Source: University of Colorado at Boulder
Summary: Researchers have uncovered a previously unknown mechanism where the human immune system tries to fight with influenza A virus.
Influenza A is commonly called as flu and caused by infection with a virus called influenza virus (has the ability to change and evolve continuously). Influenza A is a highly contagious respiratory illness different from the less severe common cold. This seasonal flu virus typically originates in birds and make its way to humans. It kills around 12,000 to 56,000 people in the U.S annually. Just as flu season comes into full gear, researchers from the University of Colorado at Boulder and the University of Texas at Austin have uncovered a previously unknown mechanism where the human innate immune system tries to fight with influenza A virus. The findings were published in the journal Cell Host and Microbe.
The research mainly focuses on two important molecular players in the influenza infection – one is the human protein TRIM 25 (plays a key role in the human immune response to flu infection) and the other is also a protein NS1 found in all the strains of influenza A virus and it binds to TRIM25 to keep it from doing its job. Through a series of lab tests, researchers revealed two important findings – TRIM25 acts earlier than previously believed by latching like a “molecular clamp” on to flu virus to keep the virus off from replication; NS1 can block the function of TRIM25 which enables to circumvent the immune response and cause infection.
Researchers observed that TRIM25 has the ability to crush influenza virus but the human form was less active. To find how TRIM25 crushes the virus, they combined purified TRIM25 and purified viral Ribonucleoproteins (vRNPs) which house the influenza genome and used electron microscopy to check. Researchers believe that new therapeutics could be designed to block the NS1 protein which helps in blocking all the strains of influenza virus.
More Information: Nicholas R. Meyerson et al, “Nuclear TRIM25 Specifically Targets Influenza Virus Ribonucleoproteins to Block the Onset of RNA Chain Elongation”, Cell Host and Microbe. DOI: dx.doi.org/10.1016/j.chom.2017.10.003