# Immunometabolic regulation of enteric viral infection > **NIH NIH F31** · WASHINGTON UNIVERSITY · 2024 · $35,482 ## Abstract Project Summary/Abstract Obesity is a global health concern as it is a risk factor for several of the leading causes of death such as heart disease, kidney disease, and type 2 diabetes. Obesity drives dysregulated inflammation, which has been shown to be a risk factor for increased morbidity and mortality in certain pulmonary viral infections such as influenza A and SARS-CoV-2. Yet it is unknown how diet induced obesity (DIO)-associated inflammation impacts the immune response to viruses that infect the gastrointestinal tract. It has been well-established that DIO drives dynamic changes in intestinal immunity, including alterations in interferon gamma and IgA production. Specifically, DIO induces skewing towards type I immunity, which is protective against intracellular pathogens like viruses. Norovirus (NV) is one of the most prevalent gut viruses, as it is the number one cause of acute viral gastroenteritis worldwide. However, the effects of DIO induced type 1, or anti-viral, skewing on immunity to NV have yet to be elucidated. My new preliminary data indicate that mice placed on a high fat diet (HFD) prior to infection with persistent murine NV (MNV) strain CR6 clear the infection in just 28 days, while mice fed normal chow (NC) remain persistently infected. This clearance appears to be independent of MNV receptor expression and viral tropism. Additionally, we found that obese patients with symptoms of gastroenteritis are less likely to test positive for NV than symptomatic lean controls, which further supports our mouse model indicating a HFD is protective against NV infection in both mice and humans. We also observe changes in the humoral response to MNV in our mouse model, as HFD-fed mice have an increase in serum MNV specific IgG and decrease in both serum and secretory MNV specific IgA in comparison to infected mice on NC. These findings lead to my central hypothesis that obesity drives alterations in intestinal immunity that promote an anti-viral state and protect against norovirus infection. I have proposed two aims to address this hypothesis. In Aim 1, I will elucidate the role of DIO-mediated changes in B and T cell responses in protection against MNV infection. In Aim 2, I will determine the role of interferon signaling in DIO-associated clearance of MNV. This novel work will advance our understanding of the relationship between diet and immunity to NV infection. This work also has translational potential as it may provide insight to treatment for NV, as there is currently no vaccine for this common virus. ## Key facts - **NIH application ID:** 10901522 - **Project number:** 1F31AI183832-01 - **Recipient organization:** WASHINGTON UNIVERSITY - **Principal Investigator:** Jasmine Wright - **Activity code:** F31 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 2024 - **Award amount:** $35,482 - **Award type:** 1 - **Project period:** 2024-08-01 → 2026-07-31 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/10901522 ## Citation > US National Institutes of Health, RePORTER application 10901522, Immunometabolic regulation of enteric viral infection (1F31AI183832-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10901522. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*