Publications by authors named "Giovanni Crivicich"
Article Synopsis
- Gain-of-function mutations in STING lead to STING-associated vasculopathy with onset in infancy (SAVI), which is marked by systemic inflammation, skin issues, and lung disease.
- A new STING variant (F269S) was discovered in a SAVI patient; this variant causes abnormal activation of immune pathways and an increase in circulating naïve T cells in the patient's bone marrow.
- The STING F269S variant enhances protein signaling and protects against viral infections but disrupts immune function, contributing to inflammation and damage in endothelial cells, thereby linking immune and lung diseases.
The interferon-induced transmembrane proteins (IFITM) are implicated in several biological processes, including antiviral defense, but their modes of action remain debated. Here, taking advantage of pseudotyped viral entry assays and replicating viruses, we uncover the requirement of host co-factors for endosomal antiviral inhibition through high-throughput proteomics and lipidomics in cellular models of IFITM restriction. Unlike plasma membrane (PM)-localized IFITM restriction that targets infectious SARS-CoV2 and other PM-fusing viral envelopes, inhibition of endosomal viral entry depends on lysines within the conserved IFITM intracellular loop.
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