The study also describes how viruses escape control when the protein is absent. This knowledge could lead to better treatments for patients with persistent viral infections, the researchers say.
Hundreds of millions of people around the world live with such incurable infections, including HIV, hepatitis B and hepatitis C.
The study was published online Wednesday, in the June 14, 2012 issue of the scientific journal Cell Host & Microbe.
A team led by virologist Michael Oldstone , a Scripps Research professor, studied the course of infection in mice genetically engineered so they don't make the protein, called TLR7. This protein plays a key role in infection from a class of viruses that store their genetic information in RNA, a molecule similar to DNA. These include HIV, the virus that causes AIDS, hepatitis B and C, and influenza.
The protein-deficient mice were infected with lymphocytic choriomeningitis virus , or LCMV; a virus scientists commonly used to probe the immune system. Normal mice can clear the infection in 60 to 90 days. The protein-deficient mice could not clear the virus at all.
Scientists then explored at the microscopic level how the immune system failed to kill the virus. The mice produced defective immune cells called T cells and B cells, less able to do their job of attacking pathogens. The scientists described the T cells as "exhausted," similiar to the state of human T cells exhausted by HIV infection.
“A number of phenomena that LCMV uses to cause a persistent infection is the same that HIV, hepatitis C and B use,” Oldstone said in a Scripps press release on the study. “That's what makes our observation important. It means that if you understood what is in the environment with loss of TLR7 signaling and how to correct that, you'd have a better chance of treating those persistent human infections.
"We know how to treat it in the mouse, and people are working very hard to do the treatments in humans," Oldstone said.
Pursuing another angle of virus research, Oldstone and colleagues published a paper in 2010 that showed that blocking another protein in mice boosted their immune "memory" of previous infections. They said the research could lead to more potent vaccines for people.
And in 2011, Oldstone and colleagues published a paper showing how a potentially fatal excessive immune response to flu infection might be controlled .
The new research was funded by the U.S. National Institutes of Health.
Other authors of the paper, "Toll-like receptor 7 is required for effective adaptive immune responses that prevent persistent virus infection," were John R. Teijaro, Megan J. Welch, Daniel M. Fremgen, and Karl von Tiehl of Scripps Research; Elina I. Zuniga of UC San Diego; Shawn D. Blackburn and E. John Wherry of the University of Pennsylvania School of Medicine; and Richard A. Flavell of Yale University.