# Project 4 - Study of KSHV Carcinogenesis

> **NIH NIH P01** · UNIV OF NORTH CAROLINA CHAPEL HILL · 2020 · $281,390

## Abstract

Project 4 
Project Summary Abstract 
 Kaposi sarcoma associated herpesvirus (KSHV) reprograms cells upon infection. This reprogramming 
of cell fate furthers lytic viral replication and latent genome persistence. One other outcome of this 
reprogramming is cellular transformation, such that KSHV-infected cells give rise to human cancer. KSHV 
reprograms endothelial cells to adopt a lymphatic phenotype, as opposed to a vascular phenotype. KSHV 
induces hyperplasia of these lymphatic endothelial cells. This eventually leads to complete transformation 
and the emergence of Kaposi sarcoma (KS). KSHV reprograms B cells, though it is unclear exactly which 
subset and what the direct outcome is. Eventually this, too, leads to complete transformation and the 
emergence of signature, KSHV-associated, B cell malignancies, i.e. a subclass of multicentric Castleman's 
disease (MCD) and primary effusion lymphoma (PEL). We hypothesize that this reprogramming is 
mediated, at least in part, by viral microRNAs, some of which are secreted in the form of vesicles. We will 
investigate the function of the viral microRNAs either within the cell or circulating in blood (exosome) in 
culture and in mouse models.

## Key facts

- **NIH application ID:** 9986674
- **Project number:** 5P01CA019014-41
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **Principal Investigator:** Dirk P Dittmer
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $281,390
- **Award type:** 5
- **Project period:** — → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9986674

## Citation

> US National Institutes of Health, RePORTER application 9986674, Project 4 - Study of KSHV Carcinogenesis (5P01CA019014-41). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9986674. Licensed CC0.

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