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Updated: Aug 25, 2026

Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein
Published on: April 21, 2015
The M1 matrix protein controls the filamentous phenotype of influenza A virus
1School of Animal and Microbial Sciences, University of Reading, Whiteknights, Reading RG6 6AJ, UK.
Abstract:
We show that most isolates of influenza A induce filamentous changes in infected cells in contrast to A/WSN/33 and A/PR8/34 strains which have undergone extensive laboratory passage and are mouse-adapted. Using reverse genetics, we created recombinant viruses in the naturally filamentous genetic background of A/Victoria/3/75 and established that this property is regulated by the M1 protein sequence, but that the phenotype is complex and several residues are involved. The filamentous phenotype was lost when the amino acid at position 41 was switched from A to V, at the same time, this recombinant virus also became insensitive to the antibody 14C2. On the other hand, the filamentous phenotype could be fully transferred to a virus containing RNA segment 7 of the A/WSN/33 virus by a combination of three mutations in both the amino and carboxy regions of the M1 protein. This observation suggests that an interaction among these regions of M1 may occur during assembly.
Insights
Most influenza A virus isolates cause filamentous changes in cells, unlike lab-adapted strains. The M1 protein
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Influenza A virus strains exhibit varied cell morphology post-infection.
- Laboratory passage and mouse adaptation can alter viral characteristics, including cell shape induction.
Purpose of the Study:
- To investigate the viral factors regulating filamentous changes in influenza A virus-infected cells.
- To identify specific viral proteins and mutations responsible for the filamentous phenotype.
Main Methods:
- Utilized reverse genetics to create recombinant influenza A viruses.
- Introduced mutations into the M1 protein of influenza A virus.
- Assessed viral morphology and antibody sensitivity of recombinant viruses.
Main Results:
- Most wild-type influenza A virus isolates induce filamentous changes, unlike highly passaged strains.
- The M1 protein regulates the filamentous phenotype, with specific residues involved.
- A mutation at position 41 of the M1 protein abolished the filamentous phenotype and conferred antibody resistance.
- Transfer of the filamentous phenotype was achieved by introducing three mutations in the M1 protein.
Conclusions:
- The M1 protein sequence is a key determinant of the filamentous phenotype in influenza A virus-infected cells.
- Specific regions and residues within the M1 protein, potentially interacting, govern this complex trait.
- Understanding these viral properties can inform studies on influenza virus evolution and pathogenesis.
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