Why people with HIV age rapidly?

Study points at the source of rapid aging, chronic inflammation in people living with HIV

Researchers have finally pinpointed at the source of rapid aging and chronic inflammation in people with HIV in a study published in journal PLOS Biology. 

Scientists at the University of Alberta have discovered that white blood cells called neutrophils play a role in impaired T cell functions and counts, as well as the associated chronic inflammation that is common with the virus.

Neutrophils make up about 60 to 80 per cent of circulating immune cells in the blood. However, unlike other types of white blood cells, neutrophils are extremely short-lived and cannot be frozen and thawed like other immune cells, making them extremely difficult to examine. And despite them being in abundance, their role in the context of HIV has not been very well defined.

In the new study researchers examined the fresh blood of 116 people living with HIV and 60 individuals without the virus. They ran comprehensive sequencing on all the genes expressed in the neutrophils from both groups to determine any differences between them and found that not all HIV-infected individuals have similar types of neutrophils. As HIV progresses in the body, neutrophils become more activated and more potent, and in turn activate the body’s T cells, which likely causes some of the problems associated with HIV infection such as inflammation and rapid aging.

Researchers say that neutrophils act like an early alarm system. When they detect a dangerous entity such as an invading microbe, they release proteins to signal other immune cells to the danger. This activation can be high or low, or more or less potent, depending on the severity of the danger and the reaction of other immune cells.

One of the proteins released by neutrophils is galectin-9, which Elahi previously linked to severe inflammation and cytokine storms in COVID-19 patients. Researchers reported that when neutrophils sense a danger such as an infection, they become stressed and release the galectin-9. As the protein begins to saturate the blood, it can interact with different immune cells. For example, the team found that galectin-9 reacted strongly with T cells and made them more susceptible to HIV infection, causing a cascading effect that leads to a hyper-immune response and inflammation.

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