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POST-COVID SYNDROME AND ITS 
IMMUNOPATHOLOGICAL MECHANISMS. 
THE ROLE OF AUTOIMMUNITY
Ryabkova V.A., MD-Student
1
, Gavrilova N.Y., MD, PhD
1
,
1
Laboratory of the Mosaics of Autoimmunity, Saint Petersburg State University, 
Russia
2
Department of Biosciences, Biotechnologies, and Biopharmaceutics, University 
of Bari, Italy
3
Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Aviv 
University School of Medicine, Tel-Hashomer, Israel 
Academic Supervisors: 
2
Kanduc D, PhD, Prof., 
1
Churilov LP, MD., PhD, Prof., 
1,3
Shoenfeld Y. MD, FRCP, MaACR, Prof.
Increasing evidence suggests a strong association between the 
COVID-19 infection and autoimmunity. Possible mechanism of the 
autoimmune phenomena in COVID-19 are molecular mimicry and 
hyperstimulation of the immune system by the virus [1].
A term “post-acute COVID-19 syndrome“ has been coined for the 
persistence of symptoms or development of sequelae beyond 4 weeks 
from the onset of acute symptoms of COVID-19 [2]. Recent meta-
analysis revealed that 80% of the patients that were infected with SARS-
CoV-2 developed one or more long-term symptoms [3]. Neuropsychiatric, 
rheumatic, respiratory, cardiovascular, gastrointestinal, and endocrine 
manifestations were identified. It was shown that prevalence of the most 
symptoms have even risen in 7-9 months compared to the early recovery 
period [4].
Potential mechanisms contributing to the pathophysiology of post-
acute COVID-19 include: (1) direct viral invasion or persistence; (2) 
immunologic aberrations and inflammatory damage in response to the 
acute infection; and (3) expected sequelae of post-critical illness [2]. 
However, most cases of post-COVID-19 syndrome developed after non 
severe COVID-19.
While there is no evidence for any hypothesis of post-COVID-19 
syndrome’s pathogenesis, it can be suggested that autoantibodies, which 
are detected during acute COVID-19 can persist and play a role in the 

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development of post-COVID-19 manifestations. The appearance and 
progression of symptoms some time after resolution of acute COVID-19 
(see above) favors this hypothesis.
The prevalence of several pathogenic autoantibodies in acute 
COVID-19 is comparable to that in autoimmune diseases [5]. In a small 
study of nine COVID-19 patients five had autoantibodies for at least 
seven months [6]. Interestingly, that autoantibodies were detected in 5/5 
patients with reported persistent symptoms and 2/4 without continued 
symptoms.
We established a patient registry of post-acute COVID-19 syndrome 
on 2/04/21 and as at 18/04/21 it includes 81 patients. 77,8% of patients are 
women. The mean age of patients is 44 years old (age range 11-77 years). 
79% of patients have not been hospitalized during acute infection (i.e. 
have developed post-acute COVID-19 syndrome following mild acute 
COVID-19). 74% of patients reported fatigue/extreme tiredness among 
their symptoms. While 68% of patients have reported the symptoms of 
post-acute COVID-19 syndrome immediately after the acute phase of 
infection, 38% of patients experienced temporary improvement after acute 
COVID-19 before the manifestation of post-acute COVID-19 syndrome. 
The enrollment of patients and the analysis of the registry is continuing.
Our current research project on the post-acute-COVID-19 syndrome 
consist of two phases. The first phase can be passed online by the