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Updated: Feb 27, 2026
Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Differential replication of Foot-and-mouth disease viruses in mice determine lethality
Marco Cacciabue1, María Soledad García-Núñez2, Fernando Delgado3
1Instituto de Biotecnología, Instituto Nacional de Tecnología Agropecuaria (INTA), De los Reseros y N. Repetto s/n, (1686) Hurlingham, Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina.
Abstract:
Adult C57BL/6J mice have been used to study Foot-and-mouth disease virus (FMDV) biology. In this work, two variants of an FMDV A/Arg/01 strain exhibiting differential pathogenicity in adult mice were identified and characterized: a non-lethal virus (A01NL) caused mild signs of disease, whereas a lethal virus (A01L) caused death within 24-48h independently of the dose used. Both viruses caused a systemic infection with pathological changes in the exocrine pancreas. Virus A01L reached higher viral loads in plasma and organs of inoculated mice as well as increased replication in an ovine kidney cell line. Complete consensus sequences revealed 6 non-synonymous changes between A01L and A10NL genomes that might be linked to replication differences, as suggested by in silico prediction studies. Our results highlight the biological significance of discrete genomic variations and reinforce the usefulness of this animal model to study viral determinants of lethality.
Insights
Two Foot-and-mouth disease virus (FMDV) variants showed different lethal effects in mice. Genomic variations influence FMDV pathogenicity and lethality, highlighting the mouse model
Area of Science:
- Virology
- Pathogen Biology
- Animal Models
Background:
- Adult C57BL/6J mice are utilized for Foot-and-mouth disease virus (FMDV) research.
- FMDV causes significant economic losses in livestock globally.
- Understanding viral determinants of pathogenicity is crucial for disease control.
Purpose of the Study:
- To identify and characterize FMDV variants with differing pathogenicity in adult mice.
- To investigate the biological significance of genomic variations on FMDV lethality.
- To validate the utility of the mouse model for studying FMDV virulence factors.
Main Methods:
- Isolation and characterization of two FMDV A/Arg/01 variants (A01NL - non-lethal, A01L - lethal).
- Assessment of pathogenicity and systemic infection in adult C57BL/6J mice.
- Viral load quantification in plasma and organs, and replication studies in ovine kidney cells.
- Genomic sequencing and comparative analysis of the two FMDV variants.
Main Results:
- A lethal FMDV variant (A01L) caused death within 24-48h in mice, irrespective of dose.
- Both variants induced systemic infection and pancreatic pathology.
- A01L exhibited higher viral loads in mice and enhanced replication in ovine kidney cells.
- Six non-synonymous genomic differences were identified between A01L and A01NL, potentially influencing replication.
Conclusions:
- Discrete genomic variations significantly impact FMDV pathogenicity and lethality.
- The adult mouse model effectively demonstrates viral determinants of FMDV lethality.
- Further research into specific genetic changes can elucidate FMDV virulence mechanisms.
