MECANISME PATOGENETICE ALE SINDROMULUI POST COVID

Abstract

Introducere. Patogenia sindromului Post Covid este controversată iar studiile clinice şi fundamentale necesită a fi prioritate. Analiza literaturii confirmă risc de stop cardiac, insuficienţă cardiacă, embolie pulmonară, accident vascular cerebral la bolnavii cu forme grave de Covid în anam-neza. Scop. Evidenţierea mecanismelor patogenetice ale sindromului Post Covid, pentru a determina probabilitatea consecinţelor pe termen lung şi strategiile de management, bazate pe verigile patogenetice. Materiale si metode. În procesul de cercetare a problemei sindromului Post Covid a fost revizuită literatura de specialitate disponibilă pe platformele informaţionale internaţionale precum PubMed, MedScape, Medline şi Hinari. De asemenea, au fost utilizate resursele informaţionale disponibile ale Librăriei Medicale a USMF „Nicolae Testemiţanu”. Rezultate. Au fost sugerate mai multe ipoteze pentru etiopatogenia sindromului Post Covid - cum ar fi: rezervoare persistente de SARS-CoV-2 în ţesuturi; dereglări imune cu sau fără reactivarea agenţilor patogeni subiacenţi, impactul SARS-CoV-2 asupra micro-biotei, mimetismul molecular, coagularea intravasculară a sângelui cu disfuncţie endotelială, semnalizare disfuncţion-ală în trunchiul cerebral. S-a raportat prezenţa celulelor T nefuncţionale, număr redus de celule de memorie efectoare CD4+ şi CD8+, expresie crescută a PD1 pe celulele de memorie, celule imune superactivate, lipsă de celule T şi B naive, supraexpresie de IF tip I. Concluzii. Sunt necesare studii fundamentale şi clinice pentru a elabora tratamente pentru bolnavi cu Covid lung, care ar aborda mecanismele patogenetice ipotetice, inclusiv persistenţa virală, neuroinflamaţia, hipercoagularea sângelui şi autoimunitatea ce induc şi menţin leziunile poliorganice.

Introduction. The pathogenesis of Post-COVID Syndrome is controversial, and both clinical and fundamental studies need to be prioritized. A review of the literature confirms the risk of cardiac arrest, heart failure, pulmonary embolism, stroke, and diabetes in patients with a history of severe COVID-19. Objective. Highlighting the mechanisms of post-COVID Syndrome is essential in order to determine the potential for long-term consequences and to develop strategies based on the underlying pathogenetic pathways. Materials and methods. In the research process on the issue of post-COVID Syndrome, the specialized literature available on international informational platforms such as PubMed, MedScape, Medline, and Hinari was reviewed. Additionally, the informational resources available at the Medical Library of Nicolae Testemitanu’ State University of Medicine and Pharmacy were used. Results. Several hypotheses have been suggested for the etiopathogenesis of post-COVID Syndrome, such as persistent SARS-CoV-2 reservoirs in tissues; immune dysregulation with or without reactivation of underlying pathogens; the impact of SARS-CoV-2 on the microbiota; molecular mimicry; microvascular blood coagulation with endothelial dysfunction; and dysfunctional signaling in the brainstem. Reports have indicated the presence of dysfunctional T cells, reduced numbers of CD4+ and CD8+ effector memory cells, increased PD1 expression on memory cells, hyperactivated immune cells, a lack of naive T and B cells, and overexpression of type I Interferon. Conclusions. Fundamental and clinical studies are needed to develop treatments for patients with post-COVID that would target the hypothetical pathogenetic mechanisms, including viral persistence, neuroinflammation, excessive blood coagulation, and autoimmunity, which induce and sustain multi-organ damage.