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Related Experiment Video

Updated: Jun 21, 2026

Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein

Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein

Published on: April 21, 2015

Influenza A virus M1 blocks the classical complement pathway through interacting with C1qA.

Junjie Zhang^1,2, Gang Li^1,2, Xiaoling Liu^3,1

¹Graduate University of Chinese Academy of Sciences, Beijing 100101, PR China.

The Journal of General Virology

|August 7, 2009

Summary

Influenza A virus M1 protein binds to complement C1qA, inhibiting the host immune response. This interaction enhances viral propagation and reduces host survival, highlighting M1's role in immune evasion.

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Area of Science:

Virology
Immunology
Structural Biology

Background:

Influenza A virus matrix protein (M1) is crucial for viral replication.
The host complement system is a key component of innate immunity against viral infections.

Purpose of the Study:

To investigate the interaction between influenza A virus M1 protein and the complement system.
To elucidate the role of M1-complement interaction in viral pathogenesis and immune evasion.

Main Methods:

In vitro binding assays to assess M1-C1qA interaction.
Functional assays including haemolysis inhibition and complement-mediated neutralization.
In vivo studies using a mouse model of influenza A infection.

Main Results:

Influenza A M1 protein directly binds to complement C1qA via its N-terminal domain.
M1 inhibits the classical complement pathway by blocking C1qA-IgG interaction and preventing haemolysis.
M1 confers resistance to complement-mediated viral neutralization in vitro.
Administration of M1 protein increases viral load in mouse lungs and reduces survival rates.

Conclusions:

Influenza A M1 protein actively subverts the host innate immune system by interacting with complement C1qA.
This interaction is a critical mechanism for viral immune evasion and pathogenesis.
Targeting M1-complement interactions could represent a novel therapeutic strategy against influenza A virus.