0240 GMT November 14, 2019
The study has shed light on a potential new element of human immunity against HIV-1 and could provide a powerful new strategy – perhaps as part of an HIV vaccine – to limit the severity of the disease, which affects 35 million people worldwide and for which there is no cure, Medical Xpress reported.
Transmitted through bodily fluids, the HIV-1 virus thrives by infecting and destroying key immune cells, known as CD4 T cells that ordinarily would mount an effective defense against the virus and initiate the antiviral activity of other immune cells. Scientists have long known that a substance produced by CD4 T cells called Interleukin-21 (IL-21) plays an important role in the immune system by activating immune cells that specialize in killing viruses like HIV-1 and driving the production of antibodies that attack them. But it was unclear how IL-21 might affect the early stages of HIV-1 infection that allows the virus to grow and spread unabated soon after a person is exposed.
Researchers conducted two studies to uncover this effect. The researchers created a culture from human tissues, primarily spleen and lymph node tissue. After exposing the cells to IL-21, they introduced HIV-1 and found that after 72 hours, cultures with IL-21 contained more than two-thirds less virus than those that didn't receive the treatment.
The second model tested IL-21 in mice transplanted with human stem cells to create a physiological environment as close as possible to that in people. Over the course of two weeks, the mice began producing IL-21, and the effect held steady: After 14 days, more than half of the mice with IL-21 did not display a detectable level of HIV-1, with IL-21 reducing both the incidence and magnitude of disease.
An analysis of the results suggested that IL-21 not only jump-starts the immune system but also thwarts the HIV-1 virus from replicating during a critical, early window of its development, when it is concentrated in one location and hasn't yet started to spread throughout the body.