The way in which memory T cells, white blood cells that help the immune system remember virus and attack it if it comes back, slip away during chronic infections such as those caused by viruses like HIV and hepatitis has been identified by researchers at the Emory Vaccine Centre.
They have also shown that a molecule called 2B4 on memory cells causes them to slow down during persistent infections.
The results have implications for vaccine design.
The authors emphasize the importance of having vaccines that encourage the immune system to quickly control a potentially chronic infection or prevent it from gaining a foothold - a task that some experimental vaccines against HIV's cousin SIV have accomplished.
"In a chronic infection, the memory T cells become so tightly regulated that they eventually are ineffective," said first author Erin West, an Emory graduate student in immunology and molecular pathogenesis.
West and her colleagues studied mice infected by a meningitis virus, which establishes a chronic infection.
They tracked naive T cells as well as memory T cells' responses to infections that varied in dose and persistence.
A molecule called 2B4 appears on memory T cells that are activated during chronic infections and slows them down, the Emory team found.
This level of regulation probably helps control the immune system and prevents it from developing dangerous over-inflammation, West said.
Blocking 2B4 might be a way to enhance immune responses against chronic infections, but more information is needed about how it works, she concluded.
The results are published online this week in the journal Immunity.