University of Turin, Italy
Student: Gloria Griffante, Ph.D. fellow
Supervisor: Prof. Santo Landolfo, M.D.
Co-Supervisor: Prof. Marco de Andrea
Human Cytomegalovirus (HCMV) is a widespread β-Herpesvirus carried by 70% up to 90% of the human population. Following primary infection, HCMV establishes a lifelong latency in cells of the myeloid lineage, where reactivation is often driven by inflammation. Autoimmune diseases (AID) are characterized by chronic inflammation due to an abnormal immune response against the body’s own tissue. In genetically predisposed patients, increasing evidence suggests that HCMV is involved in the pathogenesis of AID, but whether it initiates or supports the development of AID is still not known. Although several hypothesis have been postulated, the exact mechanisms HCMV relies on to prime an autoimmune response remain elusive.
Some post-translational modifications (PTM) are known to be inflammation-dependent conditions and their dysregulation has been associated with a spectrum of AIDs, cancer, and neurodegenerative disorders.
Against this background, we aim to characterize PTMs that might be relevant in the etiopathogenesis of AID during infection with HCMV in vitro, using as experimental model Human Foreskin Fibroblasts (HFFs), permissive to Merlin as strain of HCMV.
These findings may shed light on the contribution of infection with HCMV to the pathogenesis of AIDs and provide possible medical interventions in their treatment.