Northwestern Medicine scientists have identified the cellular mechanisms that cause immune cells to differentiate and ultimately lose function during viral infection, findings that could improve treatments to control chronic infections, according to a study published in the Proceedings of the National Academy of Sciences.
During viral infection and in the case of cancer, CD4+ helper T-cells release cytokines, or small signaling proteins, that activate and “give permission” to other immune cells to control and clear viral pathogens.
In certain viral infections, such as lymphocytic choriomeningitis virus (LCMV), which is spread by infected rodents, CD4+ T-cells differentiate into different subpopulations, including one subset of progenitor CD4+ T-cells that replenish type 1 helper (Th1) and follicular helper (Tfh) T-cells.





