Mitochondrial immunity

Credit: PROFESSORS PIETRO M. MOTTA © TOMONORI NAGURO / PHOTO RESEARCHERS" /> Credit: PROFESSORS PIETRO M. MOTTA © TOMONORI NAGURO / PHOTO RESEARCHERS The paper: R.B. Seth et al., "Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-κB and IRF3." Cell, 122:669-82, 2005. (Cited in 77 papers.) The finding: The innate immune system recognizes viral infections inside cells with RIG-I and triggers type I in

Charles Q. Choi
Jan 1, 2007
<figcaption> Credit: PROFESSORS PIETRO M. MOTTA © TOMONORI NAGURO / PHOTO RESEARCHERS</figcaption>
Credit: PROFESSORS PIETRO M. MOTTA © TOMONORI NAGURO / PHOTO RESEARCHERS

The paper:

R.B. Seth et al., "Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-κB and IRF3." Cell, 122:669-82, 2005. (Cited in 77 papers.)

The finding:

The innate immune system recognizes viral infections inside cells with RIG-I and triggers type I interferon responses with IRF3 and NF-κB. Zhijian Chen's group at the University of Texas Southwestern Medical Center in Dallas discovered a critical missing link in this pathway in mitochondria, a protein they dubbed MAVS.

The surprise:

MAVS is the first mitochondrial protein known to play a direct signaling role in an immune response.

The follow-up:

Subsequent work has shown hepatitis C virus protease NS3/4A can cleave MAVS from the mitochondrion to inactivate the protein and suppress host immunity, notes Ruslan Medzhitov at Yale University in New Haven, Conn.

The work ahead:

"Right now...

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