# Genetic architecture of host response to tickborne disease in Peromyscus leucopus

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA-IRVINE · 2022 · $235,007

## Abstract

PROJECT SUMMARY (Administrative supplement)
 For the administrative supplement a fourth specific aim is added to the project: Functional
consequences of naturally-occurring genetic variants for responses of Peromyscus to Borreliella burgdorferi.
The parent project principally entails forward genetics approaches to identify the traits and ultimately
characterize the mechanisms for the white-footed deermouse's capacity to serve as a major reservoir for
several zoonotic agents, including the cause of Lyme disease, while maintaining fitness in the presence of
persistent infection. In the course of the project to date, we have made discoveries that justify a new line of
investigation that takes a reverse genetics approach. The discoveries represent both innate and aquired
immunity in Peromyscus immunity: (1) Structural variants in the Nos2 gene of P. leucopus populations that
could account for an attenuated production of nitric oxide and reactive nitrogen species during infection. (2)
Evidence in Peromyscus of an inactivated Fcgr1 gene that encodes the high-affinity IgG Fc receptor protein
(FcγR1 or CD64) of macrophages and other phagocytes. (3) An association between a MHC class II gene
and the antibody response to the OspA protein of Borreliella burgdorferi. The new aim comprises four sub-
aims: (A) host response phenotypes of variants of the Nos2 gene and its 3’-UTR in P. leucopus, (B) functional
effects of mutant Fcgr1 of Peromyscus, (C) variation of MHC II genes and antibodies to OspA after
immunization, and (D) high-throughput discovery and annotation of structural variants segregating in the
colony. The new research supported by this administrative supplement is anticipated to have both basic
research and translational research and application impacts. The findings may also guide clinical research on
persisting illness in patients with Lyme disease and other tickborne infections.

## Key facts

- **NIH application ID:** 10625699
- **Project number:** 3R01AI157513-03S1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA-IRVINE
- **Principal Investigator:** Alan G. Barbour
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $235,007
- **Award type:** 3
- **Project period:** 2020-09-17 → 2025-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10625699

## Citation

> US National Institutes of Health, RePORTER application 10625699, Genetic architecture of host response to tickborne disease in Peromyscus leucopus (3R01AI157513-03S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10625699. Licensed CC0.

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