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Broad phenotypic alterations and potential dysfunction of lymphocytes in individuals clinically recovered from
Jingyi Yang1,2,3, Maohua Zhong4,2,3, Ejuan Zhang2,3
1Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China.
Insights
COVID-19 recovery may lead to lasting immune cell dysfunction. Clinically recovered individuals show altered T and B cell populations, suggesting profound and persistent effects on the immune system post-infection.
Area of Science:
- Immunology
- Virology
- Hematology
Background:
- Millions have recovered from COVID-19, but their long-term immune status remains unclear.
- Understanding post-COVID-19 immune cell dynamics is crucial for assessing long-term health outcomes.
Purpose of the Study:
- To comparatively analyze lymphocyte populations in clinically recovered (CR) COVID-19 patients versus healthy donors.
- To investigate potential immune dysfunction persisting after clinical recovery from SARS-CoV-2 infection.
Main Methods:
- Comparative analysis of peripheral blood mononuclear cells (PBMCs) from CR cohort and age/sex-matched healthy donors.
- Flow cytometry to assess frequencies of various T cell (CD4+, CD8+), B cell, and lymphocyte subsets, including memory and effector populations.
- Quantification of key immune markers like IFN-γ, IL-4, IL-17A, PD-1, granzyme B, and T-bet.
Main Results:
- CR cohort exhibited altered CD8+ T cell profiles with increased effector/memory cells but reduced cytotoxic/cytokine-producing subsets (Tc1, Tc2, Tc17).
- CD4+ T cells were decreased in frequency, particularly central memory cells, with lower PD-1 expression and reduced Th1, Th2, Th17, and Tfh cell frequencies.
- B cell analysis revealed a lower proportion of switched memory B cells, despite elevated CD71 activation marker; cytotoxic lymphocytes showed diminished IFN-γ, granzyme B, and T-bet.
- Immune alterations persisted for 4–11 weeks post-discharge without signs of recovery.
Conclusions:
- Severe acute respiratory syndrome coronavirus 2 infection causes profound and lasting phenotypic changes in lymphocytes.
- These alterations suggest potential immune dysfunction persisting even after clinical recovery from COVID-19.
- Further research is needed to understand the clinical implications of these persistent immune changes.
Abstract:
Although millions of patients have clinically recovered from COVID-19, little is known about the immune status of lymphocytes in these individuals. In this study, the peripheral blood mononuclear cells of a clinically recovered (CR) cohort were comparatively analyzed with those of an age- and sex-matched healthy donor cohort. We found that CD8+ T cells in the CR cohort had higher numbers of effector T cells and effector memory T cells but lower Tc1 (IFN-γ+), Tc2 (IL-4+), and Tc17 (IL-17A+) cell frequencies. The CD4+ T cells of the CR cohort were decreased in frequency, especially the central memory T cell subset. Moreover, CD4+ T cells in the CR cohort showed lower programmed cell death protein 1 (PD-1) expression and had lower frequencies of Th1 (IFN-γ+), Th2 (IL-4+), Th17 (IL-17A+), and circulating follicular helper T (CXCR5+PD-1+) cells. Accordingly, the proportion of isotype-switched memory B cells (IgM-CD20hi) among B cells in the CR cohort showed a significantly lower proportion, although the level of the activation marker CD71 was elevated. For CD3-HLA-DR- lymphocytes in the CR cohort, in addition to lower levels of IFN-γ, granzyme B and T-bet, the correlation between T-bet and IFN-γ was not observed. Additionally, by taking into account the number of days after discharge, all the phenotypes associated with reduced function did not show a tendency toward recovery within 4‒11 weeks. The remarkable phenotypic alterations in lymphocytes in the CR cohort suggest that severe acute respiratory syndrome coronavirus 2 infection profoundly affects lymphocytes and potentially results in dysfunction even after clinical recovery.
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