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Updated: Jun 19, 2026
Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
STUDIES ON THE MECHANISM OF ADAPTATION OF INFLUENZA VIRUS TO MICE
1Laboratories of the International Health Division of The Rockefeller Foundation, New York.
Abstract:
1. When strains of influenza A virus which have been isolated in chick embryos are introduced into the mouse lung, the virus multiplies readily and achieves initially a titer which is as high as is even obtained, even after repeated passage. The high initial titer of virus may be unaccompanied by any lethal or visible pathogenic effects; but with four or five mouse passages the agent becomes lethal in high titer and causes extensive pulmonary consolidation, though its capacity to multiply in the lung has not increased. In one example the adaptation to mouse lung was accompanied by increasing capacity to agglutinate guinea pig red cells without a corresponding increase in agglutinating power for chicken cells. Influenza B virus, in preliminary tests, did not behave in a similar fashion. 2. The adaptation of influenza A virus to mice is accompanied by changes in antigenic pattern, as detected by cross-tests with the agglutination inhibition method. Two strains, initially similar, with passage, changed in pattern along divergent paths so that they became not only unlike the parent strains but unlike each other. This finding has important implications for the interpretation of the strain difference problem in human influenza.
Insights
Influenza A virus adapted to mouse lungs becomes lethal and changes antigenically. This adaptation process impacts influenza strain evolution and detection, offering insights into human influenza.
Area of Science:
- Virology
- Immunology
- Pathology
Background:
- Influenza A virus is typically isolated in chick embryos.
- Adaptation studies are crucial for understanding viral evolution and pathogenicity.
Purpose of the Study:
- To investigate the adaptation of influenza A virus in the mouse lung model.
- To analyze changes in pathogenicity and antigenic properties during mouse adaptation.
Main Methods:
- Inoculation of influenza A virus strains into mouse lungs.
- Serial passage in mice to observe adaptation.
- Agglutination tests with red blood cells.
- Antigenic characterization using agglutination inhibition tests.
Main Results:
- Influenza A virus readily multiplied in mouse lungs, achieving high initial titers.
- Repeated mouse passage led to increased lethality and pulmonary consolidation without enhanced viral replication.
- Adaptation altered the virus's ability to agglutinate red blood cells and its antigenic pattern.
- Influenza B virus did not exhibit similar adaptation in preliminary tests.
Conclusions:
- Mouse lung adaptation of influenza A virus induces significant pathogenic and antigenic changes.
- Divergent antigenic evolution was observed in adapted strains, complicating strain identification.
- Findings have implications for understanding influenza A virus strain diversity and diagnostics.
