Study on the effects of influenza virus infection on host cell protein SUMOization.

Influenza A virus is a highly contagious and pathogenic virus that is susceptible to both humans and many animals.
effective replication of the virus within the host cell is based on the virus interacting with many different proteins of the host at different stages of infection to inhibit or promote the activation of the cell signaling path.
In post-transcription regulation, the modification of target proteins by SUMO-like proteins (small ubiquitin-like modification, Small Ubiquitin-like MOdifier) is an important mechanism for regulating protein activity, stability, in-cell positioning, and protein interoperability.
previous studies have shown that influenza viruses are widely associated with the SUMO system in host cells during infection, mainly focusing on the virus's own proteins, such as NS1, NS2, PB1, NP, and M1.
, however, how does the SUMO state of the host cell protein and the SUMOization of the host protein affect the virus infection after the virus infection? The problem remains unclear.
Hongxuan, a researcher in the Wildlife Epidemic Research Group at the Institute of Zoology of the Chinese Academy of Sciences, led a team that conducted exploratory studies on the effects of influenza virus infection on the host cell protein SUMO.
team used cell infection models and mass spectrometromety methods to analyze and identify the virus-infected cell SUMO protein, and found that the host cell's MEK1 protein is the target protein of SUMO1, the DEGREE of the MEK1 protein is regulated by H5N1 virus infection.
further observation, it was found that increasing the SUMO level of MEK1 would significantly inhibit the infection of the virus, while lowering the SUMOization level of MEK1 would significantly promote the level of virus replication.
further studies have found that improving the expression of influenza virus HA protein in the cell membrane promotes phosphate of THEK1 protein, while gradually reducing THEMOization of MEK1 protein.
Therefore, the study reveals a new mechanism for influenza viruses to promote virus replication by inhibiting host cell signaling path pathfages, which is important for the future treatment and prevention of influenza viruses by studying preparations that promote the SUMOization of host cells.
is a special negative regulation principle model of sumo-based ERK signal path.
under the conditions of HA expression treatment (A) and viral infection treatment (B), the dynamic changes of MEK1 SUMOization and phosphate show a similar trend, but the treatment of viral infection obviously lags behind membrane expression HA treatment.
, the researchers proposed a model hypothesis that the influenza virus activation ERK signaling path is negatively regulated (C) by SUMO-based MEK1.
influenza virus promotes vRNP nucleation through HA-regulated ERK path, which is the switch of the ERK path from MEK1 SUMOization to phosphorylation.
the study was published online February 6 under the title HA Triggers the switch from MEK1 SUMOylation to Phosphorylation of the ERK pathway in influenza A virus-infected Cells and the Helps of Its Infection Microbiology Frontiers (Front.Cell.Infect.Microbiol).
first author of this article is Wang Chengmin, Liu Huimin and Luo Jing are equal contributors, and the communication author is He Hongxuan.
the project was funded by the National Major Research and Development Program (2016YFD0500300) and the Beijing Poultry Innovation Team (CARS-PSTP) project of the National Modern Agricultural Industry Technology System.
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