Language
English
Publication Date
1-16-2024
Journal
mBio
DOI
10.1128/mbio.02145-23
PMID
38112482
PMCID
PMC10790754
PubMedCentral® Posted Date
12-19-2023
PubMedCentral® Full Text Version
Post-print
Abstract
Many viruses exploit host Ca2+ signaling to facilitate their replication; however, little is known about how Ca2+ signals from different host and viral channels contribute to the overall dysregulation of Ca2+ signaling or promote virus replication. Using cells lacking IP3R, a host ER Ca2+ channel, we delineated intracellular Ca2+ signals within virus-infected cells and intercellular Ca2+ waves (ICWs), which increased Ca2+ signaling in neighboring, uninfected cells. In infected cells, IP3R was dispensable for rotavirus-induced Ca2+ signaling and replication, suggesting the rotavirus NSP4 viroporin supplies these signals. However, IP3R-mediated ICWs increase rotavirus replication kinetics and spread, indicating that the Ca2+ signals from the ICWs may prime nearby uninfected cells to better support virus replication upon eventual infection. This "pre-emptive priming" of uninfected cells by exploiting host intercellular pathways in the vicinity of virus-infected cells represents a novel mechanism for viral reprogramming of the host to gain a replication advantage.
Keywords
Endoplasmic Reticulum, Host Microbial Interactions, Rotavirus, Signal Transduction, Viral Nonstructural Proteins, Humans, Calcium Signaling, Inositol 1, 4, 5-Trisphosphate Receptors, rotavirus, calcium signaling, replication, purinergic signaling, live imaging
Published Open-Access
yes
Recommended Citation
Perry, Jacob L; Scribano, Francesca J; Gebert, John T; et al., "Host IP3R Channels Are Dispensable for Rotavirus Ca2+ Signaling but Critical for Intercellular Ca2+ Waves That Prime Uninfected Cells for Rapid Virus Spread" (2024). Faculty, Staff and Students Publications. 8093.
https://digitalcommons.library.tmc.edu/baylor_docs/8093