Patrizia Caposio
Oregon Health & Science University, OR·Microbiology & Immunology
Human cytomegalovirus (HCMV) is a herpes virus that infects most of the world's population and then persists silently for life, a state called latency. When the immune system is weakened, as in people receiving solid organ or stem cell transplants, the virus can reawaken and cause serious illness and death.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Genetics
- Topics
human cytomegalovirus
herpesvirus
viral latency
- Grants
- 2 known grants, through Jul 2027
What they work on
- Define and functionally characterize the UL8 interactome during HCMV infection, building on proximity-sensor results that linked the viral protein pUL8 to the RhoA, Wnt and EGFR signaling pathways.
- Dissect the host cell signaling shaped jointly by the viral proteins pUL7 and pUL8, including non-canonical Wnt signaling via RhoA, and test how it controls viral latency and reactivation.
- Investigate how UL7, UL8 and HCMV microRNAs such as miR-UL112-3p and miR-US5-1 inactivate FOXO transcription factors, and whether this protects infected CD34+ hematopoietic progenitor cells from apoptosis and promotes latency.
- Provide and standardize the humanized huNSG mouse platform, the only small animal model supporting HCMV latency and reactivation, so viral growth and dissemination of mutants and treatments can be compared quantitatively across program projects.
More about the research
One of its hiding places is CD34+ hematopoietic progenitor cells, the bone-marrow cells that give rise to blood cells. This work asks how specific viral genes rewire the signaling pathways of infected cells to control whether the virus stays dormant or reactivates, and it supports a program project with a shared animal-model resource.
Why it matters
Cytomegalovirus reactivation remains a major cause of illness and death in solid organ and stem cell transplant recipients. Pinpointing the viral genes and host signaling pathways, such as Wnt, RhoA, EGFR and FOXO, that decide whether the virus stays latent or reawakens could identify targets for drugs that keep the virus dormant, and the humanized mouse platform offers a way to test such interventions in a system that supports the full viral life cycle.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
William Britt
University of Alabama at Birmingham, AL·Microbiology & Immunology
Define how the essential envelope glycoprotein complex gM/gN interacts with membrane-associated outer tegument proteins to drive envelopment of human cytomegalovirus in the cell's assembly compartment.
Angus C Wilson
New York University, NY·Microbiology & Immunology
Identify the viral reactivation signature that neurons recognize when latent HSV-1 reawakens, using cultured primary neurons as a model of latency and reactivation together with single-cell technologies.
Donna Neumann
University of Wisconsin-Madison, WI·Microbiology & Immunology
Define how chromatin insulators in the HSV-1 genome form loops that silence viral genes during latency, using human neurons and Chromosome Conformation Capture circular sequencing (4C-seq).
The school
Oregon Health & Science University: 24 labs on PI Pages, $545M a year on research, 54 research doctorates a year.
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