An infection with COVID-19 may be associated with long-term damage of the cellular immune system even after mild cases, according to new research published in the journal Allergy.1 The authors of the study said the findings can contribute to the understanding of pathomechanisms underlying long COVID.
Long COVID has become a well-known medical issue following an infection with the SARS-CoV-2 virus and impacted 6.9% of adults in the United States in 2022.2 The condition encompasses several respiratory and neurologic symptoms, including cognitive impairment, fatigue, and sleep and memory loss.3 However, there is currently little data on the long-term impact of COVID-19 on the immune system.
Key Takeaways
- COVID-19 may cause long-term damage to the cellular immune system even in mild cases, with significant reductions in immune cell counts observed up to 10 months post-infection.
- Recovered COVID-19 patients showed fewer circulating neutrophils, granulocytes, monocytes, and lymphocytes compared to non-infected individuals, indicating persistent immune activation and potential immune system impairment.
- The study highlights the complexity of long COVID's impact on various organs, including the lungs, kidneys, cardiovascular, and nervous systems, emphasizing the need for further research to understand these mechanisms and their long-term implications.
“[I]t is well-known that distinct viral infections have a long-term impact on the immune system and the overall immune homeostasis of those infected and may lead to disease-typical, organ-specific post-viral complications,” the authors wrote. “The polymorphic clinical and organ-pathological pattern of long-COVID-19 is, however, unique in its complexity. It affects the lungs, causing fibrotic changes with dyspnea, the kidneys, leading to kidney-failure, the cardiovascular system, resulting in heart palpitations and pathological orthostasis as well as the nervous system.”
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Investigators from the Medical University of Vienna conducted a study to determine the long-term impact of COVID-19 on the immune system. Data was gathered from a previous case-control study that was conducted between May 11, 2020, and August 20, 2020, when SARS-CoV-2 Wuhan Hu-1 was the only circulating strain.
The study cohort included 106 unvaccinated patients who had a COVID-19 infection confirmed by a rtPCR test. Cellular and humoral immune parameters were checked 10 weeks and 10 months after the patients’ initial COVID-19 infection. Of the included participants, 44 were male, 54 were female, and the median age was 51 years. Patients were excluded if they presented with equal or elevated antibody levels at the end of the observational 10-month period.
Investigators found that patients who had recovered from COVID-19 had significantly fewer circulating neutrophils at 10 weeks compared to individuals who had never been infected with the virus. COVID-19 patients also had reduced absolute granulocyte, monocyte, and lymphocyte counts at 10 months post-infection compared to noninfected individuals. The cellular changes were associated with a change from Th1- to Th2-dominated serum cytokine patterns.
Additionally, declines of nucleocapsid- and spike protein-specific antibody levels were associated with younger age and fewer types of specific B memory cells.
"Not entirely unexpectedly, 10 weeks after the infection, the convalescent patients showed clear signs of immune activation of both their T and B cells, in contrast to healthy study subjects," Winfried Pickl, a principal investigator on the study, said in a release.4 "Even after mild disease progression, we found a significant reduction of immune cells in the blood."
Study limitations include that only patients with a mild COVID-19 disease course who cured their disease at home were included, that symptoms reported by study participants were subjective, and that patient samples were collected during the first wave of the pandemic, which limits the findings to only a single strain of the virus.
“[O]ur results provide a possible explanation that certain manifestations of long-COVID-19 may be associated with damage of the cellular immune system by SARS-CoV-2,” the authors concluded. “This hypothesis can now be investigated in appropriate study populations in detail in the future and this may contribute to the understanding of pathomechanisms underlying long-COVID-19.”
READ MORE: COVID-19 Resource Center
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References
1. Kratzer B, Gattinger P, Trapin D, et al. Differential decline of SARS-CoV-2-specific antibody levels, innate and adaptive immune cells, and shift of Th1/inflammatory to Th2 serum cytokine levels long after first COVID-19. Allergy. 2024 Jul 14. doi: 10.1111/all.16210. Epub ahead of print. PMID: 39003594.
2. Ford ND, Agedew A, Dalton AF, Singleton J, Perrine CG, Saydah S. Notes from the Field: Long COVID Prevalence Among Adults — United States, 2022. MMWR Morb Mortal Wkly Rep 2024;73:135–136. DOI: http://dx.doi.org/10.15585/mmwr.mm7306a4.
3. Davis HE, McCorkell L, Vogel JM, et al. Long COVID: major findings, mechanisms and recommendations. Nat Rev Microbiol. 21, 133–146 (2023). https://doi.org/10.1038/s41579-022-00846-2
