Postmortem examination of three SARS-CoV-2-positive autopsies including histopathologic and immunohistochemical analysis

Abstract

This paper describes three autopsy cases with postmortem diagnosis of SARS-CoV-2 infection, with detailed macroscopic examination as well as advanced microscopic studies of organ tissues collected using hematoxylin-eosin stains and immunohistochemical markers. Two of the cases were admitted briefly in the County Clinical Emergency Hospital of Sibiu, and one was found deceased at his home address. All three autopsies were completed at the County morgue, in the COVID-19 restricted area, using complete protective equipment. The lungs of the patients seemed to be the center organ of invasion and pathogenesis of the novel coronavirus with diffuse areas of condensation, subpleural retraction zones but with different aspect of the classic bacterial bronchopneumonia. Microscopic evaluation revealed viral cytopathic effect of type II pneumocytes with a couple of cells that presented cytoplasmic and nuclear inclusions and who tend to form clusters mimicking multinucleated giant cells. Hyaline membranes and destruction of the alveolar wall as well as microthrombi formation within the small blood vessels were constantly found in almost all our three cases. The spleen had sustained white pulp atrophy with absence of lymphoid follicles. There were no microscopic signs of viral infection on the myocardium or the other organs.

COVID-19 and the Heart: A Systematic Review of Cardiac Autopsies

“…Twelve studies explored the presence of SARS-CoV-2 within the myocardium using different techniques ( Table 2 ) ( 8 , 9 , 17 , 19 , 23 , 24 , 29 , 30 , 39 , 41 , 44 , 48 ). In those studies, SARS-CoV-2 was detected in 50 of 105 hearts (47%).…”

“…Myocardial ischemia, thrombosis, and cardiac dilatation were the most dominant acute findings ( Figure 2 ). Prevalence of the non-specific myocardial edema (ME) was 100% in the six studies reporting it ( 6 , 15 , 19 , 35 , 44 , 45 ). The highly prevalent chronic cardiac pathologies not only reflect the impact of cardiac comorbidities but also complicated the histopathological interpretation.…”

Myocarditis is rare in COVID-19 autopsies: cardiovascular findings across 277 postmortem examinations

“…Additional COVID-19 autopsy manuscripts were identified based on the citations of these manuscripts. This resulted in 22 studies with at least two autopsies reported (Supplemental Table 1) 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 . Individual case reports were excluded.…”

Effect of mutations in the SARS-CoV-2 spike protein on protein stability, cleavage, and cell-cell fusion function

“…The S2 subunit of S mediates both viral-cell fusion and cell-cell fusion [40][41][42], with cell-cell fusion readily observed both in a laboratory setting and in the lungs of SARS-CoV-2 infected patients [40][41][42][43][44][45]. To better understand the requirements and contribution of cellular proteases to S2 mediated cell-cell fusion, we performed syncytia and reporter gene assays.…”

“…However, when S1/S2 border cleavage is blocked, viral entry can be mediated through endosomal compartments with proteolytic cleavage carried out by a member of the cathepsin family, similar to the entry pathway of SARS-CoV [10,35,[37][38][39]. In addition to promoting virus-cell fusion during viral particle entry, S can also promote cell-cell fusion, a pathogenic effect observed in the lungs of COVID-19 patients where neighboring cells fuse together to form large multi-nucleated cells, termed syncytia [40][41][42][43][44][45]. While the role of cellular proteases and S cleavage in viral entry is being extensively investigated, insight into the cleavage requirements for cell-cell fusion in SARS-CoV-2 remains more limited.…”