A human protein called TRIM25, which was recently discovered to play an important role in the human immune response to flu infection; and a protein called NS1 present in all strains of the influenza.
TRIM25 acts earlier than previously believed, latching on to a critical and unique flu virus structure like a molecular clamp to keep the virus from replicating as soon as TRIM25 detects this unique structure. NS1 produced by the flu virus can block this function of TRIM25, enabling flu to circumvent the immune response and cause infection.
TRIM25 fought off flu by switching on interferon response- a complex signaling pathway that strengthens cells through the body to fight off pathogens. But not all strains of influenza block this interferon signaling pathway. TRIM25 is also a restriction factor - a special protein present in the fastest-acting arm of the immune system, before spreading infection. Restriction factors lie in wait to detect a virus in the cells.
Flu uses its NS1 protein to evade TRIM25's early flu-fighting response, the researchers infected transgenic cell lines loaded with nonhuman primate versions of TRIM25 with the human influenza virus. They discovered that the cells fought off the virus far better than human versions of the TRIM25 protein.
TRIM25 has the capacity to crush influenza, the researchers combined purified TRIM25 with purified viral ribonucleoproteins (vRNPs)- eight-piece protein chains that house the influenza genome and used state-of-the-art electron microscopy to take pictures of what happened.
They found that TRIM25 appears to swiftly recognize the unique structure of vRNPs and clamps down on them to keep them from replicating inside the cell. Other experiments confirmed that the NS1 protein in flu virus inhibits this function. They also found that TRIM25 is also present in the cell nucleus, which is the same cellular location where flu replication occurs.
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