Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

4.9K
Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
4.9K
Viral Recombination00:57

Viral Recombination

23.2K
Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
23.2K
Infection01:20

Infection

7.0K
When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
7.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Subtype-specific functions of basal IFNλs.

Journal of virology·2026
Same author

Assessment of Epithelial Barrier Integrity by TEER and FITC-Dextran Permeability Assays.

Bio-protocol·2026
Same author

Stage-specific regulation of KSHV infection by HIF-1α.

Journal of virology·2026
Same author

The vaginal microbiome, papillomavirus infection, and cervical cancer: established associations in search of model systems and mechanistic answers.

mBio·2026
Same author

Basal IFNλ2/3 signaling is required for ISG expression and viral control in human intestinal epithelial cells.

PLoS pathogens·2026
Same author

Hypoxia Affects Stem Cell Fate in Patient-Derived Ileum Enteroids in a HIF-1α-Dependent Manner.

Cells·2026

Related Experiment Video

Updated: May 26, 2025

Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
10:49

Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus

Published on: January 28, 2019

8.5K

Rotavirus Spreads in a Spatially Controlled Manner.

Gianna V Passarelli1, Patricio Doldan2, Camila Metz-Zumaran1,2

  • 1Department of Molecular Genetics and Microbiology, College of Medicine, University of Florida, Gainesville, FL 32601, USA.

Cells
|February 25, 2025
PubMed
Summary

Rotavirus infection spreads spatially. Secondary infections occur faster due to high viral titers, not cell priming or calcium signaling, requiring virus release and protease access.

Keywords:
rotavirusspatial virus replicationvirus spread

More Related Videos

Simplified Reverse Genetics Method to Recover Recombinant Rotaviruses Expressing Reporter Proteins
11:40

Simplified Reverse Genetics Method to Recover Recombinant Rotaviruses Expressing Reporter Proteins

Published on: April 17, 2020

8.4K
Author Spotlight: Investigating Viral Disruption of Intestinal Epithelial Signaling – Research Insights and Future Directions
08:01

Author Spotlight: Investigating Viral Disruption of Intestinal Epithelial Signaling – Research Insights and Future Directions

Published on: January 19, 2024

1.2K

Related Experiment Videos

Last Updated: May 26, 2025

Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
10:49

Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus

Published on: January 28, 2019

8.5K
Simplified Reverse Genetics Method to Recover Recombinant Rotaviruses Expressing Reporter Proteins
11:40

Simplified Reverse Genetics Method to Recover Recombinant Rotaviruses Expressing Reporter Proteins

Published on: April 17, 2020

8.4K
Author Spotlight: Investigating Viral Disruption of Intestinal Epithelial Signaling – Research Insights and Future Directions
08:01

Author Spotlight: Investigating Viral Disruption of Intestinal Epithelial Signaling – Research Insights and Future Directions

Published on: January 19, 2024

1.2K

Area of Science:

  • Virology
  • Cell Biology
  • Infectious Diseases

Background:

  • Rotavirus causes significant global mortality, particularly in children.
  • Understanding rotavirus replication dynamics is crucial for developing effective interventions.
  • Previous studies indicate complex spatial patterns in viral spread.

Purpose of the Study:

  • To elucidate the mechanisms driving the accelerated kinetics of secondary rotavirus infections.
  • To investigate the roles of viral release, protease accessibility, and calcium signaling in rotavirus spread.
  • To determine factors contributing to the spatial control of rotavirus replication.

Main Methods:

  • Live-cell imaging of MA104 cells infected with rotavirus.
  • Trypsin neutralization assays to assess viral infectivity.
  • Pharmacological inhibition of calcium signaling pathways.
  • Quantification of viral titers and infection rates.

Main Results:

  • Rotavirus replication and spread exhibit spatial control, with secondary infections occurring in areas surrounding initially infected cells.
  • Secondary rotavirus infections require extracellular virus release and accessibility to proteases.
  • Calcium waves, critical for initial infection, are not essential for secondary infection establishment.
  • High viral titers released from primary infections are sufficient to accelerate secondary infection rates.

Conclusions:

  • The accelerated rate of secondary rotavirus infection is primarily driven by high viral loads and the requirement for extracellular virus release and protease activity.
  • Calcium signaling plays a role in the initial infection phase but is dispensable for subsequent rounds of infection.
  • Rotavirus spread is a spatially regulated process influenced by viral release kinetics and environmental factors.