Single avian flu viral protein can increase period of infectivity

Accessory protein in avian influenza viruses able to shut down chicken immune response and increase length of time virus can be transmitted.

New research led by scientists at The Pirbright Institute in the U.K. has shown how an influenza virus protein called PB1-F2 is able to shut down two pathways of the chicken immune response to increase the length of time the virus can be transmitted, according to an announcement from the institute.

The PB1-F2 protein of influenza viruses is an accessory protein, meaning it is not essential for replication. However, the majority of avian influenza viruses (93%) are able to produce the PB1-F2 protein, which is not the case for human (43%) and swine (48%) influenza viruses

“The fact the protein is conserved at such a high rate in avian influenza strains indicated to us that this protein must provide some sort of advantage for the survival of the virus in birds,” said Dr. Holly Shelton, head of the Influenza Viruses Group at Pirbright. “Our previous research has shown that PB1-F2 prolongs the length of the transmission window in chickens. This new research, published in the Journal of General Virology, was aimed at identifying the mechanism of how PB1-F2 does this.”

According to the institute, the team found that PB1-F2 interferes with two key pathways that the chicken's immune system uses to control viral infections: the interferon and the NF-κB dependent responses. In the interferon response, infected cells release proteins called interferons, which heighten the antiviral defenses of other cells around them and activate immune cells. NF-κB is a protein complex that can induce and regulate the inflammatory response in order to call immune cells to the site of infection.

PB1-F2 inhibits these pathways by attaching to proteins essential to them, the researchers explained. One of these is a cellular protein called MAVS, and binding to it PB1-F2 prevents activation of the interferon response. PB1-F2 can also bind to another protein called IKKβ, preventing it from activating NF-κB. By interrupting these two pathways, PB1-F2 can help increase viral replication.

“Of particular interest was the fact that different PB1-F2 proteins localize to specific areas of the cell, and this then dictates which pathway the protein would interact with. At the moment, we don’t know if there is a reason one pathway is favored over another or if one pathway is more effective at increasing viral replication, so these are areas we are now looking into,” Shelton added.

Through understanding how influenza viruses interact with the avian host, such as how PB1-F2 proteins prevent cells from mounting an effective antiviral response, better strategies can be devised that can prevent virus replication, thus reducing disease burden and enhancing virus control in birds.

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