LC8 has actually been show to play an active role in replication of central nervous system-attacking viruses.
A molecule thought to be crucial in ferrying the rabies virus into the brain apparently isn’t. The finding may change the way scientists think about how central nervous system-attacking viruses, such as herpes viruses, invade the brain and cause disease, according to scientists at Jefferson Medical College of Thomas Jefferson University.
Viruses, such as rabies, must be actively transported to the brain and central nervous system. The LC8 protein was thought to tether viruses to the cellular transport machinery. However, the researchers discovered that this protein complex is instead a transcription factor that plays a role in virus reproduction.
To understand the role of LC8 in rabies disease in the brain, the team compared a rabies virus strain with the LC8 binding domain to a virus lacking it. They showed that in mice that were infected with rabies without the LC8 binding domain the virus was still able to infect the brain but did not cause the disease. However, the virus’ ability to reproduce was greatly diminished.
“What we found has nothing to do with transport,” says Matthias Schnell, Ph.D., professor of microbiology and immunology. “We saw that the virus was weakened if we removed the LC8 binding site and viral replication and transcription were affected. We didn’t find a difference in the initial viral entry in the central nervous system.”
The results of the study are online in the Proceedings of the National Academy of Sciences.
