Unveiling the Pathological Mechanisms of Death Induced by SARS-CoV-2 Viral Pneumonia.

Abstract

In this comprehensive study of 15 deceased patients with confirmed SARS-CoV-2 infection, spanning a time frame of 1 to 68 days from confirmation to death, autopsies were meticulously conducted with stringent safety measures. Clinical, laboratory, histopathological, and molecular analyses were integrated, shedding light on diverse pulmonary lesions, including acute inflammatory changes, vascular abnormalities, and aberrant regenerative processes. Immunohistochemical analysis, utilizing various markers, successfully identified the SARS-CoV-2 nucleocapsid antigen within infected tissue cells and also revealed what type of inflammatory cells are involved in COVID-19 pathogenesis. Molecular investigations through rt-qPCR revealed the persistent presence and varying quantities of viral genes, even after 68 days. Moreover, the viral nucleocapsid was present even in patients who died after 50 days of infection onset. Employing statistical analyses such as Chi-square and phi coefficient tests, significant associations among microscopic lesions and their correlation with molecular and immunohistochemical findings were elucidated. We could draw a map of what kind of lesions were a direct consequence of viral invasion and what lesions where secondary to the acute immunological response. This integrative approach enhances our understanding of the intricate relationships between pathological features, providing valuable insights into the multifaceted landscape of COVID-19 pathogenesis.