Mice with Tmprss2 protein deficiency are resistant to certain flu viruses, says study.
Whether it is H1N1, H5N1 or H7N9: The flu virus influenza A exists in many different types as its two coating proteins haemagglutinin (HA) and neuraminidase (NA) can be combined in various ways.
Scientists from the Helmholtz Centre for Infection Research (HZI) in Braunschweig have been able to show how important those enzymes are for the progression of the infection.
Mice with a mutation in the gene for the protease Tmprss2 do not become infected by flu viruses containing haemagglutinin type H1. They are resistant against H1N1, the pathogen responsible for seasonal influenza epidemics, the "swine flu" and the "Spanish flu", which caused an epidemic in 1918.
"These mice do not lose weight and their lungs are almost not impacted," Professor Klaus Schughart, head of the Department "Infection Genetics" at the HZI, said. "Even though the virus still multiplies no active viral particles are formed which would infect the neighbouring cells." The infection is quickly terminated.
As the protease Tmprrs2 is a host factor it is an ideal intervention point for new drugs. So far, treatments, such as the well-known Tamiflu, attack parts of the virus.
They have decisive disadvantages: The virus can become resistant and the therapy no longer takes effect. This problem does not occur when the medication intervenes with the metabolism of the patient. Furthermore, the mice Schughart and his team examined did not show any abnormalities.
The study was published in the scientific journal PLOS Pathogens.