Braunschweig - The lack of an endogenous enzyme that influenza viruses need for replication makes mice resistant to flu. This is shown by experiments in PLOS Pathogens (2013; doi: 10.1371 / journal.ppat.1003774), which show new starting point for treatment.
Like all viruses, the pathogens of influenza depend on cell enzymes to reproduce that they misuse for the purpose of replication. Without these "host factors", the chain of infection breaks down quickly, as scientists from the Braunschweig Helmholtz Center for Infection Research are now using the example of the H1N1 influenza virus, the causative agent of "swine flu" from 2009 and the dreaded "Spanish flu" of 1918 / 20.
The researchers removed the gene for the protease Tmprss2, which is present in the cells, from the genome of mice activates hemagglutinin A. The viruses need the activated hemagglutinin in order to be able to infect other cells. The protein is the anchor with which they dock on the cell membrane.
Without Tmprss2, the chain of infection is quickly interrupted, which the team led by Prof. Klaus Schughart also noticed in their experimental animals. The knockout mice lacking the gene for Tmprss2 suffered no weight loss after exposure to influenza viruses and their lungs were hardly damaged. Although the animals were infected, Schughart reports, only inactive viruses were formed that cannot endanger the animals.
Schughart believes it is possible that some people are naturally immune to influenza due to mutations in the Tmprss2 gene. However, such cases have not yet been described.
The enzyme Tmprss2 would also be suitable as an approach for therapy. Gene therapy that would remove or switch off the gene would not be an option in humans. The development of drugs that, in the event of an infection, block the enzyme - ideally only temporarily - would be possible. The tolerance could be good. In any case, the lack of Tmprss2 had no discernible disadvantages in the mice, as Schughart assures.
A Tmprss2 blocker would also have the advantage that the viruses could not develop resistance as easily as oseltamivir and other flu medicines. These agents attack components of the virus that the virus can change through mutations. This is not possible with the Tmprss2 gene, which is part of the human genome.