COVID-19 was a new type of infection caused by a novel coronavirus, SARS-CoV-2, and a challenge for our naïve immune system. With no pre-existing adaptive immunity, SARS-CoV-2 spread rapidly worldwide in the beginning of 2020. The pandemic caused enormous pressure on healthcare systems and medical organizations, leading to global isolation protocols and the development of new vaccines in record-breaking time.

However, serum levels of neutralizing antibodies declined a few months after the immunization, although some protection was seen in epidemiological studies. In addition, many patients reported symptoms lasting even months after the acute SARS-CoV-2 infection. The condition was named “long COVID” or “post-COVID-19 condition” (PCC). However, little is known about the pathophysiological basis of the condition.

In this thesis, I studied cellular immunity generated by COVID-19 vaccination in healthcare workers, immunocompetent COVID-19 patients, and immunocompromised individuals. Moreover, I assessed the role of inflammation, humoral immunity, and hypocortisolism in PCC in a 24-month follow-up of COVID-19 inpatient and outpatient cohorts.

I showed that SARS-CoV-2 vaccination induces long-lasting cellular immunity in healthy individuals and immunocompromised patients, possibly protecting against severe disease. The prevalence of PCC decreased from 51.2% in three months to 18.3% over the 24-month follow-up period. Patients with PCC had elevated levels of anti-SARS-CoV-2 antibodies compared to recovered individuals. Interestingly, the clustering of patients to subgroups revealed that patients with fatigue, myalgia, or ongoing respiratory problems seemed to have elevated serum levels of interleukin six and high-sensitivity C-reactive protein. In contrast, patients with cognitive problems seemed to have lower cortisol levels. Unfortunately, the subgroup sizes were too small for proper statistical analysis.