The thymus, the immune system’s training school, was better preserved in people with treated HIV

The thymus is a small organ behind the breastbone. It is where T cells, the immune cells that recognise and destroy infected cells, are trained. Young T cells that leave it are called naïve T cells: they have not yet met their target and give the immune system its range. After puberty the thymus is gradually replaced by fat, a process called thymic involution. It happens faster in men, smokers and people with a higher body mass index, and it is thought to contribute to the weakening of the immune system and the low-grade, long-lasting inflammation (inflammaging) of old age.

HIV attacks T cells and, when untreated, damages the thymus. The common assumption has been that people living with HIV therefore lose their thymus faster and age prematurely in their immune system. A Danish study tested this, and found the opposite.

What they did

Researchers in Copenhagen used two existing studies with chest CT scans: 654 people with HIV aged 40 or older, diagnosed a median of 16 years earlier, and 637 people from the general population matched by age and sex. Two readers who did not know who had HIV graded each thymus from 0 (completely fat) to 3 (mostly soft tissue). They also measured a marker in blood that shows recent T-cell production by the thymus (TRECs, small DNA circles left over when a new T cell is made).

What they found

Most adults had no thymus tissue left: grade 0 in 73% of the general-population group and in 63% of people with HIV.
People with HIV more often had some left. Grades 1–3 were more common in the HIV group. Taking age, sex, smoking, weight, waist-to-hip ratio, exercise and alcohol into account, people with HIV had 1.75 times the odds of a higher thymus grade.
The tissue seemed to be working. A higher thymus grade went with more TRECs in both groups, a sign that the tissue still produced new T cells.
More thymus, less inflammation. Among people with HIV, a higher grade went with more naïve T cells, fewer worn-out (senescent) T cells and lower levels of two blood markers of inflammation, IL-6 and CRP.
Timing mattered. Within the HIV group, people diagnosed at a younger age and with a less severe low point in their T-cell count had more thymus tissue. Exposure to some older HIV drugs went with less.

What could explain it?

The authors suggest the thymus may regrow after effective HIV treatment starts. The thymus is known to regenerate after some kinds of damage, younger people do this best, and regrowth has been seen in adults within months of starting HIV treatment. Another possible explanation is survival bias: people who had more thymus tissue when infected may have been more likely to survive the years before modern treatment and so to be in the study.

What to keep in mind

This is a single snapshot, so it shows associations, not cause and effect. Less inflammation might protect the thymus rather than the other way round. Most participants were men of European descent. And the blood marker of thymus output was below the detection limit in many samples.

Why it matters

Rejuvenating the thymus is one of the big goals in immune-aging research, because a working thymus supplies fresh T cells. This study suggests that the adult thymus can be more resilient than assumed, at least in some people, and it links a better-preserved thymus to less of the chronic inflammation that drives age-related disease. The authors also point to earlier studies in the general population in which removal of the thymus or poorer thymus health went with higher mortality.