Immune Dysregulation and Persistent Symptoms: Insights into T Cell Dynamics in Post-COVID among Athletes from the CoSmo-S Study, 2026, Ringleb+

[SNT Gatchaman]

Immune Dysregulation and Persistent Symptoms: Insights into T Cell Dynamics in Post-COVID among Athletes from the CoSmo-S Study

Spoiler: Authors

Ringleb, Miriam; Bizjak, Daniel Alexander; Nieß, Andreas Michael; Notbohm, Hannah; Predel, Hans-Georg; Puta, Christian; Steinacker, Jürgen Michael; Widmann, Manuel; Zacher, Jonas; Bloch, Wilhelm; Javelle, Florian

BACKGROUND
Over 10% of all SARS-CoV-2 infections lead to persistent symptoms, a condition called post-COVID condition (PCC). For elite athletes, whose performance is central, PCC poses significant challenges. It is suggested that immune cells, particularly regulatory and effector T cells, play a key role in symptom persistence nonetheless it has not yet been investigated.

OBJECTIVE
This study investigates immune dynamics after SARS-CoV-2 infection and assesses whether symptom persistence is accompanied by T cell dysregulation in highly trained athletes.

METHODS
Thirty-six highly trained athletes were included in this study after experiencing SARS-CoV-2 infection. Athletes’ data were analyzed 2–4 weeks after infection (T0) and 3–4 months later (T1). They were categorized into two groups: those with persistent symptoms (PS) and those without (SF). Their immune cell distribution was assessed via flow cytometry.

RESULTS
In the PS group, there was an increase in T helper (Th) cell 17 and Th2 cells from T0 to T1, whereas in the SF group, these cell types either decreased or remained unchanged, respectively. Furthermore, Th1 cells decreased and natural (NK) cells increased from T0 to T1 in the PS group, while no changes were observed in the SF group. No changes were observed in Tregs nor in other cell types.

CONCLUSION
This dysregulation of the immune system toward humoral immunity indexed by a rise in Th2 and Th17 cells and a decrease in Th1 cells over time could be indicative of a possible virus persistence contributing to persistent symptoms.

CLINICAL TRIAL REGISTRATION
The study has been registered in the German Clinical Trials Register (DRKS00023717).

Web | DOI | PDF | Journal of Clinical Immunology | Open Access

 

[Mortal Machinery]

At a cursory look, Figure 2 appears to show some real differences between groups. I do not have enough understanding of the methods or statistics to say whether they are as significant as the authors claim.

 

[forestglip]

Caption for the above figure:

Participants’ levels of (A) Th1, (B) Th2, (C) NK cells, (D) Th17, (E) Treg, (F) Naïve T cells, (G) Treg/Naïve T cell ratio, (H) Th1/Th2 ratio, (I) Th17/Treg ratio from T0 to T1.

Data are presented as adjusted means for baseline levels ± standard error.

At T0, 16 athletes were in the PS group and 14 were in the SF. At T1, eight were included in the PS group and ten in the SF group.

Only post hoc results from the time-by-group interaction are presented.

Solid line: PS [persistent symptoms]; dashed line: SF [symptom free].

Time differences are presented using the following symbols; *: p < .050, **: p < .010, ***: p < .001.

Group differences are presented using the following symbols; #: p < .050, ##: p < .010, ###: p < .001

 

[Mortal Machinery]

Thanks for the assist @forestglip.

Reading through this paper, there are definite limitations, some of which the authors acknowledge.
There is also almost a 50% decrease in the number of participants/samples from T0 vs. T1 (30 vs 18), which would have some impact on results I assume.

Side note: It seems like having participants undergo maximum effort exercise testing only 2-4 weeks post acute infection - especially those still experiencing symptoms - runs the risk of potentially making some worse. Would any have recovered and not developed LC if they had taken a bit more time off? Who knows.

In my own case I sometimes wonder if I could have avoided developing ME (not LC) had I not attempted to resume training so soon.

 

[Jonathan Edwards]

I get the impression that we may see a slew of papers claiming this or that T cell population shift, when we are just looking at chance variations. Hundreds of labs are probably trying their hand at this and the junior authors will need papers out of it. Reporting in terms of TH17 and TH2 subsets isn't what i would like to see. Too much pre-interpretation and not enough raw data as usual.