic immunity; Antivirals.
A key focus of our research is virus-induced senescence (VIS)—a cellular response to viral infection characterized by stable cell cycle arrest and a pro-inflammatory secretory profile known as the senescence-associated secretory phenotype (SASP). They study how VIS contributes to tissue inflammation and dysfunction, using cytomegalovirus (CMV) and BK polyomavirus (BKPyV) as infection models, with particular emphasis on the kidney transplant setting. Their goal is to identify therapeutic strategies to target VIS and restore homeostasis.
In collaboration with the Laboratory of Viral Pathogenesis at the University of Turin, where the IRVIn’s PI is currently based, we also explore how viruses, including herpesviruses and coronaviruses, manipulate post-translational modifications (PTMs) such as citrullination—a process mediated by peptidyl-arginine deiminases (PADs). PAD dysregulation is linked to autoimmunity and cancer, and this line of investigation aims to clarify how viral infections contribute to autoimmune disease and identify novel host-targeting antivirals (HTAs).
A third research area focuses on IFI16, an interferon-inducible protein that functions as a damage-associated molecular pattern (DAMP) when released extracellularly during infection. IFI16 activates TLR4 signaling, amplifying inflammation in synergy with microbial components such as LPS. They seek to elucidate how IFI16 contributes to inflammation in viral, bacterial, and autoimmune contexts.
Together, their work aims to uncover the molecular links between viral infections, inflammation, and immune-mediated disease.
GROUP MEMBERS
Marco De Andrea
Group Leader
Associate Professor
Stefano Garagnani
PhD Student
Federica Castiglioni
PhD Student
Mirco Romanelli
PhD Student
Vincenzo Cantaluppi
Co-leader
(Kidney-transplant unit)
Full Professor
Marisa Gariglio
Co-leader (Virology unit)
Full Professor
Anna Gerbi
PhD Student
For any information, please contact
corefacilities.ipazia@uniupo.it
or segreteria.caad@uniupo.
CAAD
Center for Translational Research on
Autoimmune and Allergic Disease
Centro di Ricerca Traslazionale
sulle Malattie Autoimmuni e Allergiche
Corso Trieste 15/A
Novara – 28100 (ITALY)