COVID-19 in Children: Molecular Profile and Pathological Features

Abstract

Although the World Health Organization has declared the end of the COVID-19 pandemic, doctors continue to register new cases of the disease among both adults and children. Unfortunately, the course of COVID-19 in children can have a severe form, with death being a potential outcome. The absence of published works discussing the pathological morphology of COVID-19 in children prevents the objective analysis of the disease’s pathogenesis, including among the adult population. In this vein, the objective of our study is to identify the morphological features of the lungs’ involvement and evaluate virus–host interactions in the case of COVID-19 in patients at a pediatric medical practice. We present the results of the study of the lungs of three children who died due to COVID-19, highlighting the predominant involvement of their respiratory organs at different stages of the disease (5, 21, and 50 days). This article presents data obtained from histopathological and immunohistochemical investigations, taking into account the results of clinical and laboratory indicators and intravital and postmortem SARS-CoV-2 PCR investigations. The common finding of all of the examined COVID-19 cases is the involvement of the endothelium in microcirculation vessels, which are considered to be a primary target of various pathogenic influencing factors. We also discuss both the significance of apoptosis as a result of virus–host interactions and the most likely cause of endothelium cell destruction. The results of this study could be useful for the development of endothelium-protective therapy to prevent the progression of disseminated intravascular coagulation syndrome.

Are Endomyocardial Ventricular Biopsies Useful for Assessing Myocardial Fibrosis?

“…Recently, there has been much evidence that novel coronavirus infection may damage not only the respiratory tract but also the cardiovascular system. Many authors have pointed to vascular-mediated myocardial damage in the acute period of infection with the development of hemorrhage, necrosis, and thrombosis, which will inevitably lead to the formation of foci of replacement fibrosis [ 32 , 33 , 34 , 35 , 36 , 37 ]. Moreover, in the postacute period of coronavirus infection in a part of patients, we can also see persisting damage in the myocardium, which can potentially lay the foundation for the formation of autoinflammatory diseases and promote progressive collagen deposition in the interstitium [ 38 ].…”