Serum Level of Anti-Nucleocapsid, but Not Anti-Spike Antibody, Is Associated with Improvement of Long COVID Symptoms, 2022, Varnai et al

[Wyva]

Abstract

Background: Long COVID is a condition characterized by long-term sequelae persisting after the typical convalescence period of COVID-19. Previous reports have suggested the role of an unsatisfactory immune response and impaired viral clearance in the pathogenesis of long COVID syndrome. We focused on potential associations between post-vaccination changes of antibody titers and the severity of long COVID symptoms and factors influencing the state of remission observed in patients with long COVID after vaccination.

Methods: The severity of long COVID symptoms and serum anti-SARS-CoV-2 spike (S-Ig) and nucleocapsid (NC-Ig) levels were assessed in 107 post-COVID subjects at two time points: at baseline, and 17–24 weeks later. Besides, vaccination status was also assessed. Symptoms were evaluated based on the Chalder fatigue scale (CFQ-11) and visual analogue scale (VAS).

Results: Serum level of S-Ig and NC-Ig at baseline were significantly higher in the patients with non-severe fatigue than those with severe fatigue, and this difference remained significant at follow-up in the case of NC-Ig. NC-Ig level above median was as an independent predictor for complete remission at follow-up. The difference in NC-Ig levels in subgroup analyses (severe fatigue vs. non-severe fatigue; complete remission vs. incomplete remission or progression) was found to be significant only in patients who received vaccination.

Conclusions: The immune response against the SARS-CoV-2 nucleocapsid may play a more important role than the spike in the course of long-term COVID syndrome.

Open access: https://www.mdpi.com/2076-393X/10/2/165/htm

 

[Wyva]

This is a new paper from the same Hungarian team who published this one last year: Severe Fatigue and Memory Impairment Are Associated with Lower Serum Level of Anti-SARS-CoV-2 Antibodies in pw Post-COVID (...), 2021, Molnar et al

Again, they mention CFS:

Chronic fatigue syndrome (CFS) is frequently preceded by a viral infection [16], but the molecular mechanisms underlying these post-acute presentations have yet to be elucidated. Post-infectious sequelae have also been observed following infection by other coronaviruses such as SARS-CoV and MERS-CoV; the most common symptom is fatigue [17].

Cytotoxic activity of NK and CD8+ T cells and NK phenotypes was significantly decreased in CFS patients, suggesting significant dysregulation of the immune system in CFS patients [18]. In patients with CFS, the CD8+ T cells had reduced mitochondrial membrane potential compared with those from healthy controls and CD8+ T cells had reduced glycolysis following activation [19]. These findings indicate that patients have impaired T cell metabolism.

The T cell compartment was altered in CFS population, with increased proportions of effector memory CD8+ T cells and decreased proportions of terminally differentiated effector CD8+ T cells reflecting an altered immunological state caused by an ongoing or recent infection [20]. There is considerable evidence for dysfunction of the CD4+ and especially CD8+ T cells in chronic fatigue syndrome, and given the marked similarity to the symptoms of SARS-CoV-2-induced post COVID fatigue, the pathophysiological role of these T cells in long COVID also arises.​