# Modulation of tumorigenesis by viral exosomes

> **NIH NIH P01** · UNIV OF NORTH CAROLINA CHAPEL HILL · 2024 · $347,154

## Abstract

Project 1
Project Summary Abstract
This is a renewal application of a long-standing P01 grant. Our central hypothesis is that Extracellular
Vesicles(EVs) or “exosomes” reprogram the tumor microenvironment of Kaposi Sarcoma (KS) and that
these processes also affect neighboring EBV infected cells in the lymph nodes. In Sub-Saharan Africa,
where both KSHV and EBV are endemic, approximately 40% of KSHV shedders also shed EBV”. Hence,
we expect that even asymptomatic persons will have viral derived EVs in their circulation. About 1011 /ml
EVs circulate in human plasma, as compared to ~104 infectious KSHV particles during systemic KS. The
endothelial lining of blood and lymphatic vessels are continuously exposed to systemically circulating EVs
and these are the lineage of origin for KS. All KSHV-derived EVs carry all KSHV microRNAs. If only one in
a million plasma EVs are derived from a latent or lytic KSHV-infected cell, more KSHV miRNAs are
transferred by EVs than viral genomes by virions. New this funding period, we will probe the interaction of
KSHV EVs on EBV pathogenesis, image single EV particles, and explore novel ways to repurpose natural
EVs for targeted KS therapy.

## Key facts

- **NIH application ID:** 10852900
- **Project number:** 5P01CA019014-44
- **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:** 2024
- **Award amount:** $347,154
- **Award type:** 5
- **Project period:** 1997-05-01 → 2027-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10852900

## Citation

> US National Institutes of Health, RePORTER application 10852900, Modulation of tumorigenesis by viral exosomes (5P01CA019014-44). Retrieved via AI Analytics 2026-06-16 from https://api.ai-analytics.org/grant/nih/10852900. Licensed CC0.

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