Viral infections can kill, but a recent study shows that they can also save us. A group led by researchers from the A*STAR Singapore Institute for Clinical Sciences have provided evidence that herpes virus infections in humans can induce an immune response that can contribute to protection against other unrelated pathogens.
Herpes virus infections are very common in humans, affecting more than 90% of the population. They normally cause persistent infection, remaining in the body harmlessly for many years, but are also associated with the development of cancers such as Burkitt’s lymphoma.
The researchers evaluated CD8 T cells in 50 patients, all of whom carried herpes viruses, such as Epstein Barr virus (EBV) and human cytomegalovirus (HCMV), and who were also infected with other viruses.
T cells are the immune system’s first line of defense. When activated by infectious agents, they kill infected cells and retain a memory of the microbe so that they can respond to future infections. Herpes viruses are known to alter the composition of the body’s T-cell repertoire, so that up to 20% of T cells are specific to them.
The researchers found that patients with acute hepatitis B virus infection had a greatly expanded T-cell population, containing activated T cells specific not only to HBV, but also to EBV and HCMV. Similar findings were observed in the T-cell populations of patients infected with dengue fever, influenza and adenovirus.
They then went on to investigate how herpes virus-specific T cells might be activated by other infections. They purified T cells from the healthy volunteers carrying EBV and HCMV, then incubated them with signaling molecules called cytokines—known to be produced in response to infection—to mimic the T-cell activation observed in patients with viral infections.
In all of the samples, one particular cytokine called interleukin-15 was found to activate herpes virus-specific T cells. These results suggest that interleukin-15 produced during new viral infections can contribute to the activation of herpes virus-specific T cells.
These findings show that activation of herpes virus-specific T cells is a common feature of the human immune response to infection by other viruses. As well as contributing to the immune response to current infections, this mechanism may also prevent the reactivation of persistent herpes viruses. The researchers believe that the ability of persistent viruses to leave a functional imprint on T cells has deeper consequences that require further elucidation.