Can a past coronavirus infection weaken your immune system for a long time?
A past coronavirus infection can temporarily disrupt the immune system, and in Long COVID possibly for an extended period. If you have persistent symptoms following your infection, it is worthwhile discussing this with your doctor, including with a view to rehabilitation.
During an acute coronavirus infection, the immune system's so-called attack cells (the T-cells that clear viruses) become functionally exhausted. They display more inhibitory signals on their surface and work less effectively. At the same time, the virus suppresses the way the immune system is informed about the presence of threats, which further limits the response.
In people who continue to experience prolonged symptoms after a coronavirus infection, known as Long COVID, signs of chronic inflammation and T-cell exhaustion can still be detected in the blood more than six months later, compared with people who have fully recovered. That pattern has been found in two independent groups of participants. In addition, small studies also show disruptions in the gene activity of immune cells, particularly around antigen presentation (the mechanism by which the immune system recognises threats) and signalling molecules. The groups in these studies are small, so firm conclusions cannot yet be drawn.
In people who have been seriously ill and were discharged from hospital at least six months earlier, lower numbers of immune cells and a less diverse immune defence repertoire have still been measured compared with healthy individuals. A diverse repertoire is important for recognising a wide range of pathogens. Two immune signalling molecules that support the growth and survival of immune cells were significantly reduced. An encouraging finding: people who followed a rehabilitation programme after discharge had nearly normal values, whereas people without rehabilitation did not reach those levels. This is based on a single study, however, in which no one was randomly assigned.
In people with an already weakened immune system, the coronavirus can hide for extended periods in tissues outside the respiratory tract. This leads to ongoing dysregulation of the immune system and also increases the risk of new virus variants emerging. How large the group is in which this occurs is not precisely known. There are also theoretical models describing how viruses can accelerate T-cell exhaustion via small regulatory molecules inside the cell, but this has not yet been established as a confirmed mechanism in large clinical studies.
This answer is based on several review articles that summarise existing literature, supplemented by a number of smaller studies following people after a coronavirus infection. The findings on T-cell exhaustion are reasonably consistent across these sources. However, the direct studies in humans have small participant numbers (groups of 15 to 28 people) and are not designed in a way that allows cause and effect to be fully established: it is clear that the changes exist, but how long they persist in the average patient, and to what extent this is clinically noticeable, has not yet been sufficiently investigated.
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