# Calcium signaling in Calicivirus infection and replication

> **NIH NIH F31** · BAYLOR COLLEGE OF MEDICINE · 2022 · $46,752

## Abstract

PROJECT SUMMARY/ABSTRACT
Enteric viruses such as human norovirus (HuNoV) and rotavirus (RV) remain the leading causes of acute viral
gastroenteritis, of which there are over 700 million annual cases worldwide. Despite the prevalence of these
enteric pathogens, there are persistent gaps in knowledge in how both viruses disrupt homeostatic
cellular processes to enhance their replication. In addition to sharing clinical manifestations of disease,
members of both Reoviridae and Caliciviridae families are known to dysregulate calcium signaling during the
course of infection through the function of a viral ion channel, or viroporin. RV viroporin-induced calcium
dysregulation has been shown to initiate an ADP-mediated paracrine signaling cascade that ultimately results
in ER calcium release from neighboring uninfected cells, a cellular phenomenon known as intercellular
calcium waves. In addition to proximal cell dysregulation, RV NSP4 viroporin activity initiates a cellular
process known as store-operated calcium entry (SOCE). Preliminary data in the Tulane virus system, a
closely related human norovirus surrogate, has shown both an analogous intercellular calcium signaling
phenotype and the potential to exploit SOCE pathways for enhanced replication. The objective of this
proposal is to characterize the calcium signaling phenotype of Tulane and human norovirus infected cells,
extending these observations to include proximal, uninfected cells, and to determine the role of dysregulated
cellular calcium signaling in viral replication. Aim 1 of this project proposes to characterize aberrant calcium
signaling in infected and proximal, uninfected cells following Tulane and human norovirus infection. Aim 2 will
determine the contributions of store operated calcium entry pathways to virus replication, critically linking
host cell calcium signaling dynamics to viral growth. Unveiling these features of infection will reveal
important parallels in the way that reoviruses and caliciviruses disrupt host cell signaling processes and
may suggest a potentially conserved mechanism of enhanced replication and disease progression in
gut-tropic viruses. Therefore, this proposal will provide critical insight into novel broad-spectrum antiviral
targets.

## Key facts

- **NIH application ID:** 10536331
- **Project number:** 1F31DK132942-01A1
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **Principal Investigator:** Francesca Jean Scribano
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $46,752
- **Award type:** 1
- **Project period:** 2022-07-01 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10536331

## Citation

> US National Institutes of Health, RePORTER application 10536331, Calcium signaling in Calicivirus infection and replication (1F31DK132942-01A1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10536331. Licensed CC0.

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